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胃癌治疗(PDQ®)

胃癌基本信息

发病率与死亡率

据估计，2015年中国胃癌新发病例和死亡病例分别为：

  • 新发病例：40.3万。
  • 死亡病例：29.1万。
    • 据估计，2020年美国胃癌新发病例与死亡病例数分别为：

  • 新发病例：27,600。
  • 死亡病例：11,010。

    • 流行病学

    胃癌的组织学类型主要为腺癌，占所有胃部恶性肿瘤的90%-95%，本总结重点讨论此类胃癌治疗。在美国，关于食管胃癌的解剖位置的流行病学模式正在发生变化。远端或非贲门部胃癌的发病率呈现出下降趋势。

    但是，在25-39岁人群中，非贲门部胃癌的发病率已经从0.27例/100,000人（1977-1981年）上升至0.45例/100,000人（2002-2006年）。

    这一特定年龄组人群中非贲门部胃癌发病率的升高仍需进一步研究证实。

    与非贲门部胃癌的发病率总体平稳趋势不同，一些更早期研究显示，贲门部胃腺癌的发病率从20世纪70年代中期至80年代后期每年递增4%-10%。

    同样，食管胃交界部腺癌发病率也有显著上升，从1.22例/100,000人（1973-1978年）上升至2.00例/100,000人（1985-1990年）。

    此后，发病率基本稳定在1.94例/100,000人（2003-2008年）。

    最新数据显示，虽然观察到胃贲门部癌发病率略有上升，但总体相对平稳，高加索人群中，发病率从2.4例/100,000人（1977-1981年）上升至2.9例/100,000人（2001-2006年）。

    但发病率出现这种暂时性变化的原因尚不明确。

    风险因素

    在美国人群常见的主要癌症中，胃癌发病率位列14。在中国人群常见的主要癌症中，胃癌发病率位居第3位。尽管胃癌的具体病因不详，但目前已知的风险因素如下：

  • 胃幽门螺旋杆菌感染。
  • 高龄。
  • 男性。
  • 新鲜果蔬摄入减少。
  • 高盐食物、烟熏食物和腌制食物的高摄入。
  • 慢性萎缩性胃炎。
  • 肠上皮化生。
  • 恶性贫血。
  • 胃腺瘤性息肉。
  • 胃癌家族史。
  • 吸烟。
  • 梅内特里耶病（巨大肥厚性胃炎）。
  • EB病毒
  • 家族性综合症（包括家族性腺瘤性息肉病）。

    • 预后与生存期

    胃癌患者的预后与肿瘤累及范围相关，包括淋巴结受累和肿瘤直接浸润穿透胃壁。

    肿瘤分级也可提供部分预后信息。

    超过50%的局限性远端胃癌可以治愈。然而在美国，诊断时分期仍为早期胃癌者只占所有胃癌病例的10%-20%。大部分患者已出现局部或远端转移灶。这些患者的总体5年生存率差异很大。已出现肿瘤扩散的患者的5年生存率几乎为零，而可切除的局部远端胃癌患者的生存率则可高达50%。对于近端胃癌患者，即使病变仍明确局限于局部，其5年生存率也仅有10%-15%。对于弥漫性病变的胃癌患者，姑息治疗可缓解症状，延长生存期，然而很少达到长期缓解。

    胃肠道间质肿瘤最常见于胃。（更多信息参见PDQ胃肠道间质肿瘤治疗总结。）

    相关总结内容

    下列其他PDQ总结中包含胃癌相关的信息：

  • 胃癌预防。
  • 胃癌筛查。
  • 儿童罕见癌症（儿童型胃癌）。

    • 参考文献

  • American Cancer Society: Cancer Facts and Figures 2020. Atlanta, Ga: American Cancer Society, 2020. Available online. Last accessed January 17, 2020.
  • Anderson WF, Camargo MC, Fraumeni JF, et al.: Age-specific trends in incidence of noncardia gastric cancer in US adults. JAMA 303 (17): 1723-8, 2010.
  • Blot WJ, Devesa SS, Kneller RW, et al.: Rising incidence of adenocarcinoma of the esophagus and gastric cardia. JAMA 265 (10): 1287-9, 1991.
  • Buas MF, Vaughan TL: Epidemiology and risk factors for gastroesophageal junction tumors: understanding the rising incidence of this disease. Semin Radiat Oncol 23 (1): 3-9, 2013.
  • Kurtz RC, Sherlock P: The diagnosis of gastric cancer. Semin Oncol 12 (1): 11-8, 1985.
  • Scheiman JM, Cutler AF: Helicobacter pylori and gastric cancer. Am J Med 106 (2): 222-6, 1999.
  • Fenoglio-Preiser CM, Noffsinger AE, Belli J, et al.: Pathologic and phenotypic features of gastric cancer. Semin Oncol 23 (3): 292-306, 1996.
  • Siewert JR, Böttcher K, Stein HJ, et al.: Relevant prognostic factors in gastric cancer: ten-year results of the German Gastric Cancer Study. Ann Surg 228 (4): 449-61, 1998.
  • Nakamura K, Ueyama T, Yao T, et al.: Pathology and prognosis of gastric carcinoma. Findings in 10,000 patients who underwent primary gastrectomy. Cancer 70 (5): 1030-7, 1992.
  • Adachi Y, Yasuda K, Inomata M, et al.: Pathology and prognosis of gastric carcinoma: well versus poorly differentiated type. Cancer 89 (7): 1418-24, 2000.
    • Gastric Cancer Treatment (PDQ®)

    General Information About Gastric Cancer

    Incidence and Mortality

    Estimated new cases and deaths from gastric cancer in the United States in 2020:

  • New cases: 27,600.
  • Deaths: 11,010.

    • Epidemiology

    Management of adenocarcinoma histology, which accounts for 90% to 95% of all gastric malignancies, is discussed in this summary. There are changing epidemiologic patterns in the United States regarding the anatomic location of esophagogastric cancers, with a trend of decreased occurrence of distal or noncardia gastric cancers.

    However, in persons aged 25 to 39 years, there has been an increase in the incidence of noncardia gastric cancers from 0.27 cases per 100,000 individuals (1977–1981) to 0.45 cases per 100,000 individuals (2002–2006).

    Additional studies are needed to confirm the observed increases in noncardia gastric cancers in this specific age group.

    In contrast to the overall stable trend for noncardia gastric cancers, earlier studies demonstrated an increased incidence of adenocarcinomas of the gastric cardia of 4% to 10% per year from the mid-1970s to the late 1980s.

    Similarly, the incidence of gastroesophageal junction adenocarcinomas increased sharply, from 1.22 cases per 100,000 individuals (1973–1978) to 2.00 cases per 100,000 individuals (1985–1990).

    Since that time, the incidence has remained steady at 1.94 cases per 100,000 individuals (2003–2008).

    More recent data demonstrate that the incidence of gastric cardia cancers has been relatively stable, although an increase has been observed, from 2.4 cases per 100,000 individuals (1977–1981) to 2.9 cases per 100,000 individuals (2001–2006) in the Caucasian population.

    The reasons for these temporal changes in incidence are unclear.

    Risk Factors

    In the United States, gastric cancer ranks 14th in incidence among the major types of cancer. While the precise etiology is unknown, acknowledged risk factors for gastric cancer include the following:

  • Helicobacter pylori gastric infection.
  • Advanced age.
  • Male gender.
  • Diet low in fruits and vegetables.
  • Diet high in salted, smoked, or preserved foods.
  • Chronic atrophic gastritis.
  • Intestinal metaplasia.
  • Pernicious anemia.
  • Gastric adenomatous polyps.
  • Family history of gastric cancer.
  • Cigarette smoking.
  • Ménétrier disease (giant hypertrophic gastritis).
  • Epstein-Barr virus.
  • Familial syndromes (including familial adenomatous polyposis).

    • Prognosis and Survival

    The prognosis of patients with gastric cancer is related to tumor extent and includes both nodal involvement and direct tumor extension beyond the gastric wall.

    Tumor grade may also provide some prognostic information.

    In localized distal gastric cancer, more than 50% of patients can be cured. However, early-stage disease accounts for only 10% to 20% of all cases diagnosed in the United States. The remaining patients present with metastatic disease in either regional or distant sites. The overall survival rate in these patients at 5 years ranges from almost no survival for patients with disseminated disease to almost 50% survival for patients with localized distal gastric cancers confined to resectable regional disease. Even with apparent localized disease, the 5-year survival rate of patients with proximal gastric cancer is only 10% to 15%. Although the treatment of patients with disseminated gastric cancer may result in palliation of symptoms and some prolongation of survival, long remissions are uncommon.

    Gastrointestinal stromal tumors occur most commonly in the stomach. (Refer to the PDQ summary on Gastrointestinal Stromal Tumors Treatment for more information.)

    Related Summaries

    Other PDQ summaries containing information related to gastric cancer include the following:

  • Stomach (Gastric) Cancer Prevention.
  • Stomach (Gastric) Cancer Screening.
  • Unusual Cancers of Childhood (childhood cancer of the stomach).

    • ReferenceSection

  • American Cancer Society: Cancer Facts and Figures 2020. Atlanta, Ga: American Cancer Society, 2020. Available online. Last accessed January 17, 2020.
  • Anderson WF, Camargo MC, Fraumeni JF, et al.: Age-specific trends in incidence of noncardia gastric cancer in US adults. JAMA 303 (17): 1723-8, 2010.
  • Blot WJ, Devesa SS, Kneller RW, et al.: Rising incidence of adenocarcinoma of the esophagus and gastric cardia. JAMA 265 (10): 1287-9, 1991.
  • Buas MF, Vaughan TL: Epidemiology and risk factors for gastroesophageal junction tumors: understanding the rising incidence of this disease. Semin Radiat Oncol 23 (1): 3-9, 2013.
  • Kurtz RC, Sherlock P: The diagnosis of gastric cancer. Semin Oncol 12 (1): 11-8, 1985.
  • Scheiman JM, Cutler AF: Helicobacter pylori and gastric cancer. Am J Med 106 (2): 222-6, 1999.
  • Fenoglio-Preiser CM, Noffsinger AE, Belli J, et al.: Pathologic and phenotypic features of gastric cancer. Semin Oncol 23 (3): 292-306, 1996.
  • Siewert JR, Böttcher K, Stein HJ, et al.: Relevant prognostic factors in gastric cancer: ten-year results of the German Gastric Cancer Study. Ann Surg 228 (4): 449-61, 1998.
  • Nakamura K, Ueyama T, Yao T, et al.: Pathology and prognosis of gastric carcinoma. Findings in 10,000 patients who underwent primary gastrectomy. Cancer 70 (5): 1030-7, 1992.
  • Adachi Y, Yasuda K, Inomata M, et al.: Pathology and prognosis of gastric carcinoma: well versus poorly differentiated type. Cancer 89 (7): 1418-24, 2000.
    • 胃癌治疗(PDQ®)

    胃癌的细胞学分类

    胃腺癌主要分为两大类：

  • 肠型。
  • 弥漫型。

    • 肠型胃腺癌分化较好，肿瘤细胞多呈管状或腺体样结构排列。肠型腺癌又分管状、乳头状和粘液性腺癌。腺鳞癌罕见。

    弥漫型胃腺癌多为低分化或未分化癌，缺乏腺体样排列。临床上，弥漫型胃腺癌可浸润整个胃壁（又称皮革胃）。

    一些肿瘤兼具有肠型与弥漫型的混合特征。

    Gastric Cancer Treatment (PDQ®)

    Cellular Classification of Gastric Cancer

    There are two major types of gastric adenocarcinoma including the following:

  • Intestinal.
  • Diffuse.

    • Intestinal adenocarcinomas are well differentiated, and the cells tend to arrange themselves in tubular or glandular structures. The terms tubular, papillary, and mucinous are assigned to the various types of intestinal adenocarcinomas. Rarely, adenosquamous cancers can occur.

    Diffuse adenocarcinomas are undifferentiated or poorly differentiated, and they lack a gland formation. Clinically, diffuse adenocarcinomas can give rise to infiltration of the gastric wall (i.e., linitis plastica).

    Some tumors can have mixed features of intestinal and diffuse types.

    胃癌治疗(PDQ®)

    胃癌分期信息

    AJCC预后分期组以及TMN分期定义

    美国癌症联合委员会（AJCC）根据TMN标准（肿瘤、结节、转移灶）对胃癌提出了特定的分期。

    分期TNM描述
    分期TNM描述
    分期TNM描述
    分期TNM描述
    分期TNM描述
    0Tis, N0, M0Tis = 原位癌：上皮内肿瘤，未侵及粘膜固有层，重度不典型增生。
    N0 = 无区域淋巴结转移。
    M0 = 无远端转移。
    分期TNM描述
    IAT1, N0, M0T1 = 肿瘤侵及粘膜固有层、粘膜肌层或粘膜下层。
    –T1a = 肿瘤侵及粘膜固有层或粘膜肌层。
    –T1b = 肿瘤侵及粘膜下层。
    N0 = 无区域淋巴结转移。
    M0 = 无远端转移。
    IBT1, N1, M0T1 = 肿瘤侵及粘膜固有层、粘膜肌层或粘膜下层。
    –T1a = 肿瘤侵及粘膜固有层或粘膜肌层。
    –T1b = 肿瘤侵及粘膜下层。
    N1 = 1或2个区域淋巴结转移。
    M0 = 无远端转移。
    T2, N0, M0
    N0 = 无区域淋巴结转移。
    M0 = 无远端转移。
    分期TNM描述
    IIAT1, N2, M0T1 = 肿瘤侵及粘膜固有层、粘膜肌层或粘膜下层。
    –T1a = 肿瘤侵及粘膜固有层或粘膜肌层。
    –T1b = 肿瘤侵及粘膜下层。
    N2 = 3-6个区域淋巴结转移。
    M0 = 无远端转移。
    T2, N1, M0
    N1 = 1或2个区域淋巴结转移。
    M0 = 无远端转移。
    T3, N0, M0
    N0 = 无区域淋巴结转移。
    M0 = 无远端转移。
    IIBT1, N3a, M0T1 = 肿瘤侵及粘膜固有层、粘膜肌层或粘膜下层。
    –T1a = 肿瘤侵及粘膜固有层或粘膜肌层。
    –T1b = 肿瘤侵及粘膜下层。
    N3a = 7-15个区域淋巴结转移。
    M0 = 无远端转移。
    T2, N2, M0
    N2 = 3-6个区域淋巴结转移。
    M0 = 无远端转移。
    T3, N1, M0
    N1 = 1或2个区域淋巴结转移。
    M0 = 无远端转移。
    T4a, N0, M0T4a = 肿瘤侵及浆膜（脏层腹膜）。
    N0 = 无区域淋巴结转移。
    M0 = 无远端转移。
    分期TNM描述
    IIIAT2, N3a, M0
    N3a = 7-15个区域淋巴结转移。
    M0 = 无远端转移。
    T3, N2, M0
    N2 = 3-6个区域淋巴结转移。
    M0 = 无远端转移。
    T4a, N1, M0T4a = 肿瘤侵及浆膜（脏层腹膜）。
    N1 = 1或2个区域淋巴结转移。
    M0 = 无远端转移。
    T4a, N2, M0 T4a = 肿瘤侵及浆膜（脏层腹膜）。
    N2 = 3-6个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N0, M0
    N0 = 无区域淋巴结转移。
    M0 = 无远端转移。
    IIIBT1, N3b, M0T1 = 肿瘤侵及粘膜固有层、粘膜肌层或粘膜下层。
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    T2, N3b, M0
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    T3, N3a, M0
    N3a = 7-15个区域淋巴结转移。
    M0 = 无远端转移。
    T4a, N3a, M0T4a = 肿瘤侵及浆膜（脏层腹膜）。
    N3a = 7-15个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N1, M0
    N1 = 1或2个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N2, M0
    N2 = 3-6个区域淋巴结转移。
    M0 = 无远端转移。
    IIICT3, N3b, M0
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    T4a, N3b, M0T4a = 肿瘤侵及浆膜（脏层腹膜）。
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N3a, M0
    N3a = 7-15个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N3b, M0
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    分期TNM描述
    IV任意T，任意N，M1TX = 原发性肿瘤无法评估。
    T0 = 无原发性肿瘤的证据。
    Tis = 原位癌：上皮内肿瘤，未侵及粘膜固有层，重度不典型增生。
    T1 = 肿瘤侵及粘膜固有层、粘膜肌层或粘膜下层。
    –T1a = 肿瘤侵及粘膜固有层或粘膜肌层。
    –T1b = 肿瘤侵及粘膜下层。
    –T4a = 肿瘤侵及浆膜（脏层腹膜）。
    –T4b = 肿瘤侵及邻近结构/器官。
    NX = 区域淋巴结无法评估。
    N0 = 无区域淋巴结转移。
    N1 = 1或2个区域淋巴结转移。
    N2 = 3-6个区域淋巴结转移。
    N3 = ≥7个区域淋巴结转移。
    –N3a = 7-15个区域淋巴结转移。
    –N3b = ≥16个区域淋巴结转移。
    M1 = 远处转移。
    T = 原发性肿瘤；N = 区域淋巴结；M = 远端转移；p = 病理性。
    a经AJCC许可转载：Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    T = 原发性肿瘤；N = 区域淋巴结；M = 远端转移；p = 病理性。
    a经AJCC许可转载：Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    b原发性肿瘤可穿透固有肌层，进入胃结肠韧带或肝胃韧带，或大网膜、小网膜，但覆盖这些结构的脏层腹膜未穿透。在这种情况下，肿瘤分期为T3。如果肿瘤穿透了覆盖胃韧带或网膜的脏层腹膜，则分期为T4。
    T = 原发性肿瘤；N = 区域淋巴结；M = 远端转移；p = 病理性。
    a经AJCC许可转载：Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    b原发性肿瘤可穿透固有肌层，进入胃结肠韧带或肝胃韧带，或大网膜、小网膜，但覆盖这些结构的脏层腹膜未穿透。在这种情况下，肿瘤分期为T3。如果肿瘤穿透了覆盖胃韧带或网膜的脏层腹膜，则分期为T4。
    c胃邻近结构包括脾脏、横结肠、肝脏、膈肌、胰腺、腹壁、肾上腺、肾、小肠、腹膜后组织。
    d壁内延伸至十二指肠或食管不视为侵袭胃邻近结构，但根据任一部位的最大侵袭深度进行分期。
    T = 原发性肿瘤；N = 区域淋巴结；M = 远端转移；p = 病理性。
    a经AJCC许可转载：Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    b原发性肿瘤可穿透固有肌层，进入胃结肠韧带或肝胃韧带，或大网膜、小网膜，但覆盖这些结构的脏层腹膜未穿透。在这种情况下，肿瘤分期为T3。如果肿瘤穿透了覆盖胃韧带或网膜的脏层腹膜，则分期为T4。
    c胃邻近结构包括脾脏、横结肠、肝脏、膈肌、胰腺、腹壁、肾上腺、肾、小肠、腹膜后组织。
    d壁内延伸至十二指肠或食管不视为侵袭胃邻近结构，但根据任一部位的最大侵袭深度进行分期。
    T = 原发性肿瘤；N = 区域淋巴结；M = 远端转移；p = 病理性。
    a经AJCC许可转载：Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    b原发性肿瘤可穿透固有肌层，进入胃结肠韧带或肝胃韧带，或大网膜、小网膜，但覆盖这些结构的脏层腹膜未穿透。在这种情况下，肿瘤分期为T3。如果肿瘤穿透了覆盖胃韧带或网膜的脏层腹膜，则分期为T4。
    c胃邻近结构包括脾脏、横结肠、肝脏、膈肌、胰腺、腹壁、肾上腺、肾、小肠、腹膜后组织。
    d壁内延伸至十二指肠或食管不视为侵袭胃邻近结构，但根据任一部位的最大侵袭深度进行分期。
    分期TNM描述
    分期TNM描述
    分期TNM描述
    分期TNM描述
    IAT1, N0, M0T1 = 肿瘤侵及粘膜固有层、粘膜肌层或粘膜下层。
    –T1a = 肿瘤侵及粘膜固有层或粘膜肌层。
    –T1b = 肿瘤侵及粘膜下层。
    N0 = 无区域淋巴结转移。
    M0 = 无远端转移。
    IBT1, N1, M0T1 = 肿瘤侵及粘膜固有层、粘膜肌层或粘膜下层。
    –T1a = 肿瘤侵及粘膜固有层或粘膜肌层。
    –T1b = 肿瘤侵及粘膜下层。
    N1 = 1或2个区域淋巴结转移。
    M0 = 无远端转移。
    T2, N0, M0
    N0 = 无区域淋巴结转移。
    M0 = 无远端转移。
    分期TNM描述
    IIAT1, N2, M0T1 = 肿瘤侵及粘膜固有层、粘膜肌层或粘膜下层。
    –T1a = 肿瘤侵及粘膜固有层或粘膜肌层。
    –T1b = 肿瘤侵及粘膜下层。
    N2 = 3-6个区域淋巴结转移。
    M0 = 无远端转移。
    T2, N1, M0
    N1 = 1或2个区域淋巴结转移。
    M0 = 无远端转移。
    T3, N0, M0
    N0 = 无区域淋巴结转移。
    M0 = 无远端转移。
    IIBT1, N3a, M0T1 = 肿瘤侵及粘膜固有层、粘膜肌层或粘膜下层。
    –T1a = 肿瘤侵及粘膜固有层或粘膜肌层。
    –T1b = 肿瘤侵及粘膜下层。
    N3a = 7-15个区域淋巴结转移。
    M0 = 无远端转移。
    T2, N2, M0
    N2 = 3-6个区域淋巴结转移。
    M0 = 无远端转移。
    T3, N1, M0
    N1 = 1或2个区域淋巴结转移。
    M0 = 无远端转移。
    T4a, N0, M0T4a = 肿瘤侵及浆膜（脏层腹膜）。
    N0 = 无区域淋巴结转移。
    M0 = 无远端转移。
    分期TNM描述
    IIIAT2, N3a, M0
    N3a = 7-15个区域淋巴结转移。
    M0 = 无远端转移。
    T3, N2, M0
    N2 = 3-6个区域淋巴结转移。
    M0 = 无远端转移。
    T4a, N1, M0T4a = 肿瘤侵及浆膜（脏层腹膜）。
    N1 = 1或2个区域淋巴结转移。
    M0 = 无远端转移。
    T4a, N2, M0 T4a = 肿瘤侵及浆膜（脏层腹膜）。
    N2 = 3-6个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N0, M0
    N0 = 无区域淋巴结转移。
    M0 = 无远端转移。
    IIIBT1, N3b, M0T1 = 肿瘤侵及粘膜固有层、粘膜肌层或粘膜下层。
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    T2, N3b, M0
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    T3, N3a, M0
    N3a = 7-15个区域淋巴结转移。
    M0 = 无远端转移。
    T4a, N3a, M0T4a = 肿瘤侵及浆膜（脏层腹膜）。
    N3a = 7-15个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N1, M0
    N1 = 1或2个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N2, M0
    N2 = 3-6个区域淋巴结转移。
    M0 = 无远端转移。
    IIICT3, N3b, M0
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    T4a, N3b, M0T4a = 肿瘤侵及浆膜（脏层腹膜）。
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N3a, M0
    N3a = 7-15个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N3b, M0
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    分期TNM描述
    IV任意T，任意N，M1TX = 原发性肿瘤无法评估。
    T0 = 无原发性肿瘤的证据。
    Tis = 原位癌：上皮内肿瘤，未侵及粘膜固有层，重度不典型增生。
    T1 = 肿瘤侵及粘膜固有层、粘膜肌层或粘膜下层。
    –T1a = 肿瘤侵及粘膜固有层或粘膜肌层。
    –T1b = 肿瘤侵及粘膜下层。
    –T4a = 肿瘤侵及浆膜（脏层腹膜）。
    –T4b = 肿瘤侵及邻近结构/器官。
    NX = 区域淋巴结无法评估。
    N0 = 无区域淋巴结转移。
    N1 = 1或2个区域淋巴结转移。
    N2 = 3-6个区域淋巴结转移。
    N3 = ≥7个区域淋巴结转移。
    –N3a = 7-15个区域淋巴结转移。
    –N3b = ≥16个区域淋巴结转移。
    M1 = 远处转移。
    T = 原发性肿瘤；N = 区域淋巴结；M = 远端转移；p = 病理性。
    a经AJCC许可转载：Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    b原发性肿瘤可穿透固有肌层，进入胃结肠韧带或肝胃韧带，或大网膜、小网膜，但覆盖这些结构的脏层腹膜未穿透。在这种情况下，肿瘤分期为T3。如果肿瘤穿透了覆盖胃韧带或网膜的脏层腹膜，则分期为T4。
    T = 原发性肿瘤；N = 区域淋巴结；M = 远端转移；p = 病理性。
    a经AJCC许可转载：Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    b原发性肿瘤可穿透固有肌层，进入胃结肠韧带或肝胃韧带，或大网膜、小网膜，但覆盖这些结构的脏层腹膜未穿透。在这种情况下，肿瘤分期为T3。如果肿瘤穿透了覆盖胃韧带或网膜的脏层腹膜，则分期为T4。
    c胃邻近结构包括脾脏、横结肠、肝脏、膈肌、胰腺、腹壁、肾上腺、肾、小肠、腹膜后组织。
    d壁内延伸至十二指肠或食管不视为侵袭胃邻近结构，但根据任一部位的最大侵袭深度进行分期。
    T = 原发性肿瘤；N = 区域淋巴结；M = 远端转移；p = 病理性。
    a经AJCC许可转载：Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    b原发性肿瘤可穿透固有肌层，进入胃结肠韧带或肝胃韧带，或大网膜、小网膜，但覆盖这些结构的脏层腹膜未穿透。在这种情况下，肿瘤分期为T3。如果肿瘤穿透了覆盖胃韧带或网膜的脏层腹膜，则分期为T4。
    c胃邻近结构包括脾脏、横结肠、肝脏、膈肌、胰腺、腹壁、肾上腺、肾、小肠、腹膜后组织。
    d壁内延伸至十二指肠或食管不视为侵袭胃邻近结构，但根据任一部位的最大侵袭深度进行分期。
    T = 原发性肿瘤；N = 区域淋巴结；M = 远端转移；p = 病理性。
    a经AJCC许可转载：Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    b原发性肿瘤可穿透固有肌层，进入胃结肠韧带或肝胃韧带，或大网膜、小网膜，但覆盖这些结构的脏层腹膜未穿透。在这种情况下，肿瘤分期为T3。如果肿瘤穿透了覆盖胃韧带或网膜的脏层腹膜，则分期为T4。
    c胃邻近结构包括脾脏、横结肠、肝脏、膈肌、胰腺、腹壁、肾上腺、肾、小肠、腹膜后组织。
    d壁内延伸至十二指肠或食管不视为侵袭胃邻近结构，但根据任一部位的最大侵袭深度进行分期。
    分期TNM描述
    分期TNM描述
    分期TNM描述
    IIAT1, N2, M0T1 = 肿瘤侵及粘膜固有层、粘膜肌层或粘膜下层。
    –T1a = 肿瘤侵及粘膜固有层或粘膜肌层。
    –T1b = 肿瘤侵及粘膜下层。
    N2 = 3-6个区域淋巴结转移。
    M0 = 无远端转移。
    T2, N1, M0
    N1 = 1或2个区域淋巴结转移。
    M0 = 无远端转移。
    T3, N0, M0
    N0 = 无区域淋巴结转移。
    M0 = 无远端转移。
    IIBT1, N3a, M0T1 = 肿瘤侵及粘膜固有层、粘膜肌层或粘膜下层。
    –T1a = 肿瘤侵及粘膜固有层或粘膜肌层。
    –T1b = 肿瘤侵及粘膜下层。
    N3a = 7-15个区域淋巴结转移。
    M0 = 无远端转移。
    T2, N2, M0
    N2 = 3-6个区域淋巴结转移。
    M0 = 无远端转移。
    T3, N1, M0
    N1 = 1或2个区域淋巴结转移。
    M0 = 无远端转移。
    T4a, N0, M0T4a = 肿瘤侵及浆膜（脏层腹膜）。
    N0 = 无区域淋巴结转移。
    M0 = 无远端转移。
    分期TNM描述
    IIIAT2, N3a, M0
    N3a = 7-15个区域淋巴结转移。
    M0 = 无远端转移。
    T3, N2, M0
    N2 = 3-6个区域淋巴结转移。
    M0 = 无远端转移。
    T4a, N1, M0T4a = 肿瘤侵及浆膜（脏层腹膜）。
    N1 = 1或2个区域淋巴结转移。
    M0 = 无远端转移。
    T4a, N2, M0 T4a = 肿瘤侵及浆膜（脏层腹膜）。
    N2 = 3-6个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N0, M0
    N0 = 无区域淋巴结转移。
    M0 = 无远端转移。
    IIIBT1, N3b, M0T1 = 肿瘤侵及粘膜固有层、粘膜肌层或粘膜下层。
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    T2, N3b, M0
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    T3, N3a, M0
    N3a = 7-15个区域淋巴结转移。
    M0 = 无远端转移。
    T4a, N3a, M0T4a = 肿瘤侵及浆膜（脏层腹膜）。
    N3a = 7-15个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N1, M0
    N1 = 1或2个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N2, M0
    N2 = 3-6个区域淋巴结转移。
    M0 = 无远端转移。
    IIICT3, N3b, M0
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    T4a, N3b, M0T4a = 肿瘤侵及浆膜（脏层腹膜）。
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N3a, M0
    N3a = 7-15个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N3b, M0
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    分期TNM描述
    IV任意T，任意N，M1TX = 原发性肿瘤无法评估。
    T0 = 无原发性肿瘤的证据。
    Tis = 原位癌：上皮内肿瘤，未侵及粘膜固有层，重度不典型增生。
    T1 = 肿瘤侵及粘膜固有层、粘膜肌层或粘膜下层。
    –T1a = 肿瘤侵及粘膜固有层或粘膜肌层。
    –T1b = 肿瘤侵及粘膜下层。
    –T4a = 肿瘤侵及浆膜（脏层腹膜）。
    –T4b = 肿瘤侵及邻近结构/器官。
    NX = 区域淋巴结无法评估。
    N0 = 无区域淋巴结转移。
    N1 = 1或2个区域淋巴结转移。
    N2 = 3-6个区域淋巴结转移。
    N3 = ≥7个区域淋巴结转移。
    –N3a = 7-15个区域淋巴结转移。
    –N3b = ≥16个区域淋巴结转移。
    M1 = 远处转移。
    T = 原发性肿瘤；N = 区域淋巴结；M = 远端转移；p = 病理性。
    a经AJCC许可转载：Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    b原发性肿瘤可穿透固有肌层，进入胃结肠韧带或肝胃韧带，或大网膜、小网膜，但覆盖这些结构的脏层腹膜未穿透。在这种情况下，肿瘤分期为T3。如果肿瘤穿透了覆盖胃韧带或网膜的脏层腹膜，则分期为T4。
    c胃邻近结构包括脾脏、横结肠、肝脏、膈肌、胰腺、腹壁、肾上腺、肾、小肠、腹膜后组织。
    d壁内延伸至十二指肠或食管不视为侵袭胃邻近结构，但根据任一部位的最大侵袭深度进行分期。
    T = 原发性肿瘤；N = 区域淋巴结；M = 远端转移；p = 病理性。
    a经AJCC许可转载：Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    b原发性肿瘤可穿透固有肌层，进入胃结肠韧带或肝胃韧带，或大网膜、小网膜，但覆盖这些结构的脏层腹膜未穿透。在这种情况下，肿瘤分期为T3。如果肿瘤穿透了覆盖胃韧带或网膜的脏层腹膜，则分期为T4。
    c胃邻近结构包括脾脏、横结肠、肝脏、膈肌、胰腺、腹壁、肾上腺、肾、小肠、腹膜后组织。
    d壁内延伸至十二指肠或食管不视为侵袭胃邻近结构，但根据任一部位的最大侵袭深度进行分期。
    T = 原发性肿瘤；N = 区域淋巴结；M = 远端转移；p = 病理性。
    a经AJCC许可转载：Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    b原发性肿瘤可穿透固有肌层，进入胃结肠韧带或肝胃韧带，或大网膜、小网膜，但覆盖这些结构的脏层腹膜未穿透。在这种情况下，肿瘤分期为T3。如果肿瘤穿透了覆盖胃韧带或网膜的脏层腹膜，则分期为T4。
    c胃邻近结构包括脾脏、横结肠、肝脏、膈肌、胰腺、腹壁、肾上腺、肾、小肠、腹膜后组织。
    d壁内延伸至十二指肠或食管不视为侵袭胃邻近结构，但根据任一部位的最大侵袭深度进行分期。
    分期TNM描述
    分期TNM描述
    IIIAT2, N3a, M0
    N3a = 7-15个区域淋巴结转移。
    M0 = 无远端转移。
    T3, N2, M0
    N2 = 3-6个区域淋巴结转移。
    M0 = 无远端转移。
    T4a, N1, M0T4a = 肿瘤侵及浆膜（脏层腹膜）。
    N1 = 1或2个区域淋巴结转移。
    M0 = 无远端转移。
    T4a, N2, M0 T4a = 肿瘤侵及浆膜（脏层腹膜）。
    N2 = 3-6个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N0, M0
    N0 = 无区域淋巴结转移。
    M0 = 无远端转移。
    IIIBT1, N3b, M0T1 = 肿瘤侵及粘膜固有层、粘膜肌层或粘膜下层。
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    T2, N3b, M0
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    T3, N3a, M0
    N3a = 7-15个区域淋巴结转移。
    M0 = 无远端转移。
    T4a, N3a, M0T4a = 肿瘤侵及浆膜（脏层腹膜）。
    N3a = 7-15个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N1, M0
    N1 = 1或2个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N2, M0
    N2 = 3-6个区域淋巴结转移。
    M0 = 无远端转移。
    IIICT3, N3b, M0
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    T4a, N3b, M0T4a = 肿瘤侵及浆膜（脏层腹膜）。
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N3a, M0
    N3a = 7-15个区域淋巴结转移。
    M0 = 无远端转移。
    T4b, N3b, M0
    N3b = ≥16个区域淋巴结转移。
    M0 = 无远端转移。
    分期TNM描述
    IV任意T，任意N，M1TX = 原发性肿瘤无法评估。
    T0 = 无原发性肿瘤的证据。
    Tis = 原位癌：上皮内肿瘤，未侵及粘膜固有层，重度不典型增生。
    T1 = 肿瘤侵及粘膜固有层、粘膜肌层或粘膜下层。
    –T1a = 肿瘤侵及粘膜固有层或粘膜肌层。
    –T1b = 肿瘤侵及粘膜下层。
    –T4a = 肿瘤侵及浆膜（脏层腹膜）。
    –T4b = 肿瘤侵及邻近结构/器官。
    NX = 区域淋巴结无法评估。
    N0 = 无区域淋巴结转移。
    N1 = 1或2个区域淋巴结转移。
    N2 = 3-6个区域淋巴结转移。
    N3 = ≥7个区域淋巴结转移。
    –N3a = 7-15个区域淋巴结转移。
    –N3b = ≥16个区域淋巴结转移。
    M1 = 远处转移。
    T = 原发性肿瘤；N = 区域淋巴结；M = 远端转移；p = 病理性。
    a经AJCC许可转载：Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    b原发性肿瘤可穿透固有肌层，进入胃结肠韧带或肝胃韧带，或大网膜、小网膜，但覆盖这些结构的脏层腹膜未穿透。在这种情况下，肿瘤分期为T3。如果肿瘤穿透了覆盖胃韧带或网膜的脏层腹膜，则分期为T4。
    c胃邻近结构包括脾脏、横结肠、肝脏、膈肌、胰腺、腹壁、肾上腺、肾、小肠、腹膜后组织。
    d壁内延伸至十二指肠或食管不视为侵袭胃邻近结构，但根据任一部位的最大侵袭深度进行分期。
    T = 原发性肿瘤；N = 区域淋巴结；M = 远端转移；p = 病理性。
    a经AJCC许可转载：Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    b原发性肿瘤可穿透固有肌层，进入胃结肠韧带或肝胃韧带，或大网膜、小网膜，但覆盖这些结构的脏层腹膜未穿透。在这种情况下，肿瘤分期为T3。如果肿瘤穿透了覆盖胃韧带或网膜的脏层腹膜，则分期为T4。
    c胃邻近结构包括脾脏、横结肠、肝脏、膈肌、胰腺、腹壁、肾上腺、肾、小肠、腹膜后组织。
    d壁内延伸至十二指肠或食管不视为侵袭胃邻近结构，但根据任一部位的最大侵袭深度进行分期。
    分期TNM描述
    IV任意T，任意N，M1TX = 原发性肿瘤无法评估。
    T0 = 无原发性肿瘤的证据。
    Tis = 原位癌：上皮内肿瘤，未侵及粘膜固有层，重度不典型增生。
    T1 = 肿瘤侵及粘膜固有层、粘膜肌层或粘膜下层。
    –T1a = 肿瘤侵及粘膜固有层或粘膜肌层。
    –T1b = 肿瘤侵及粘膜下层。
    –T4a = 肿瘤侵及浆膜（脏层腹膜）。
    –T4b = 肿瘤侵及邻近结构/器官。
    NX = 区域淋巴结无法评估。
    N0 = 无区域淋巴结转移。
    N1 = 1或2个区域淋巴结转移。
    N2 = 3-6个区域淋巴结转移。
    N3 = ≥7个区域淋巴结转移。
    –N3a = 7-15个区域淋巴结转移。
    –N3b = ≥16个区域淋巴结转移。
    M1 = 远处转移。
    T = 原发性肿瘤；N = 区域淋巴结；M = 远端转移；p = 病理性。
    a经AJCC许可转载：Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    b原发性肿瘤可穿透固有肌层，进入胃结肠韧带或肝胃韧带，或大网膜、小网膜，但覆盖这些结构的脏层腹膜未穿透。在这种情况下，肿瘤分期为T3。如果肿瘤穿透了覆盖胃韧带或网膜的脏层腹膜，则分期为T4。
    c胃邻近结构包括脾脏、横结肠、肝脏、膈肌、胰腺、腹壁、肾上腺、肾、小肠、腹膜后组织。
    d壁内延伸至十二指肠或食管不视为侵袭胃邻近结构，但根据任一部位的最大侵袭深度进行分期。

    参考文献

  • Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    • Gastric Cancer Treatment (PDQ®)

    Stage Information for Gastric Cancer

    AJCC Prognostic Stage Groups and TNM Definitions

    The American Joint Committee on Cancer (AJCC) has designated staging by TNM (tumor, node, metastasis) classification to define gastric cancer.

    StageTNMDescription
    StageTNMDescription
    StageTNMDescription
    StageTNMDescription
    StageTNMDescription
    0Tis, N0, M0Tis = Carcinoma in situ: intraepithelial tumor without invasion of the lamina propria, high-grade dysplasia.
    N0 = No regional lymph node metastasis.
    M0 = No distant metastasis.
    StageTNMDescription
    IAT1, N0, M0T1 = Tumor invades lamina propria, muscularis mucosae, or submucosa.
    –T1a = Tumor invades lamina propria or muscularis mucosae.
    –T1b = Tumor invades submucosa.
    N0 = No regional lymph node metastasis.
    M0 = No distant metastasis.
    IBT1, N1, M0T1 = Tumor invades lamina propria, muscularis mucosae, or submucosa.
    –T1a = Tumor invades lamina propria or muscularis mucosae.
    –T1b = Tumor invades submucosa.
    N1 = Metastases in 1 or 2 regional lymph nodes.
    M0 = No distant metastasis.
    T2, N0, M0
    N0 = No regional lymph node metastasis.
    M0 = No distant metastasis.
    StageTNMDescription
    IIAT1, N2, M0T1 = Tumor invades lamina propria, muscularis mucosae, or submucosa.
    –T1a = Tumor invades lamina propria or muscularis mucosae.
    –T1b = Tumor invades submucosa.
    N2 = Metastases in 3 to 6 regional lymph nodes.
    M0 = No distant metastasis.
    T2, N1, M0
    N1 = Metastases in 1 or 2 regional lymph nodes.
    M0 = No distant metastasis.
    T3, N0, M0
    N0 = No regional lymph node metastasis.
    M0 = No distant metastasis.
    IIBT1, N3a, M0T1 = Tumor invades lamina propria, muscularis mucosae, or submucosa.
    –T1a = Tumor invades lamina propria or muscularis mucosae.
    –T1b = Tumor invades submucosa.
    N3a = Metastasis in 7 to 15 regional lymph nodes.
    M0 = No distant metastasis.
    T2, N2, M0
    N2 = Metastases in 3 to 6 regional lymph nodes.
    M0 = No distant metastasis.
    T3, N1, M0
    N1 = Metastasis in 1or 2 regional lymph nodes.
    M0 = No distant metastasis.
    T4a, N0, M0T4a = Tumor invades serosa (visceral peritoneum).
    N0 = No regional lymph node metastasis.
    M0 = No distant metastasis.
    StageTNMDescription
    IIIAT2, N3a, M0
    N3a = Metastasis in 7 to 15 regional lymph nodes.
    M0 = No distant metastasis.
    T3, N2, M0
    N2 = Metastasis in 3 to 6 regional lymph nodes.
    M0 = No distant metastasis.
    T4a, N1, M0T4a = Tumor invades serosa (visceral peritoneum).
    N1 = Metastasis in 1or 2 regional lymph nodes.
    M0 = No distant metastasis.
    T4a, N2, M0 T4a = Tumor invades serosa (visceral peritoneum).
    N2 = Metastasis in 3 to 6 regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N0, M0
    N0 = No regional lymph node metastasis.
    M0 = No distant metastasis.
    IIIBT1, N3b, M0T1 = Tumor invades lamina propria, muscularis mucosae, or submucosa.
    N3b = Metastases in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    T2, N3b, M0
    N3b = Metastases in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    T3, N3a, M0
    N3a = Metastasis in 7 to 15 regional lymph nodes.
    M0 = No distant metastasis.
    T4a, N3a, M0T4a = Tumor invades serosa (visceral peritoneum).
    N3a = Metastasis in 7 to 15 regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N1, M0
    N1 = Metastasis in 1or 2 regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N2, M0
    N2 = Metastasis in 3 to 6 regional lymph nodes.
    M0 = No distant metastasis.
    IIICT3, N3b, M0
    N3b = Metastasis in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    T4a, N3b, M0T4a = Tumor invades serosa (visceral peritoneum).
    N3b = Metastasis in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N3a, M0
    N3a = Metastasis in 7 to 15 regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N3b, M0
    N3b = Metastasis in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    StageTNMDescription
    IVAny T, Any N, M1TX = Primary tumor cannot be assessed.
    T0 = No evidence of primary tumor.
    Tis = Carcinoma in situ: intraepithelial tumor without invasion of the lamina propria, high-grade dysplasia.
    T1 = Tumor invades lamina propria, muscularis mucosae, or submucosa.
    –T1a = Tumor invades lamina propria or muscularis mucosae.
    –T1b = Tumor invades submucosa.
    –T4a = Tumor invades serosa (visceral peritoneum).
    –T4b = Tumor invades adjacent structures/organs.
    NX = Regional lymph node(s) cannot be assessed.
    N0 = No regional lymph node metastasis.
    N1 = Metastases in 1 or 2 regional lymph nodes.
    N2 = Metastases in 3 to 6 regional lymph nodes.
    N3 = Metastases in ≥7 regional lymph nodes.
    –N3a = Metastases in 7 to 15 regional lymph nodes.
    –N3b = Metastases in 16 or more regional lymph nodes.
    M1 = Distant metastasis.
    T = primary tumor; N = regional lymph node; M = distant metastasis; p = pathological.
    aReprinted with permission from AJCC: Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    T = primary tumor; N = regional lymph node; M = distant metastasis; p = pathological.
    aReprinted with permission from AJCC: Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    bA tumor may penetrate the muscularis propria with extension into the gastrocolic or gastrohepatic ligaments, or into the greater or lesser omentum, without perforation of the visceral peritoneum covering these structures. In this case, the tumor is classified T3. If there is perforation of the visceral peritoneum covering the gastric ligaments or the omentum, the tumor should be classified T4.
    T = primary tumor; N = regional lymph node; M = distant metastasis; p = pathological.
    aReprinted with permission from AJCC: Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    bA tumor may penetrate the muscularis propria with extension into the gastrocolic or gastrohepatic ligaments, or into the greater or lesser omentum, without perforation of the visceral peritoneum covering these structures. In this case, the tumor is classified T3. If there is perforation of the visceral peritoneum covering the gastric ligaments or the omentum, the tumor should be classified T4.
    cThe adjacent structures of the stomach include the spleen, transverse colon, liver, diaphragm, pancreas, abdominal wall, adrenal gland, kidney, small intestine, and retroperitoneum.
    dIntramural extension to the duodenum or esophagus is not considered invasion of an adjacent structure, but is classified using the depth of the greatest invasion in any of these sites.
    T = primary tumor; N = regional lymph node; M = distant metastasis; p = pathological.
    aReprinted with permission from AJCC: Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    bA tumor may penetrate the muscularis propria with extension into the gastrocolic or gastrohepatic ligaments, or into the greater or lesser omentum, without perforation of the visceral peritoneum covering these structures. In this case, the tumor is classified T3. If there is perforation of the visceral peritoneum covering the gastric ligaments or the omentum, the tumor should be classified T4.
    cThe adjacent structures of the stomach include the spleen, transverse colon, liver, diaphragm, pancreas, abdominal wall, adrenal gland, kidney, small intestine, and retroperitoneum.
    dIntramural extension to the duodenum or esophagus is not considered invasion of an adjacent structure, but is classified using the depth of the greatest invasion in any of these sites.
    T = primary tumor; N = regional lymph node; M = distant metastasis; p = pathological.
    aReprinted with permission from AJCC: Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    bA tumor may penetrate the muscularis propria with extension into the gastrocolic or gastrohepatic ligaments, or into the greater or lesser omentum, without perforation of the visceral peritoneum covering these structures. In this case, the tumor is classified T3. If there is perforation of the visceral peritoneum covering the gastric ligaments or the omentum, the tumor should be classified T4.
    cThe adjacent structures of the stomach include the spleen, transverse colon, liver, diaphragm, pancreas, abdominal wall, adrenal gland, kidney, small intestine, and retroperitoneum.
    dIntramural extension to the duodenum or esophagus is not considered invasion of an adjacent structure, but is classified using the depth of the greatest invasion in any of these sites.
    StageTNMDescription
    StageTNMDescription
    StageTNMDescription
    StageTNMDescription
    IAT1, N0, M0T1 = Tumor invades lamina propria, muscularis mucosae, or submucosa.
    –T1a = Tumor invades lamina propria or muscularis mucosae.
    –T1b = Tumor invades submucosa.
    N0 = No regional lymph node metastasis.
    M0 = No distant metastasis.
    IBT1, N1, M0T1 = Tumor invades lamina propria, muscularis mucosae, or submucosa.
    –T1a = Tumor invades lamina propria or muscularis mucosae.
    –T1b = Tumor invades submucosa.
    N1 = Metastases in 1 or 2 regional lymph nodes.
    M0 = No distant metastasis.
    T2, N0, M0
    N0 = No regional lymph node metastasis.
    M0 = No distant metastasis.
    StageTNMDescription
    IIAT1, N2, M0T1 = Tumor invades lamina propria, muscularis mucosae, or submucosa.
    –T1a = Tumor invades lamina propria or muscularis mucosae.
    –T1b = Tumor invades submucosa.
    N2 = Metastases in 3 to 6 regional lymph nodes.
    M0 = No distant metastasis.
    T2, N1, M0
    N1 = Metastases in 1 or 2 regional lymph nodes.
    M0 = No distant metastasis.
    T3, N0, M0
    N0 = No regional lymph node metastasis.
    M0 = No distant metastasis.
    IIBT1, N3a, M0T1 = Tumor invades lamina propria, muscularis mucosae, or submucosa.
    –T1a = Tumor invades lamina propria or muscularis mucosae.
    –T1b = Tumor invades submucosa.
    N3a = Metastasis in 7 to 15 regional lymph nodes.
    M0 = No distant metastasis.
    T2, N2, M0
    N2 = Metastases in 3 to 6 regional lymph nodes.
    M0 = No distant metastasis.
    T3, N1, M0
    N1 = Metastasis in 1or 2 regional lymph nodes.
    M0 = No distant metastasis.
    T4a, N0, M0T4a = Tumor invades serosa (visceral peritoneum).
    N0 = No regional lymph node metastasis.
    M0 = No distant metastasis.
    StageTNMDescription
    IIIAT2, N3a, M0
    N3a = Metastasis in 7 to 15 regional lymph nodes.
    M0 = No distant metastasis.
    T3, N2, M0
    N2 = Metastasis in 3 to 6 regional lymph nodes.
    M0 = No distant metastasis.
    T4a, N1, M0T4a = Tumor invades serosa (visceral peritoneum).
    N1 = Metastasis in 1or 2 regional lymph nodes.
    M0 = No distant metastasis.
    T4a, N2, M0 T4a = Tumor invades serosa (visceral peritoneum).
    N2 = Metastasis in 3 to 6 regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N0, M0
    N0 = No regional lymph node metastasis.
    M0 = No distant metastasis.
    IIIBT1, N3b, M0T1 = Tumor invades lamina propria, muscularis mucosae, or submucosa.
    N3b = Metastases in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    T2, N3b, M0
    N3b = Metastases in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    T3, N3a, M0
    N3a = Metastasis in 7 to 15 regional lymph nodes.
    M0 = No distant metastasis.
    T4a, N3a, M0T4a = Tumor invades serosa (visceral peritoneum).
    N3a = Metastasis in 7 to 15 regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N1, M0
    N1 = Metastasis in 1or 2 regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N2, M0
    N2 = Metastasis in 3 to 6 regional lymph nodes.
    M0 = No distant metastasis.
    IIICT3, N3b, M0
    N3b = Metastasis in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    T4a, N3b, M0T4a = Tumor invades serosa (visceral peritoneum).
    N3b = Metastasis in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N3a, M0
    N3a = Metastasis in 7 to 15 regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N3b, M0
    N3b = Metastasis in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    StageTNMDescription
    IVAny T, Any N, M1TX = Primary tumor cannot be assessed.
    T0 = No evidence of primary tumor.
    Tis = Carcinoma in situ: intraepithelial tumor without invasion of the lamina propria, high-grade dysplasia.
    T1 = Tumor invades lamina propria, muscularis mucosae, or submucosa.
    –T1a = Tumor invades lamina propria or muscularis mucosae.
    –T1b = Tumor invades submucosa.
    –T4a = Tumor invades serosa (visceral peritoneum).
    –T4b = Tumor invades adjacent structures/organs.
    NX = Regional lymph node(s) cannot be assessed.
    N0 = No regional lymph node metastasis.
    N1 = Metastases in 1 or 2 regional lymph nodes.
    N2 = Metastases in 3 to 6 regional lymph nodes.
    N3 = Metastases in ≥7 regional lymph nodes.
    –N3a = Metastases in 7 to 15 regional lymph nodes.
    –N3b = Metastases in 16 or more regional lymph nodes.
    M1 = Distant metastasis.
    T = primary tumor; N = regional lymph node; M = distant metastasis; p = pathological.
    aReprinted with permission from AJCC: Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    bA tumor may penetrate the muscularis propria with extension into the gastrocolic or gastrohepatic ligaments, or into the greater or lesser omentum, without perforation of the visceral peritoneum covering these structures. In this case, the tumor is classified T3. If there is perforation of the visceral peritoneum covering the gastric ligaments or the omentum, the tumor should be classified T4.
    T = primary tumor; N = regional lymph node; M = distant metastasis; p = pathological.
    aReprinted with permission from AJCC: Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    bA tumor may penetrate the muscularis propria with extension into the gastrocolic or gastrohepatic ligaments, or into the greater or lesser omentum, without perforation of the visceral peritoneum covering these structures. In this case, the tumor is classified T3. If there is perforation of the visceral peritoneum covering the gastric ligaments or the omentum, the tumor should be classified T4.
    cThe adjacent structures of the stomach include the spleen, transverse colon, liver, diaphragm, pancreas, abdominal wall, adrenal gland, kidney, small intestine, and retroperitoneum.
    dIntramural extension to the duodenum or esophagus is not considered invasion of an adjacent structure, but is classified using the depth of the greatest invasion in any of these sites.
    T = primary tumor; N = regional lymph node; M = distant metastasis; p = pathological.
    aReprinted with permission from AJCC: Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    bA tumor may penetrate the muscularis propria with extension into the gastrocolic or gastrohepatic ligaments, or into the greater or lesser omentum, without perforation of the visceral peritoneum covering these structures. In this case, the tumor is classified T3. If there is perforation of the visceral peritoneum covering the gastric ligaments or the omentum, the tumor should be classified T4.
    cThe adjacent structures of the stomach include the spleen, transverse colon, liver, diaphragm, pancreas, abdominal wall, adrenal gland, kidney, small intestine, and retroperitoneum.
    dIntramural extension to the duodenum or esophagus is not considered invasion of an adjacent structure, but is classified using the depth of the greatest invasion in any of these sites.
    T = primary tumor; N = regional lymph node; M = distant metastasis; p = pathological.
    aReprinted with permission from AJCC: Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    bA tumor may penetrate the muscularis propria with extension into the gastrocolic or gastrohepatic ligaments, or into the greater or lesser omentum, without perforation of the visceral peritoneum covering these structures. In this case, the tumor is classified T3. If there is perforation of the visceral peritoneum covering the gastric ligaments or the omentum, the tumor should be classified T4.
    cThe adjacent structures of the stomach include the spleen, transverse colon, liver, diaphragm, pancreas, abdominal wall, adrenal gland, kidney, small intestine, and retroperitoneum.
    dIntramural extension to the duodenum or esophagus is not considered invasion of an adjacent structure, but is classified using the depth of the greatest invasion in any of these sites.
    StageTNMDescription
    StageTNMDescription
    StageTNMDescription
    IIAT1, N2, M0T1 = Tumor invades lamina propria, muscularis mucosae, or submucosa.
    –T1a = Tumor invades lamina propria or muscularis mucosae.
    –T1b = Tumor invades submucosa.
    N2 = Metastases in 3 to 6 regional lymph nodes.
    M0 = No distant metastasis.
    T2, N1, M0
    N1 = Metastases in 1 or 2 regional lymph nodes.
    M0 = No distant metastasis.
    T3, N0, M0
    N0 = No regional lymph node metastasis.
    M0 = No distant metastasis.
    IIBT1, N3a, M0T1 = Tumor invades lamina propria, muscularis mucosae, or submucosa.
    –T1a = Tumor invades lamina propria or muscularis mucosae.
    –T1b = Tumor invades submucosa.
    N3a = Metastasis in 7 to 15 regional lymph nodes.
    M0 = No distant metastasis.
    T2, N2, M0
    N2 = Metastases in 3 to 6 regional lymph nodes.
    M0 = No distant metastasis.
    T3, N1, M0
    N1 = Metastasis in 1or 2 regional lymph nodes.
    M0 = No distant metastasis.
    T4a, N0, M0T4a = Tumor invades serosa (visceral peritoneum).
    N0 = No regional lymph node metastasis.
    M0 = No distant metastasis.
    StageTNMDescription
    IIIAT2, N3a, M0
    N3a = Metastasis in 7 to 15 regional lymph nodes.
    M0 = No distant metastasis.
    T3, N2, M0
    N2 = Metastasis in 3 to 6 regional lymph nodes.
    M0 = No distant metastasis.
    T4a, N1, M0T4a = Tumor invades serosa (visceral peritoneum).
    N1 = Metastasis in 1or 2 regional lymph nodes.
    M0 = No distant metastasis.
    T4a, N2, M0 T4a = Tumor invades serosa (visceral peritoneum).
    N2 = Metastasis in 3 to 6 regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N0, M0
    N0 = No regional lymph node metastasis.
    M0 = No distant metastasis.
    IIIBT1, N3b, M0T1 = Tumor invades lamina propria, muscularis mucosae, or submucosa.
    N3b = Metastases in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    T2, N3b, M0
    N3b = Metastases in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    T3, N3a, M0
    N3a = Metastasis in 7 to 15 regional lymph nodes.
    M0 = No distant metastasis.
    T4a, N3a, M0T4a = Tumor invades serosa (visceral peritoneum).
    N3a = Metastasis in 7 to 15 regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N1, M0
    N1 = Metastasis in 1or 2 regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N2, M0
    N2 = Metastasis in 3 to 6 regional lymph nodes.
    M0 = No distant metastasis.
    IIICT3, N3b, M0
    N3b = Metastasis in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    T4a, N3b, M0T4a = Tumor invades serosa (visceral peritoneum).
    N3b = Metastasis in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N3a, M0
    N3a = Metastasis in 7 to 15 regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N3b, M0
    N3b = Metastasis in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    StageTNMDescription
    IVAny T, Any N, M1TX = Primary tumor cannot be assessed.
    T0 = No evidence of primary tumor.
    Tis = Carcinoma in situ: intraepithelial tumor without invasion of the lamina propria, high-grade dysplasia.
    T1 = Tumor invades lamina propria, muscularis mucosae, or submucosa.
    –T1a = Tumor invades lamina propria or muscularis mucosae.
    –T1b = Tumor invades submucosa.
    –T4a = Tumor invades serosa (visceral peritoneum).
    –T4b = Tumor invades adjacent structures/organs.
    NX = Regional lymph node(s) cannot be assessed.
    N0 = No regional lymph node metastasis.
    N1 = Metastases in 1 or 2 regional lymph nodes.
    N2 = Metastases in 3 to 6 regional lymph nodes.
    N3 = Metastases in ≥7 regional lymph nodes.
    –N3a = Metastases in 7 to 15 regional lymph nodes.
    –N3b = Metastases in 16 or more regional lymph nodes.
    M1 = Distant metastasis.
    T = primary tumor; N = regional lymph node; M = distant metastasis; p = pathological.
    aReprinted with permission from AJCC: Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    bA tumor may penetrate the muscularis propria with extension into the gastrocolic or gastrohepatic ligaments, or into the greater or lesser omentum, without perforation of the visceral peritoneum covering these structures. In this case, the tumor is classified T3. If there is perforation of the visceral peritoneum covering the gastric ligaments or the omentum, the tumor should be classified T4.
    cThe adjacent structures of the stomach include the spleen, transverse colon, liver, diaphragm, pancreas, abdominal wall, adrenal gland, kidney, small intestine, and retroperitoneum.
    dIntramural extension to the duodenum or esophagus is not considered invasion of an adjacent structure, but is classified using the depth of the greatest invasion in any of these sites.
    T = primary tumor; N = regional lymph node; M = distant metastasis; p = pathological.
    aReprinted with permission from AJCC: Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    bA tumor may penetrate the muscularis propria with extension into the gastrocolic or gastrohepatic ligaments, or into the greater or lesser omentum, without perforation of the visceral peritoneum covering these structures. In this case, the tumor is classified T3. If there is perforation of the visceral peritoneum covering the gastric ligaments or the omentum, the tumor should be classified T4.
    cThe adjacent structures of the stomach include the spleen, transverse colon, liver, diaphragm, pancreas, abdominal wall, adrenal gland, kidney, small intestine, and retroperitoneum.
    dIntramural extension to the duodenum or esophagus is not considered invasion of an adjacent structure, but is classified using the depth of the greatest invasion in any of these sites.
    T = primary tumor; N = regional lymph node; M = distant metastasis; p = pathological.
    aReprinted with permission from AJCC: Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    bA tumor may penetrate the muscularis propria with extension into the gastrocolic or gastrohepatic ligaments, or into the greater or lesser omentum, without perforation of the visceral peritoneum covering these structures. In this case, the tumor is classified T3. If there is perforation of the visceral peritoneum covering the gastric ligaments or the omentum, the tumor should be classified T4.
    cThe adjacent structures of the stomach include the spleen, transverse colon, liver, diaphragm, pancreas, abdominal wall, adrenal gland, kidney, small intestine, and retroperitoneum.
    dIntramural extension to the duodenum or esophagus is not considered invasion of an adjacent structure, but is classified using the depth of the greatest invasion in any of these sites.
    StageTNMDescription
    StageTNMDescription
    IIIAT2, N3a, M0
    N3a = Metastasis in 7 to 15 regional lymph nodes.
    M0 = No distant metastasis.
    T3, N2, M0
    N2 = Metastasis in 3 to 6 regional lymph nodes.
    M0 = No distant metastasis.
    T4a, N1, M0T4a = Tumor invades serosa (visceral peritoneum).
    N1 = Metastasis in 1or 2 regional lymph nodes.
    M0 = No distant metastasis.
    T4a, N2, M0 T4a = Tumor invades serosa (visceral peritoneum).
    N2 = Metastasis in 3 to 6 regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N0, M0
    N0 = No regional lymph node metastasis.
    M0 = No distant metastasis.
    IIIBT1, N3b, M0T1 = Tumor invades lamina propria, muscularis mucosae, or submucosa.
    N3b = Metastases in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    T2, N3b, M0
    N3b = Metastases in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    T3, N3a, M0
    N3a = Metastasis in 7 to 15 regional lymph nodes.
    M0 = No distant metastasis.
    T4a, N3a, M0T4a = Tumor invades serosa (visceral peritoneum).
    N3a = Metastasis in 7 to 15 regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N1, M0
    N1 = Metastasis in 1or 2 regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N2, M0
    N2 = Metastasis in 3 to 6 regional lymph nodes.
    M0 = No distant metastasis.
    IIICT3, N3b, M0
    N3b = Metastasis in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    T4a, N3b, M0T4a = Tumor invades serosa (visceral peritoneum).
    N3b = Metastasis in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N3a, M0
    N3a = Metastasis in 7 to 15 regional lymph nodes.
    M0 = No distant metastasis.
    T4b, N3b, M0
    N3b = Metastasis in 16 or more regional lymph nodes.
    M0 = No distant metastasis.
    StageTNMDescription
    IVAny T, Any N, M1TX = Primary tumor cannot be assessed.
    T0 = No evidence of primary tumor.
    Tis = Carcinoma in situ: intraepithelial tumor without invasion of the lamina propria, high-grade dysplasia.
    T1 = Tumor invades lamina propria, muscularis mucosae, or submucosa.
    –T1a = Tumor invades lamina propria or muscularis mucosae.
    –T1b = Tumor invades submucosa.
    –T4a = Tumor invades serosa (visceral peritoneum).
    –T4b = Tumor invades adjacent structures/organs.
    NX = Regional lymph node(s) cannot be assessed.
    N0 = No regional lymph node metastasis.
    N1 = Metastases in 1 or 2 regional lymph nodes.
    N2 = Metastases in 3 to 6 regional lymph nodes.
    N3 = Metastases in ≥7 regional lymph nodes.
    –N3a = Metastases in 7 to 15 regional lymph nodes.
    –N3b = Metastases in 16 or more regional lymph nodes.
    M1 = Distant metastasis.
    T = primary tumor; N = regional lymph node; M = distant metastasis; p = pathological.
    aReprinted with permission from AJCC: Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    bA tumor may penetrate the muscularis propria with extension into the gastrocolic or gastrohepatic ligaments, or into the greater or lesser omentum, without perforation of the visceral peritoneum covering these structures. In this case, the tumor is classified T3. If there is perforation of the visceral peritoneum covering the gastric ligaments or the omentum, the tumor should be classified T4.
    cThe adjacent structures of the stomach include the spleen, transverse colon, liver, diaphragm, pancreas, abdominal wall, adrenal gland, kidney, small intestine, and retroperitoneum.
    dIntramural extension to the duodenum or esophagus is not considered invasion of an adjacent structure, but is classified using the depth of the greatest invasion in any of these sites.
    T = primary tumor; N = regional lymph node; M = distant metastasis; p = pathological.
    aReprinted with permission from AJCC: Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    bA tumor may penetrate the muscularis propria with extension into the gastrocolic or gastrohepatic ligaments, or into the greater or lesser omentum, without perforation of the visceral peritoneum covering these structures. In this case, the tumor is classified T3. If there is perforation of the visceral peritoneum covering the gastric ligaments or the omentum, the tumor should be classified T4.
    cThe adjacent structures of the stomach include the spleen, transverse colon, liver, diaphragm, pancreas, abdominal wall, adrenal gland, kidney, small intestine, and retroperitoneum.
    dIntramural extension to the duodenum or esophagus is not considered invasion of an adjacent structure, but is classified using the depth of the greatest invasion in any of these sites.
    StageTNMDescription
    IVAny T, Any N, M1TX = Primary tumor cannot be assessed.
    T0 = No evidence of primary tumor.
    Tis = Carcinoma in situ: intraepithelial tumor without invasion of the lamina propria, high-grade dysplasia.
    T1 = Tumor invades lamina propria, muscularis mucosae, or submucosa.
    –T1a = Tumor invades lamina propria or muscularis mucosae.
    –T1b = Tumor invades submucosa.
    –T4a = Tumor invades serosa (visceral peritoneum).
    –T4b = Tumor invades adjacent structures/organs.
    NX = Regional lymph node(s) cannot be assessed.
    N0 = No regional lymph node metastasis.
    N1 = Metastases in 1 or 2 regional lymph nodes.
    N2 = Metastases in 3 to 6 regional lymph nodes.
    N3 = Metastases in ≥7 regional lymph nodes.
    –N3a = Metastases in 7 to 15 regional lymph nodes.
    –N3b = Metastases in 16 or more regional lymph nodes.
    M1 = Distant metastasis.
    T = primary tumor; N = regional lymph node; M = distant metastasis; p = pathological.
    aReprinted with permission from AJCC: Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    bA tumor may penetrate the muscularis propria with extension into the gastrocolic or gastrohepatic ligaments, or into the greater or lesser omentum, without perforation of the visceral peritoneum covering these structures. In this case, the tumor is classified T3. If there is perforation of the visceral peritoneum covering the gastric ligaments or the omentum, the tumor should be classified T4.
    cThe adjacent structures of the stomach include the spleen, transverse colon, liver, diaphragm, pancreas, abdominal wall, adrenal gland, kidney, small intestine, and retroperitoneum.
    dIntramural extension to the duodenum or esophagus is not considered invasion of an adjacent structure, but is classified using the depth of the greatest invasion in any of these sites.

    ReferenceSection

  • Stomach. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp. 203–20.
    • 胃癌治疗(PDQ®)

    治疗方案概述

    根治性手术是实现治愈目标的标准治疗方法。但是，由于肿瘤床复发或区域淋巴结转移而引起的局部治疗失败，以及由于血行转移或腹膜种植转移而引起的远处治疗失败，其发生率仍居高不下。

    因此，应考虑由多学科团队进行全面的分期并评估，以确定新辅助、围手术期和辅助联合化疗、手术和外照射放疗的疗效。

    一些欧洲研究者评估了单独使用围手术期化疗且不进行放疗的疗效。

    首先，在一项III期随机临床试验（MRC-ST02 [NCT00002615]）中，将患II期及以上胃腺癌、食管下段三分之一腺癌患者随机分配至两组，一组在手术前后接受3个疗程的表柔比星、顺铂并连续注射5-氟尿嘧啶（5-FU）（ECF）治疗，另一组接受单独手术治疗。与手术组相比，接受围手术期化疗组患者总生存率（OS）显著提高（死亡风险比[HR]，0.75；95%置信区间[CI]：0.60-0.93；P = 0.009）。

    [证据等级：1iiA]

    另外，在随机III期AIO-FLOT4临床试验（NCT01216644）中，T2期或以上和/或淋巴结阳性的可切除病灶患者接受了围手术期表柔比星、顺铂和5-FU或卡培他滨（ECF / ECX）（手术前、后各三个疗程）或围手术期多西他赛、奥沙利铂和5-FU /亚叶酸（FLOT）（手术前、后各四个疗程，每个疗程为两周）。OS显著增加，从35个月（接受ECF / ECX）增加到50个月（接受FLOT）（HR，0.77；95％CI，0.63-0.94；P = 0.012）。

    在一项III期组间临床试验（SWOG-9008 [NCT01197118]）中，将559例患IB至IV（M0）期胃和食管胃交界部可切除腺癌的患者随机分配至两组，一组接受单独手术治疗，另一组接受手术联合术后化疗（5-FU与亚叶酸）和同步放疗（45Gy）。中位随访时间超过10年时，接受辅助联合治疗的患者的生存期明显延长。

    [证据等级：1iiA]辅助放化疗组的中位OS为35个月，单独手术组则为27个月（P=0.0046）。放化疗组的无复发中位生存期为27个月，而单独手术组为19个月（P < 0.001）。

    参考文献

  • Gunderson LL, Sosin H: Adenocarcinoma of the stomach: areas of failure in a re-operation series (second or symptomatic look) clinicopathologic correlation and implications for adjuvant therapy. Int J Radiat Oncol Biol Phys 8 (1): 1-11, 1982.
  • Cunningham D, Allum WH, Stenning SP, et al.: Perioperative chemotherapy versus surgery alone for resectable gastroesophageal cancer. N Engl J Med 355 (1): 11-20, 2006.
  • Al-Batran SE, Homann N, Pauligk C, et al.: Perioperative chemotherapy with fluorouracil plus leucovorin, oxaliplatin, and docetaxel versus fluorouracil or capecitabine plus cisplatin and epirubicin for locally advanced, resectable gastric or gastro-oesophageal junction adenocarcinoma (FLOT4): a randomised, phase 2/3 trial. Lancet 393 (10184): 1948-1957, 2019.
  • Smalley SR, Benedetti JK, Haller DG, et al.: Updated analysis of SWOG-directed intergroup study 0116: a phase III trial of adjuvant radiochemotherapy versus observation after curative gastric cancer resection. J Clin Oncol 30 (19): 2327-33, 2012.
    • Gastric Cancer Treatment (PDQ®)

    Treatment Option Overview

    Radical surgery represents the standard form of therapy that has curative intent. However, the incidences of local failure in the tumor bed and regional lymph nodes, and distant failures via hematogenous or peritoneal routes, remain high.

    As such, comprehensive staging and evaluation with a multidisciplinary team to determine roles of neoadjuvant, perioperative, and adjuvant combination chemotherapy, surgery, and external-beam radiation therapies should be considered.

    Investigators in Europe evaluated the role of perioperative chemotherapy without radiation therapy.

    Initially, in a randomized phase III trial (MRC-ST02 [NCT00002615]), patients with stage II or higher adenocarcinoma of the stomach or of the lower third of the esophagus were assigned to receive three cycles of epirubicin, cisplatin, and continuous infusion 5-fluorouracil (5-FU) (ECF) before and after surgery or to receive surgery alone. Compared with the surgery group, the perioperative chemotherapy group had a significantly higher overall survival (OS) (hazard ratio [HR]death, 0.75; 95% confidence interval [CI], 0.60–0.93; P = .009).

    [Level of evidence: 1iiA]

    In addition, in the randomized phase III AIO-FLOT4 trial (NCT01216644), patients with resectable disease that was stage T2 or higher and/or node positive received either perioperative epirubicin, cisplatin, and 5-FU or capecitabine (ECF/ECX) (three cycles before and after surgery) or perioperative docetaxel, oxaliplatin, and 5-FU/leucovorin (FLOT) (four 2-week cycles before and after surgery). OS was significantly increased from 35 months with ECF/ECX to 50 months with FLOT (HR, 0.77; 95% CI, 0.63–0.94; P = .012).

    In a phase III Intergroup trial (SWOG-9008 [NCT01197118]), 559 patients with completely resected stage IB to stage IV (M0) adenocarcinoma of the stomach and gastroesophageal junction were randomly assigned to receive either surgery alone or surgery plus postoperative chemotherapy (5-FU and leucovorin) and concurrent radiation therapy (45 Gy). With a median follow-up of more than 10 years, a significant survival benefit was reported for patients who received adjuvant combined modality therapy.

    [Level of evidence: 1iiA] Median OS was 35 months for the adjuvant chemoradiation therapy group and 27 months for the surgery-alone arm (P = .0046). Median relapse-free survival was 27 months in the chemoradiation arm compared with 19 months in the surgery-alone arm (P < .001).

    ReferenceSection

  • Gunderson LL, Sosin H: Adenocarcinoma of the stomach: areas of failure in a re-operation series (second or symptomatic look) clinicopathologic correlation and implications for adjuvant therapy. Int J Radiat Oncol Biol Phys 8 (1): 1-11, 1982.
  • Cunningham D, Allum WH, Stenning SP, et al.: Perioperative chemotherapy versus surgery alone for resectable gastroesophageal cancer. N Engl J Med 355 (1): 11-20, 2006.
  • Al-Batran SE, Homann N, Pauligk C, et al.: Perioperative chemotherapy with fluorouracil plus leucovorin, oxaliplatin, and docetaxel versus fluorouracil or capecitabine plus cisplatin and epirubicin for locally advanced, resectable gastric or gastro-oesophageal junction adenocarcinoma (FLOT4): a randomised, phase 2/3 trial. Lancet 393 (10184): 1948-1957, 2019.
  • Smalley SR, Benedetti JK, Haller DG, et al.: Updated analysis of SWOG-directed intergroup study 0116: a phase III trial of adjuvant radiochemotherapy versus observation after curative gastric cancer resection. J Clin Oncol 30 (19): 2327-33, 2012.
    • 胃癌治疗(PDQ®)

    0期胃癌

    0期胃癌的标准治疗方案

    0期胃癌的标准治疗方案包括以下：

  • 手术。
  • 内镜黏膜切除术（EMR）。

    • 手术

    0期胃癌指局限于粘膜层的胃癌。日本的0期胃癌临床诊断经验表明，接受胃切除术与淋巴结清扫术后，患者的5年生存率可达90%以上。一项美国的系列临床研究亦证实了上述结果。

    内镜黏膜切除术（EMR）

    在日本和整个亚洲，已在具有良好风险特征（Tis或T1a，直径≤2 cm，主要为分化型，无溃疡）且淋巴结转移风险较低的早期肿瘤患者中进行了EMR研究。黏膜内肿瘤发生淋巴结转移的风险低于黏膜下肿瘤。

    应考虑根据上述标准严格筛选患者，由经验丰富的内镜医师进行治疗，并进行密切监测。

    证据（EMR）：

  • 一项EMR前瞻性试验纳入了1987年至1998年在东京接受治疗的445例粘膜内癌患者（共479个肿瘤）。对于具有黏膜下浸润、血管受累和（或）切缘阳性证据的患者，建议完全切除肿瘤。在405例粘膜内病变患者中，278例接受了完全切除，2%局部复发患者接受了根治性治疗，中位随访时间为38个月时无病生存率达100%。在不完全切除/切除情况无法评价的患者中，127例患者中18例出现局部复发，随之行根治性手术。
  • [证据等级：3iiiDii]

    • 当前临床试验

    使用高级临床试验检索工具查找NCI支持的癌症临床试验（当前正在招募患者）。可通过试验地点、治疗类型、药物名称和其他标准缩小检索范围。还可获得关于临床试验的基本信息。

    参考文献

  • Green PH, O'Toole KM, Slonim D, et al.: Increasing incidence and excellent survival of patients with early gastric cancer: experience in a United States medical center. Am J Med 85 (5): 658-61, 1988.
  • Japanese Gastric Cancer Association: Japanese gastric cancer treatment guidelines 2014 (ver. 4). Gastric Cancer 20 (1): 1-19, 2017.
  • Ono H, Kondo H, Gotoda T, et al.: Endoscopic mucosal resection for treatment of early gastric cancer. Gut 48 (2): 225-9, 2001.
    • Gastric Cancer Treatment (PDQ®)

    Stage 0 Gastric Cancer

    Standard Treatment Options for Stage 0 Gastric Cancer

    Standard treatment options for stage 0 gastric cancer include the following:

  • Surgery.
  • Endoscopic mucosal resection (EMR).

    • Surgery

    Stage 0 is gastric cancer confined to mucosa. Experience in Japan, where stage 0 is diagnosed frequently, indicates that more than 90% of patients treated by gastrectomy with lymphadenectomy will survive beyond 5 years. An American series has confirmed these results.

    Endoscopic mucosal resection (EMR)

    EMR has been studied in Japan and throughout Asia in patients with early-stage tumors with good-risk features (Tis or T1a, diameter ≤2 cm, predominantly differentiated type, without ulcerative findings) that have a lower risk of nodal metastasis. Intramucosal tumors have a lower risk of nodal metastasis than submucosal tumors.

    Careful patient selection by the above criteria, treatment with an experienced endoscopist, and close surveillance should be considered.

    Evidence (EMR):

  • A prospective trial of EMR included 445 patients with intramucosal carcinoma (a total of 479 tumors) treated in Tokyo between 1987 and 1998. Complete resection was recommended for patients with evidence of submucosal invasion, blood vessel involvement, and/or positive margins. Of the 405 patients with intramucosal disease, 278 underwent complete resection, with 2% local recurrence treated with curative intent and 100% disease-free survival at a median follow-up of 38 months. In those with incomplete/inevaluable resections, 18 of 127 patients recurred locally and underwent curative surgery.
  • [Level of evidence: 3iiiDii]

    • Current Clinical Trials

    Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available.

    ReferenceSection

  • Green PH, O'Toole KM, Slonim D, et al.: Increasing incidence and excellent survival of patients with early gastric cancer: experience in a United States medical center. Am J Med 85 (5): 658-61, 1988.
  • Japanese Gastric Cancer Association: Japanese gastric cancer treatment guidelines 2014 (ver. 4). Gastric Cancer 20 (1): 1-19, 2017.
  • Ono H, Kondo H, Gotoda T, et al.: Endoscopic mucosal resection for treatment of early gastric cancer. Gut 48 (2): 225-9, 2001.
    • 胃癌治疗(PDQ®)

    I期胃癌

    I期胃癌的标准治疗方案

    I期胃癌的标准治疗方案如下所示：

  • 采用以下手术方式之一进行手术切除：
  • 远端胃大部切除术（如果病变不是位于胃底或贲门食管交界处）。
  • 近端胃大部切除术或全胃切除术，均同时行远端食管切除术（如果病变累及贲门）。这些肿瘤常累及食管黏膜下淋巴管。
  • 全胃切除术（如果肿瘤弥漫累及胃部或出现在胃体中，并延伸至距离贲门或胃窦6 cm范围以内）。

    • 在行上述手术时，建议进行区域淋巴结清扫。不常规进行脾切除术。

  • 对经过选择的IA期胃癌患者行内镜下粘膜切除术（EMR）。
  • 对淋巴结阳性（T1 N1）和肌层浸润性（T2 N0）疾病患者进行术后放化疗或围手术期化疗。

    • 手术切除

    手术切除（包括区域淋巴结清扫术）是I期胃癌患者的首选治疗方法。

    如果病变未累及贲门食管交界部，亦未弥漫累及胃部，首选胃大部切除术，因为研究已证实其生存率与全胃切除术相当，并且可使并发症发生率降低。

    [证据等级：1iiA] 病变累及贲门时，为达到根治性目的，应进行近端胃大部切除术或全胃切除术（包括切除足够长的食管）。若病变弥漫全胃，需行全胃切除术。至少应手术切除胃大弯和胃小弯的胃周围区域淋巴结。值得注意的是，I期胃癌患者可能有胃周围淋巴结转移。

    内镜黏膜切除术（EMR）

    在日本和整个亚洲，已在具有良好风险特征（Tis或T1a，直径≤2 cm，主要为分化型，无溃疡）且淋巴结转移风险较低的早期肿瘤患者中进行了EMR研究。黏膜内肿瘤发生淋巴结转移的风险低于黏膜下肿瘤。

    应考虑根据上述标准严格筛选患者，由经验丰富的内镜医师进行治疗，并进行密切监测。

    证据（EMR）：

  • 一项EMR前瞻性试验纳入了1987年至1998年在东京接受治疗的445例粘膜内癌患者（共479个肿瘤）。对于具有黏膜下浸润、血管受累和（或）切缘阳性证据的患者，建议完全切除肿瘤。在405例粘膜内病变患者中，278例接受了完全切除，2%局部复发患者接受了根治性治疗，中位随访时间为38个月时无病生存率达100%。在不完全切除/切除情况无法评价的患者中，127例患者中18例出现局部复发，随之行根治性手术。
  • [证据等级：3iiiDii]

    • 术后放化疗

    对于淋巴结阳性（T1 N1）或肌层浸润（T2 N0）病变患者，术后应考虑进行放化疗。

    证据（术后放化疗）：

  • 一项前瞻性多中心III期临床试验（SWOG-9008 [NCT01197118]）评估了术后联合放化疗 VS.单独手术治疗在559例完全可切除的IB期至IV期（M0）胃和食管胃交界处腺癌患者中的疗效，研究表明接受辅助联合治疗的患者生存率显著升高。
  • [证据等级：1iiA]
  • 在随访期为10年以上时，辅助放化疗组的中位生存期为35个月，单独手术组则为27个月（P= 0.0046）。
  • 放化疗组的无复发中位生存期为27个月，而单独手术组为19个月（P < 0.001）。主要观察到局部复发风险有所改善（从手术治疗组的47％改善为放化疗组的29％）。
  • 然而，试验中仅36例患者为IB期肿瘤（每组18例患者）。

    • 由于IB期肿瘤患者在完全切除后的预后相对良好，因此本组辅助放化疗的有效性并不明显。

    围手术期化疗

    一些欧洲研究者评估了单独使用围手术期化疗且不进行放疗的疗效。

    证据（围手术期化疗）：

  • 在随机III期AIO-FLOT4临床试验（NCT01216644）中，716例可切除的IB期至III期胃或胃食管腺癌患者随机接受多西他赛、奥沙利铂和氟尿嘧啶（5-FU）/亚叶酸钙（FLOT）围手术期化疗；或表柔比星、顺铂和5-FU或卡培他滨（ECF/ECX）治疗。
  • [证据等级：1iiA]
  • FLOT治疗组的中位总生存期（OS）为50个月，而ECF/ECX治疗组为35个月（风险比[HR]，0.77；95%置信区间，0.63–0.94；P = 0.012）。
  • FLOT治疗组的手术切缘阴性率为85%，ECF/ECX治疗组为78%（P = 0.0162）。
  • 两组的毒性发生率相似（ECF/ECX治疗组住院率达26%，FLOT治疗组住院率达25%）。然而，产生的副作用类型不同，ECF/ECX治疗组恶心、血栓栓塞事件和贫血的发生率更高，而FLOT治疗组3/4级感染、中性粒细胞减少症、腹泻和神经病变的发生率更高。

    • 根据临床评估确定的I期胃癌治疗方案

    根据临床评估确定的I期胃癌治疗方案如下所示：

  • 新辅助放化疗，例如已结束的SWOG-S0425试验中和已完成的RTOG-9904（NCT00003862）。

    • 当前临床试验

    使用高级临床试验检索工具查找NCI支持的癌症临床试验（当前正在招募患者）。可通过试验地点、治疗类型、药物名称和其他标准缩小检索范围。还可获得关于临床试验的基本信息。

    参考文献

  • Brennan MF, Karpeh MS: Surgery for gastric cancer: the American view. Semin Oncol 23 (3): 352-9, 1996.
  • Smalley SR, Benedetti JK, Haller DG, et al.: Updated analysis of SWOG-directed intergroup study 0116: a phase III trial of adjuvant radiochemotherapy versus observation after curative gastric cancer resection. J Clin Oncol 30 (19): 2327-33, 2012.
  • Al-Batran SE, Homann N, Pauligk C, et al.: Perioperative chemotherapy with fluorouracil plus leucovorin, oxaliplatin, and docetaxel versus fluorouracil or capecitabine plus cisplatin and epirubicin for locally advanced, resectable gastric or gastro-oesophageal junction adenocarcinoma (FLOT4): a randomised, phase 2/3 trial. Lancet 393 (10184): 1948-1957, 2019.
  • Bozzetti F, Marubini E, Bonfanti G, et al.: Subtotal versus total gastrectomy for gastric cancer: five-year survival rates in a multicenter randomized Italian trial. Italian Gastrointestinal Tumor Study Group. Ann Surg 230 (2): 170-8, 1999.
  • Japanese Gastric Cancer Association: Japanese gastric cancer treatment guidelines 2014 (ver. 4). Gastric Cancer 20 (1): 1-19, 2017.
  • Ono H, Kondo H, Gotoda T, et al.: Endoscopic mucosal resection for treatment of early gastric cancer. Gut 48 (2): 225-9, 2001.
  • Kelsen DP: Postoperative adjuvant chemoradiation therapy for patients with resected gastric cancer: intergroup 116. J Clin Oncol 18 (21 Suppl): 32S-4S, 2000.
  • Cunningham D, Allum WH, Stenning SP, et al.: Perioperative chemotherapy versus surgery alone for resectable gastroesophageal cancer. N Engl J Med 355 (1): 11-20, 2006.
  • Ajani JA, Winter K, Okawara GS, et al.: Phase II trial of preoperative chemoradiation in patients with localized gastric adenocarcinoma (RTOG 9904): quality of combined modality therapy and pathologic response. J Clin Oncol 24 (24): 3953-8, 2006.
    • Gastric Cancer Treatment (PDQ®)

    Stage I Gastric Cancer

    Standard Treatment Options for Stage I Gastric Cancer

    Standard treatment options for stage I gastric cancer include the following:

  • Surgical resection with one of the following surgical procedures:
  • Distal subtotal gastrectomy (if the lesion is not in the fundus or at the cardioesophageal junction).
  • Proximal subtotal gastrectomy or total gastrectomy, both with distal esophagectomy (if the lesion involves the cardia). These tumors often involve the submucosal lymphatics of the esophagus.
  • Total gastrectomy (if the tumor involves the stomach diffusely or arises in the body of the stomach and extends to within 6 cm of the cardia or distal antrum).

    • Regional lymphadenectomy is recommended with all of the above procedures. Splenectomy is not routinely performed.

  • Endoscopic mucosal resection (EMR) for select patients with stage IA gastric cancer.
  • Postoperative chemoradiation therapy or perioperative chemotherapy for patients with node-positive (T1 N1) and muscle-invasive (T2 N0) disease.

    • Surgical resection

    Surgical resection including regional lymphadenectomy is the treatment of choice for patients with stage I gastric cancer.

    If the lesion is not in the cardioesophageal junction and does not diffusely involve the stomach, subtotal gastrectomy is the procedure of choice, because it has been demonstrated to provide equivalent survival when compared with total gastrectomy and is associated with decreased morbidity.

    [Level of evidence: 1iiA] When the lesion involves the cardia, proximal subtotal gastrectomy or total gastrectomy (including a sufficient length of esophagus) may be performed with curative intent. If the lesion diffusely involves the stomach, total gastrectomy is required. At a minimum, surgical resection includes greater and lesser curvature perigastric regional lymph nodes. Note that in patients with stage I gastric cancer, perigastric lymph nodes may contain cancer.

    Endoscopic mucosal resection (EMR)

    EMR has been studied in Japan and throughout Asia in patients with early-stage tumors with good risk features (Tis or T1a, diameter ≤2 cm, predominantly differentiated type, without ulcerative findings) that have a lower risk of nodal metastasis. Intramucosal tumors have a lower risk of nodal metastasis than submucosal tumors.

    Careful patient selection by the above criteria, treatment with an experienced endoscopist, and close surveillance should be considered.

    Evidence (EMR):

  • A prospective trial of EMR included 445 patients with intramucosal carcinoma (a total of 479 tumors) treated in Tokyo between 1987 and 1998. Complete resection was recommended for patients with evidence of submucosal invasion, blood vessel involvement, and/or positive margins. Of the 405 patients with intramucosal disease, 278 underwent complete resection, with 2% local recurrence treated with curative intent and 100% disease-free survival at a median follow-up of 38 months. In those with incomplete/inevaluable resections, 18 of 127 patients recurred locally and underwent curative surgery.
  • [Level of evidence: 3iiiDii]

    • Postoperative chemoradiation therapy

    In patients with node-positive (T1 N1) and muscle-invasive (T2 N0) disease, postoperative chemoradiation therapy may be considered.

    Evidence (postoperative chemoradiation therapy):

  • A prospective multi-institution phase III trial (SWOG-9008 [NCT01197118]) evaluated postoperative combined chemoradiation therapy versus surgery alone in 559 patients with completely resected stage IB to stage IV (M0) adenocarcinoma of the stomach and gastroesophageal junction and reported a significant survival benefit with adjuvant combined modality therapy.
  • [Level of evidence: 1iiA]
  • With more than 10 years of follow-up, median survival was 35 months for the adjuvant chemoradiation therapy group and 27 months for the surgery-alone arm (P = .0046).
  • Median relapse-free survival was 27 months in the chemoradiation arm compared with 19 months in the surgery-alone arm (P < .001). Improvement was primarily seen for locoregional recurrence risk (improvement from 47% for surgery vs. 29% for chemoradiation).
  • However, only 36 patients in the trial had stage IB tumors (18 patients in each arm).

    • Because the prognosis is relatively favorable for patients with completely resected stage IB disease, the effectiveness of adjuvant chemoradiation therapy for this group is less clear.

    Perioperative chemotherapy

    Investigators in Europe evaluated the role of perioperative chemotherapy without radiation therapy.

    Evidence (perioperative chemotherapy):

  • In the randomized phase III AIO-FLOT4 trial (NCT01216644), 716 patients with stage IB to stage III resectable gastric or gastroesophageal adenocarcinoma were randomly assigned to receive either perioperative chemotherapy with docetaxel, oxaliplatin, and fluorouracil (5-FU)/leucovorin (FLOT); or epirubicin, cisplatin, and 5-FU or capecitabine (ECF/ECX).
  • [Level of evidence: 1iiA]
  • Median overall survival was 50 months with FLOT and 35 months with ECF/ECX (hazard ratio, 0.77; 95% confidence interval, 0.63–0.94; P = .012).
  • Margin-free resection in the FLOT group was 85% versus 78% in the ECF/ECX group (P = .0162).
  • Toxicity rates were similar between groups (26% required hospitalizations in the ECF/ECX group and 25% in the FLOT group). However, types of side effects differed, with increased nausea, thromboembolic events, and anemia in the ECF/ECX group versus higher rates of grade 3/4 infections, neutropenia, diarrhea, and neuropathy in the FLOT group.

    • Treatment Options Under Clinical Evaluation for Stage I Gastric Cancer

    Treatment options under clinical evaluation for stage I gastric cancer include the following:

  • Neoadjuvant chemoradiation therapy such as in the closed SWOG-S0425 trial, and the RTOG-9904 (NCT00003862) trial, which is completed.

    • Current Clinical Trials

    Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available.

    ReferenceSection

  • Brennan MF, Karpeh MS: Surgery for gastric cancer: the American view. Semin Oncol 23 (3): 352-9, 1996.
  • Smalley SR, Benedetti JK, Haller DG, et al.: Updated analysis of SWOG-directed intergroup study 0116: a phase III trial of adjuvant radiochemotherapy versus observation after curative gastric cancer resection. J Clin Oncol 30 (19): 2327-33, 2012.
  • Al-Batran SE, Homann N, Pauligk C, et al.: Perioperative chemotherapy with fluorouracil plus leucovorin, oxaliplatin, and docetaxel versus fluorouracil or capecitabine plus cisplatin and epirubicin for locally advanced, resectable gastric or gastro-oesophageal junction adenocarcinoma (FLOT4): a randomised, phase 2/3 trial. Lancet 393 (10184): 1948-1957, 2019.
  • Bozzetti F, Marubini E, Bonfanti G, et al.: Subtotal versus total gastrectomy for gastric cancer: five-year survival rates in a multicenter randomized Italian trial. Italian Gastrointestinal Tumor Study Group. Ann Surg 230 (2): 170-8, 1999.
  • Japanese Gastric Cancer Association: Japanese gastric cancer treatment guidelines 2014 (ver. 4). Gastric Cancer 20 (1): 1-19, 2017.
  • Ono H, Kondo H, Gotoda T, et al.: Endoscopic mucosal resection for treatment of early gastric cancer. Gut 48 (2): 225-9, 2001.
  • Kelsen DP: Postoperative adjuvant chemoradiation therapy for patients with resected gastric cancer: intergroup 116. J Clin Oncol 18 (21 Suppl): 32S-4S, 2000.
  • Cunningham D, Allum WH, Stenning SP, et al.: Perioperative chemotherapy versus surgery alone for resectable gastroesophageal cancer. N Engl J Med 355 (1): 11-20, 2006.
  • Ajani JA, Winter K, Okawara GS, et al.: Phase II trial of preoperative chemoradiation in patients with localized gastric adenocarcinoma (RTOG 9904): quality of combined modality therapy and pathologic response. J Clin Oncol 24 (24): 3953-8, 2006.
    • 胃癌治疗(PDQ®)

    II期和III期胃癌

    II期和III期胃癌的标准治疗方案

    II期和III期胃癌的标准治疗方案如下所示：

  • 手术切除方案（在与多学科团队讨论围手术期和辅助治疗的疗效后）可能包括以下术式之一：
  • 远端胃大部切除术（如果病变未累及胃底或贲门食管交界处）。
  • 近端胃大部切除术或全胃切除术（如果病变累及贲门）。
  • 全胃切除术（如果肿瘤弥漫累及胃部或出现在胃体中，并延伸至距贲门6 cm以内）。

    • 在行上述手术时，建议进行区域淋巴结清扫。不常规进行脾切除术。

  • 围手术期化疗。
  • 术后（辅助）放化疗。
  • 术后（辅助）化疗。

    • 尚未进行有关辅助放化疗与围手术期化疗疗效对比的随机试验。

    手术切除

    由于局部复发和远处转移的风险较高，除手术外，还应考虑进行围手术期和术后治疗。

    对于Ⅱ期、Ⅲ期胃癌患者，以及所有符合条件进行手术的患者，手术切除肿瘤并行区域淋巴结清扫是首选的治疗方案。

    如果病变未累及贲门食管交界处，亦未弥漫累及全胃，则首选胃大部切除术。病变累及贲门时，为达到根治性目的，应进行近端胃大部切除术或全胃切除术。若病变弥漫全胃，需行全胃切除术联合相应的淋巴结清扫。扩大淋巴结清扫（D2）的作用尚不明确，译者认为，除早期胃癌外，D2淋巴结清扫的意义已经被学术界广泛认可。NCCN指南及日本胃癌治疗规约中均明确提出建议行D2淋巴结清扫。而是否需行D3及以上淋巴结清扫术尚有争议。有研究显示D3淋巴结清扫术并不增加疗效，而会导致并发症发生率的增加。

    而一部分研究报道称其会导致并发症发生率增加。

    多达15%经选择的III期患者可通过单独手术治愈，尤其是若淋巴结转移较少（<7个淋巴结）。

    围手术期化疗

    一些欧洲研究者评估了单独使用围手术期化疗且不进行放疗的疗效。

    证据（围手术期化疗）：

  • 在随机III期AIO-FLOT4临床试验（NCT01216644）中，716例可切除的IB期至III期胃或胃食管腺癌患者随机接受多西他赛、奥沙利铂和氟尿嘧啶（5-FU）/亚叶酸钙（FLOT）围手术期化疗；或表柔比星、顺铂和5-FU或卡培他滨（ECF/ECX）治疗。
  • [证据等级：1iiA]
  • FLOT治疗组的中位总生存期（OS）为50个月，而ECF/ECX治疗组为35个月（风险比[HR]，0.77；95%置信区间，0.63–0.94；P = 0.012）。
  • FLOT治疗组的手术切缘阴性率为85%，ECF/ECX治疗组为78%（P = 0.0162）。
  • 两组的毒性发生率相似（ECF/ECX治疗组住院率达26%，FLOT治疗组住院率达25%）。然而，产生的副作用类型不同，ECF/ECX治疗组恶心、血栓栓塞事件和贫血的发生率更高，而FLOT治疗组3/4级感染、中性粒细胞减少症、腹泻和神经病变的发生率更高。
  • 在一项随机III期MAGIC临床试验（NCT00002615）中，患II期及以上胃腺癌、食管下段三分之一腺癌的患者被随机分配至两组，一组在手前及术后接受3个疗程的表柔比星、顺铂并连续注射5-FU（ECF），另一组接受单独手术治疗。
  • 与手术组相比，接受围手术期化疗组患者无进展生存期显著延长（进展HR，0.66，95%CI，0.53-0.81；P< 0.001），OS也显著提高（死亡HR，0.75；95%CI，0.60-0.93；P =0.009）。
  • 围手术期化疗组的5年OS为36.3%（95%CI，29.5%-43.0%）；单独手术组则为23%（95%CI，16.6%-29.4%）。
  • [证据等级：1iiA]

    • 术后（辅助）放化疗

    未接受过新辅助治疗的II期和III期胃癌患者可考虑接受术后放化疗。

    证据（术后[辅助]放化疗）：

  • 一项前瞻性多中心III期临床试验（SWOG-9008 [NCT01197118]）评估了术后联合放化疗对比单独手术治疗在559例完全可切除的IB期至IV期（M0）胃和食管胃交界部腺癌患者中的疗效，研究表明接受辅助联合治疗的患者生存率显著升高。
  • [证据等级：1iiA]
  • 在随访期为10年以上时，辅助放化疗组的中位生存期为35个月，单独手术组则为27个月（P= 0.0046）。
  • 放化疗组的无复发中位生存期为27个月，而单独手术组为19个月（P < 0.001）。主要观察到局部复发风险有所改善（从手术治疗组的47％改善为放化疗组的29％）。
  • 然而，试验中仅36例患者为IB期肿瘤（每组18例患者）。
  • 在癌症和白血病B组研究（CALGB-80101[NCT00052910]）中尝试评价更强化的化疗方案联合放疗的疗效，结果显示无生存期获益。546例曾行IB-IV期（M0）胃或胃食管交界部腺癌根治性切除术的患者接受了术后的放疗以及安排在放疗前后的5-FU与甲酰四氢叶酸治疗，或接受了术后的放疗以及安排在放疗前后的ECF治疗。
  • 两组的5年OS率均为44%。
  • 在一项III期荷兰临床试验（CRITICS[NCT00407186]）中，788例IB期-IVA期胃/胃食管交界部腺癌患者接受了术前化疗和手术，随后随机分组接受了术后化疗或放化疗。
  • 辅助放化疗并不能提高已经接受了新辅助化疗的患者的生存期。
  • 化疗组的中位OS为43个月，而放化疗组为37个月（95%CI，0.84-1.22；P = 0.90）。

    • 术后（辅助）化疗

    一些欧洲研究者评估了单独使用术后化疗且不进行放疗的疗效。

    证据（术后[辅助]化疗）：

  • 日本研究者的一项临床研究招募了1,059例已行D2胃切除术的II期或III期胃癌患者，随机分配至两组，一组口服替吉奥（S-1，一种在美国尚未上市的口服氟嘧啶药物）一年，另一组术后仅进行随访。
  • 将患者按1:1比例随机分配。
  • S-1治疗组的3年OS为80.1%，单独手术组则为70.1%。与单独手术组相比，S-1治疗组死亡HR为0.68（95%CI：0.52-0.87；P = 0.003）。
  • [证据等级：1iiA]
  • 一些亚洲研究者评价了卡培他滨/奥沙利铂作为胃癌切除术后辅助治疗药物的疗效。在CLASSIC（NCT00411229）临床试验中，将来自韩国和中国37个中心的1,035例已行根治性D2胃切除术后的IIA、IIB、IIIA或IIIB期胃癌患者随机分配至两组，一组接受术后辅助化疗（8个疗程的卡陪他滨+奥沙利铂，每个疗程为3周），另一组仅接受术后随访。
  • 化疗组的3年无病生存率为74%，单独手术组则为59%（HR，0.56；95%CI，0.44-0.72；P<0.0001）。
  • 化疗组的3年OS为83%，单独手术组为78%（HR，0.72；95%CI，0.52-1.00；P=0.0493）。
  • [证据等级：1iiA]
  • 尚需进一步随访。

    • 临床评价中的II期和III期胃癌治疗方案

    临床评价中的II期和III期胃癌治疗方案如下所示：

  • SWOG-S0425试验和RTOG-9904试验证实了新辅助放化疗的疗效。
  • 围手术期化疗方案。

    • 所有最新确诊的II期和III期胃癌患者均应被视为临床试验的候选者。

    当前临床试验

    使用高级临床试验检索工具查找NCI支持的癌症临床试验（当前正在招募患者）。可通过试验地点、治疗类型、药物名称和其他标准缩小检索范围。还可获得关于临床试验的基本信息。

    参考文献

  • Brennan MF, Karpeh MS: Surgery for gastric cancer: the American view. Semin Oncol 23 (3): 352-9, 1996.
  • Cunningham D, Allum WH, Stenning SP, et al.: Perioperative chemotherapy versus surgery alone for resectable gastroesophageal cancer. N Engl J Med 355 (1): 11-20, 2006.
  • Smalley SR, Benedetti JK, Haller DG, et al.: Updated analysis of SWOG-directed intergroup study 0116: a phase III trial of adjuvant radiochemotherapy versus observation after curative gastric cancer resection. J Clin Oncol 30 (19): 2327-33, 2012.
  • Kitamura K, Yamaguchi T, Sawai K, et al.: Chronologic changes in the clinicopathologic findings and survival of gastric cancer patients. J Clin Oncol 15 (12): 3471-80, 1997.
  • Bonenkamp JJ, Songun I, Hermans J, et al.: Randomised comparison of morbidity after D1 and D2 dissection for gastric cancer in 996 Dutch patients. Lancet 345 (8952): 745-8, 1995.
  • Cuschieri A, Fayers P, Fielding J, et al.: Postoperative morbidity and mortality after D1 and D2 resections for gastric cancer: preliminary results of the MRC randomised controlled surgical trial.The Surgical Cooperative Group. Lancet 347 (9007): 995-9, 1996.
  • Al-Batran SE, Homann N, Pauligk C, et al.: Perioperative chemotherapy with fluorouracil plus leucovorin, oxaliplatin, and docetaxel versus fluorouracil or capecitabine plus cisplatin and epirubicin for locally advanced, resectable gastric or gastro-oesophageal junction adenocarcinoma (FLOT4): a randomised, phase 2/3 trial. Lancet 393 (10184): 1948-1957, 2019.
  • Kelsen DP: Postoperative adjuvant chemoradiation therapy for patients with resected gastric cancer: intergroup 116. J Clin Oncol 18 (21 Suppl): 32S-4S, 2000.
  • Fuchs CS, Niedzwiecki D, Mamon HJ, et al.: Adjuvant Chemoradiotherapy With Epirubicin, Cisplatin, and Fluorouracil Compared With Adjuvant Chemoradiotherapy With Fluorouracil and Leucovorin After Curative Resection of Gastric Cancer: Results From CALGB 80101 (Alliance). J Clin Oncol 35 (32): 3671-3677, 2017.
  • Cats A, Jansen EPM, van Grieken NCT, et al.: Chemotherapy versus chemoradiotherapy after surgery and preoperative chemotherapy for resectable gastric cancer (CRITICS): an international, open-label, randomised phase 3 trial. Lancet Oncol 19 (5): 616-628, 2018.
  • Sakuramoto S, Sasako M, Yamaguchi T, et al.: Adjuvant chemotherapy for gastric cancer with S-1, an oral fluoropyrimidine. N Engl J Med 357 (18): 1810-20, 2007.
  • Bang YJ, Kim YW, Yang HK, et al.: Adjuvant capecitabine and oxaliplatin for gastric cancer after D2 gastrectomy (CLASSIC): a phase 3 open-label, randomised controlled trial. Lancet 379 (9813): 315-21, 2012.
  • Ajani JA, Winter K, Okawara GS, et al.: Phase II trial of preoperative chemoradiation in patients with localized gastric adenocarcinoma (RTOG 9904): quality of combined modality therapy and pathologic response. J Clin Oncol 24 (24): 3953-8, 2006.
    • Gastric Cancer Treatment (PDQ®)

    Stages II and III Gastric Cancer

    Standard Treatment Options for Stages II and III Gastric Cancer

    Standard treatment options for stage II gastric cancer and stage III gastric cancer include the following:

  • Surgical resection (after discussion with a multidisciplinary team regarding the role of perioperative and adjuvant therapy) may include one of the following surgical procedures:
  • Distal subtotal gastrectomy (if the lesion is not in the fundus or at the cardioesophageal junction).
  • Proximal subtotal gastrectomy or total gastrectomy (if the lesion involves the cardia).
  • Total gastrectomy (if the tumor involves the stomach diffusely or arises in the body of the stomach and extends to within 6 cm of the cardia).

    • Regional lymphadenectomy is recommended with all of the above procedures. Splenectomy is not routinely performed.

  • Perioperative chemotherapy.
  • Postoperative (adjuvant) chemoradiation therapy.
  • Postoperative (adjuvant) chemotherapy.

    • No randomized trials of adjuvant chemoradiation versus perioperative chemotherapy have been undertaken.

    Surgical resection

    Due to high risk of locoregional and distant recurrence, consideration for perioperative and postoperative therapy should be considered in addition to surgery.

    Surgical resection with regional lymphadenectomy is the treatment of choice for patients with stages II and III gastric cancer and all eligible patients undergo surgery.

    If the lesion is not in the cardioesophageal junction and does not diffusely involve the stomach, subtotal gastrectomy is the procedure of choice. When the lesion involves the cardia, proximal subtotal gastrectomy or total gastrectomy may be performed with curative intent. If the lesion diffusely involves the stomach, total gastrectomy and appropriate lymph node resection may be required. The role of extended lymph node (D2) dissection is uncertain

    and in some series is associated with increased morbidity.

    As many as 15% of selected stage III patients can be cured by surgery alone, particularly if lymph node involvement is minimal (<7 lymph nodes).

    Perioperative chemotherapy

    Investigators in Europe evaluated the role of perioperative chemotherapy without radiation therapy.

    Evidence (perioperative chemotherapy):

  • In the randomized phase III AIO-FLOT4 trial (NCT01216644), 716 patients with stage IB to stage III resectable gastric or gastroesophageal adenocarcinoma were randomly assigned to receive either perioperative chemotherapy with docetaxel, oxaliplatin, and fluorouracil (5-FU)/leucovorin (FLOT) or epirubicin, cisplatin, and 5-FU or capecitabine (ECF/ECX).
  • [Level of evidence: 1iiA]
  • Median overall survival (OS) was 50 months with FLOT and 35 months with ECF/ECX (hazard ratio [HR], 0.77; 95% confidence interval [CI], 0.63–0.94; P = .012).
  • Margin-free resection in the FLOT group was 85% versus 78% in the ECF/ECX group (P = .0162).
  • Toxicity rates were similar between groups (26% required hospitalizations in the ECF/ECX group and 25% in the FLOT group). However, types of side effects differed, with increased nausea, thromboembolic events, and anemia in the ECF/ECX group versus higher rates of grade 3/4 infections, neutropenia, diarrhea, and neuropathy in the FLOT group.
  • In the randomized phase III MAGIC trial (NCT00002615), patients with stage II or higher adenocarcinoma of the stomach or of the lower third of the esophagus were assigned to receive three cycles of epirubicin, cisplatin, and continuous infusion 5-FU (ECF) before and after surgery or to receive surgery alone.
  • Compared with the surgery group, the perioperative chemotherapy group had a significantly higher likelihood of progression-free survival (HR for progression, 0.66; 95% CI, 0.53–0.81; P < .001) and of OS (HRdeath, 0.75; 95% CI, 0.60–0.93; P = .009).
  • Five-year OS was 36.3% (95% CI, 29.5%‒43.0%) for the perioperative chemotherapy group and 23% (95% CI, 16.6%‒29.4%) for the surgery group.
  • [Level of evidence: 1iiA]

    • Postoperative (adjuvant) chemoradiation therapy

    Postoperative chemoradiation therapy may be considered for patients with stages II and III gastric cancer who have not received neoadjuvant therapy.

    Evidence (postoperative [adjuvant] chemoradiation therapy):

  • A prospective multi-institution phase III trial (SWOG-9008 [NCT01197118]) evaluated postoperative combined chemoradiation therapy compared with surgery alone in 559 patients with completely resected stage IB to stage IV (M0) adenocarcinoma of the stomach and gastroesophageal junction and reported a significant survival benefit with adjuvant combined modality therapy.
  • [Level of evidence: 1iiA]
  • With more than 10 years of follow-up, median survival was 35 months for the adjuvant chemoradiation therapy arm and 27 months for the surgery-alone arm (P = .0046).
  • Median relapse-free survival was 27 months in the chemoradiation arm compared with 19 months in the surgery-alone arm (P < .001). Improvement was primarily seen for locoregional recurrence risk (improvement from 47% for surgery vs. 29% for chemoradiation).
  • However, only 36 patients in the trial had stage IB tumors (18 patients in each arm).
  • Attempts to evaluate the role of more intensive chemotherapy regimens in combination with radiation in the Cancer and Leukemia Group B study (CALGB-80101 [NCT00052910]) demonstrated no survival benefit. The 546 patients who had undergone curative resection of stage IB to stage IV (M0) gastric or gastroesophageal junction adenocarcinoma received postoperative 5-FU with leucovorin before and after radiation or postoperative ECF before and after combined radiation therapy.
  • The 5-year OS rates were 44% in both arms.
  • In a phase III Dutch trial (CRITICS [NCT00407186]) of 788 patients with stage IB to stage IVA gastric/gastroesophageal junction adenocarcinoma patients received preoperative chemotherapy and surgery, and then were randomly assigned to receive postoperative chemotherapy or chemoradiotherapy.
  • Adjuvant chemoradiation did not improve survival in those who received neoadjuvant chemotherapy.
  • Median OS was 43 months in the chemotherapy arm and 37 months in the chemoradiotherapy group (95% CI, 0.84–1.22; P = .90).

    • Postoperative (adjuvant) chemotherapy

    Investigators in Europe evaluated the role of postoperative chemotherapy without radiation therapy.

    Evidence (postoperative [adjuvant] chemotherapy):

  • Japanese investigators randomly assigned 1,059 patients with stage II or III gastric cancer who had undergone a D2 gastrectomy to receive either 1 year of S-1, an oral fluoropyrimidine not available in the United States, or follow-up after surgery alone.
  • Patients were randomly assigned in a 1:1 fashion.
  • The 3-year OS rate was 80.1% in the S-1 group and 70.1% in the surgery-only group. The HRdeath in the S-1 group, as compared with the surgery-only group, was 0.68 (95% CI, 0.52–0.87; P = .003).
  • [Level of evidence: 1iiA]
  • Investigators in Asia evaluated the role of capecitabine/oxaliplatin as adjuvant therapy after gastric cancer resection. In the CLASSIC (NCT00411229) trial, 37 centers in South Korea, China, and Taiwan randomly assigned 1,035 patients with stages IIA, IIB, IIIA, or IIIB gastric cancer who had undergone a curative D2 gastrectomy to receive adjuvant chemotherapy (eight 3-week cycles of capecitabine plus oxaliplatin) or follow-up alone after surgery.
  • The 3-year disease-free survival rate was 74% in the chemotherapy group and 59% in the surgery-alone group (HR, 0.56; 95% CI, 0.44–0.72; P < .0001).
  • The 3-year OS was 83% in the chemotherapy group and 78% in the surgery-alone group (HR, 0.72; 95% CI, 0.52–1.00; P = .0493).
  • [Level of evidence: 1iiA]
  • Further follow-up is anticipated.

    • Treatment Options Under Clinical Evaluation for Stages II and III Gastric Cancer

    Treatment options under clinical evaluation for stages II and III gastric cancer include the following:

  • Neoadjuvant chemoradiation therapy was evidenced in the SWOG-S0425 trial and the RTOG-9904 trial.
  • Perioperative chemotherapy regimens.

    • All newly diagnosed patients with stages II and III gastric cancer should be considered candidates for clinical trials.

    Current Clinical Trials

    Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available.

    ReferenceSection

  • Brennan MF, Karpeh MS: Surgery for gastric cancer: the American view. Semin Oncol 23 (3): 352-9, 1996.
  • Cunningham D, Allum WH, Stenning SP, et al.: Perioperative chemotherapy versus surgery alone for resectable gastroesophageal cancer. N Engl J Med 355 (1): 11-20, 2006.
  • Smalley SR, Benedetti JK, Haller DG, et al.: Updated analysis of SWOG-directed intergroup study 0116: a phase III trial of adjuvant radiochemotherapy versus observation after curative gastric cancer resection. J Clin Oncol 30 (19): 2327-33, 2012.
  • Kitamura K, Yamaguchi T, Sawai K, et al.: Chronologic changes in the clinicopathologic findings and survival of gastric cancer patients. J Clin Oncol 15 (12): 3471-80, 1997.
  • Bonenkamp JJ, Songun I, Hermans J, et al.: Randomised comparison of morbidity after D1 and D2 dissection for gastric cancer in 996 Dutch patients. Lancet 345 (8952): 745-8, 1995.
  • Cuschieri A, Fayers P, Fielding J, et al.: Postoperative morbidity and mortality after D1 and D2 resections for gastric cancer: preliminary results of the MRC randomised controlled surgical trial.The Surgical Cooperative Group. Lancet 347 (9007): 995-9, 1996.
  • Al-Batran SE, Homann N, Pauligk C, et al.: Perioperative chemotherapy with fluorouracil plus leucovorin, oxaliplatin, and docetaxel versus fluorouracil or capecitabine plus cisplatin and epirubicin for locally advanced, resectable gastric or gastro-oesophageal junction adenocarcinoma (FLOT4): a randomised, phase 2/3 trial. Lancet 393 (10184): 1948-1957, 2019.
  • Kelsen DP: Postoperative adjuvant chemoradiation therapy for patients with resected gastric cancer: intergroup 116. J Clin Oncol 18 (21 Suppl): 32S-4S, 2000.
  • Fuchs CS, Niedzwiecki D, Mamon HJ, et al.: Adjuvant Chemoradiotherapy With Epirubicin, Cisplatin, and Fluorouracil Compared With Adjuvant Chemoradiotherapy With Fluorouracil and Leucovorin After Curative Resection of Gastric Cancer: Results From CALGB 80101 (Alliance). J Clin Oncol 35 (32): 3671-3677, 2017.
  • Cats A, Jansen EPM, van Grieken NCT, et al.: Chemotherapy versus chemoradiotherapy after surgery and preoperative chemotherapy for resectable gastric cancer (CRITICS): an international, open-label, randomised phase 3 trial. Lancet Oncol 19 (5): 616-628, 2018.
  • Sakuramoto S, Sasako M, Yamaguchi T, et al.: Adjuvant chemotherapy for gastric cancer with S-1, an oral fluoropyrimidine. N Engl J Med 357 (18): 1810-20, 2007.
  • Bang YJ, Kim YW, Yang HK, et al.: Adjuvant capecitabine and oxaliplatin for gastric cancer after D2 gastrectomy (CLASSIC): a phase 3 open-label, randomised controlled trial. Lancet 379 (9813): 315-21, 2012.
  • Ajani JA, Winter K, Okawara GS, et al.: Phase II trial of preoperative chemoradiation in patients with localized gastric adenocarcinoma (RTOG 9904): quality of combined modality therapy and pathologic response. J Clin Oncol 24 (24): 3953-8, 2006.
    • 胃癌治疗(PDQ®)

    无法手术的复发性IV期胃癌

    无法手术的复发性IV期胃癌的标准治疗方案

    无法手术的复发性IV期胃癌患者（包括临床判断或术中判断不可切除的胃癌患者）的标准治疗方案如下所示：

  • 一线姑息性全身治疗：
  • 姑息性化疗。
  • 氟尿嘧啶（5-FU）。
  • 表柔比星、顺铂和5-FU（ECF）。
  • 表柔比星、奥沙利铂和卡培他滨（EOX）。
  • 顺铂和5-FU（CF）。
  • 5-FU、甲酰四氢叶酸和奥沙利铂。
  • 多西他赛、顺铂和5-FU。
  • 依托泊苷、甲酰四氢叶酸和5-FU（ELF）。
  • 5-FU、甲酰四氢叶酸和伊立替康。
  • 曲妥珠单抗联合化疗治疗HER2阳性肿瘤患者（免疫组化[IHC]检测为3+或荧光原位杂交[FISH]试验呈阳性）。
  • 二线姑息性全身治疗。
  • 姑息性化疗。
  • 雷莫芦单抗联合或不联合化疗。
  • 免疫治疗。
  • 错配修复缺陷（dMMR）或微卫星高度不稳定（MSI-H）肿瘤患者的二线治疗。
  • 程序性死亡配体1（PD-L1）-阳性肿瘤患者的三线治疗。
  • 帕博利珠单抗。
  • 纳武利尤单抗。
  • 腔内激光疗法、腔内支架置入或胃空肠吻合术可能有助于胃梗阻患者的治疗。
  • 姑息性放疗可缓解出血、疼痛和梗阻。
  • 姑息性切除手术适用于持续出血或梗阻的患者。

    • 一线姑息性全身治疗

    姑息性化疗

    多项临床研究比较了标准化疗和最佳支持疗法在治疗转移性胃癌中的疗效，目前的共识认为接受化疗的患者平均生存时间较接受支持疗法的患者可延长数月。

    [证据等级：1iiA]在过去二十年期间，多项随机临床试验评估了不同治疗方案（单药化疗与联合化疗）对治疗方案尚存争议的转移性胃癌患者的疗效。一项荟萃分析显示，联合化疗相较于单药化疗具有相对优势，总生存率（OS）的风险比（HR）为0.83（95%置信区间[CI]，0.74-0.93）。

    证据（姑息性化疗）：

  • 所有联合治疗方案中，ECF方案常被美国和欧洲国家作为参考标准。 在欧洲一项临床试验中，274例转移性食管-胃癌患者随机接受ECF治疗，或5-FU、多柔比星联合甲氨蝶呤（FAMTX）治疗。
  • ECF治疗组的中位生存期明显长于FAMTX治疗组（分别为8.9与5.7个月，P = 0.0009）。
  • [证据等级：1iiA]
  • 另一项临床试验比较了ECF方案与丝裂霉素、顺铂联合5-FU（MCF）治疗方案，两组患者的生存期无统计学显著差异（分别为9.4与8.7个月，P= 0.315）。
  • [证据等级：1iiA]
  • 根据REAL-2临床试验（ISRCTN51678883）的结果，奥沙利铂与卡培他滨目前常用于替换ECF治疗方案中的顺铂与5-FU。
  • 该随机临床试验中共有1002例患有晚期食管、胃食管交界部或胃癌患者入组，试验使用2×2分组方案，结果显示卡培他滨治疗的患者中位OS不劣效于5-FU治疗的患者（死亡率HR=0.86；95%CI，0.82-0.99），亦不劣效于奥沙利铂取代顺铂治疗的患者（死亡HR=0.92；95%CI，0.80-1.10）。
  • 一项国际协作临床研究中445例转移性胃癌患者随机接受多西他赛、顺铂联合5-FU（DCF）方案治疗或CF方案治疗。
  • 将疾病进展时间（TTP）作为主要终点。
  • DCF治疗组的患者TTP显著延长（DCF治疗组5.6个月；95%CI，4.9-5.9；CF治疗组3.7个月；95%CI，3.4-4.5；HR，1.47；95%CI，1.19-1.82；对数秩检验P<0.001；风险降低32%）。
  • DCF治疗组患者的中位OS明显长于CF治疗组（DCF组9.2个月；95%CI，8.4-10.6；CF治疗组8.6个月；95%CI，7.2-9.5；HR，1.29；95%CI，1.0-1.6；对数秩检验P=0.02；风险降低23%）。
  • [证据等级：1iiA]
  • 两组的毒性反应发生率均偏高。
  • 发热性中性粒细胞减少症在DCF治疗组患者中更常见（分别为29%和12%），研究表明DCF治疗组患者死亡率为10.4%，而CF治疗组则为9.4%。
  • 对于转移性胃癌患者，CF治疗方案是否可作为参考方案仍有争议。
  • 一项研究中，将245例转移性胃癌患者随机分配至CF、FAMTX或ELF治疗组，研究结果显示三组的反应率、无进展生存期或OS均无显著差异。
  • 三组患者出现3-4级中性粒细胞减少症的比例均为35%-43%，而CF治疗组患者严重恶心、呕吐的发生率更高，达26%。
  • [证据等级：1iiDiv]

    • II期临床试验显示，使用基于伊立替康或奥沙利铂的治疗方案后，患者的反应率、TTP与行ECF或CF方案治疗的患者相似，且前者毒性反应更少。

    关于任一治疗方案相对有效性优劣，目前证据存在争议。多项研究正在评估这些新治疗方案的有效性。

    曲妥珠单抗

    曲妥珠单抗可联合一线化疗药物治疗HER2阳性转移性胃腺癌。对于转移性患者，建议进行HER2检测。

    证据（曲妥珠单抗）：

  • 在一项曲妥珠单抗治疗胃癌的国际开放性III期临床试验（ToGA [NCT01041404]）中，将HER-2阳性的转移性、局部晚期无法手术或复发性胃癌或胃食管交界部癌患者随机分配至两组，分别使用联合或不联合抗HER2单克隆抗体曲妥珠单抗的化疗方案
  • 若患者IHC染色3+或FISH显示HER2/CEP17比值≥2，则认为此患者为HER2阳性。对3,665例患者的肿瘤进行HER2检测，其中810例呈阳性（22%），594例符合合格性标准接受随机分组。化疗药物包括顺铂联合5-FU亦或卡培他滨，由研究者选择。患者按照研究方案每3周接受1次治疗，共6个周期，同时每3周进行曲妥珠单抗给药，直至疾病进展、出现不可耐受的毒性反应或患者退出研究。疾病进展时禁止交叉使用曲妥珠单抗。
  • 曲妥珠单抗组患者的中位OS为13.8个月（95%CI，12-16），而单独化疗组患者为11.1个月（95%CI，10-13）（HR，0.74；95%CI，0.60-0.91；P =0.0046）。
  • [证据等级：1iiA]
  • 两组中各种不良事件发生率均无显著差异，心脏毒性反应在两组中也均罕见。

    • 二线姑息性全身治疗

    姑息性化疗

    对于一线姑息性化疗后疾病进展的患者，尚无标准的治疗方案。可接受的治疗方案包括伊立替康联合或不联合5-FU/甲酰四氢叶酸、多西他赛和紫杉醇联合或不联合雷莫芦单抗。（更多信息请参见本总结的雷莫芦单抗章节。）

    证据（姑息性化疗）：

  • 韩国研究者将既往接受过1或2种化疗方案（含氟嘧啶与铂剂）的晚期胃癌患者按2:1比例随机分配至挽救化疗组和最佳支持治疗组。
  • 挽救化疗由主治医生选择多西他赛（60 mg/m2，每3周一次）或伊立替康（150 mg/m2，每2周一次）中的一种。在入组的202例患者中，133例患者接受挽救化疗，69例患者接受最佳支持治疗。
  • 挽救化疗组中位OS为5.3个月，最佳支持治疗组则为3.8个月（HR，0.657；P=0.007）。
  • 使用多西他赛与伊立替康的患者中位OS无差异（分别为5.2与6.5个月，P=0.116）。
  • [证据等级：1iiA]

    • 雷莫芦单抗

    雷莫芦单抗是一种全人源化单克隆抗体，靶向作用于血管内皮生长因子受体-2。

    证据（雷莫芦单抗）：

  • 在一项设置了安慰剂对照的III期国际临床试验——REGARD研究（NCT00917384）中，355例接受一线5-FU-或含铂方案治疗后疾病进展的IV期胃癌或胃食管交界处癌患者按2:1比例随机分配至雷莫芦单抗组或安慰剂组。
  • 与分配至安慰剂组的患者的中位OS（3.8个月）相比，分配至雷莫芦单抗组的患者的中位OS（5.2个月）显著改善（HR，0.776；P=0.047）。
  • 雷莫芦单抗组的高血压发生率高于安慰剂组。
  • [证据等级：1iiA]

    • 雷莫芦单抗是一种对顺铂或5-FU耐药的IV期胃癌的可行性治疗药物。

  • 在一项双盲III期国际临床试验——RAINBOW研究（NCT01170663）中，将665例患者随机分配，在第1、8和15天接受紫杉醇（80 mg/m2）治疗，每28天一次，一组在第1和15天添加雷莫芦单抗（8 mg/kg），另一组在第1天和第15天添加安慰剂。
  • 与分配至安慰剂组的患者的中位OS（7.4个月）相比，分配至雷莫芦单抗组的患者的中位OS（9.6个月）显著改善（HR，0.807；P=0.017）。
  • ≥3级中性粒细胞减少症、疲乏、高血压和腹痛在雷莫芦单抗治疗组中更常见。
  • [证据等级：1iA]

    • 紫杉醇和雷莫芦单抗联合治疗是IV期胃癌或胃食管交界部癌患者可接受的二线化疗方案。

    免疫治疗

    检查点抑制剂，尤其是程序性死亡1（PD-1）抑制剂，正在被积极研究用于治疗胃癌和胃食管癌。建议对转移性胃腺癌患者进行dMMR（IHC染色）或MSI聚合酶链反应检测以及PD-L1联合阳性评分（美国CPS评分）。

    dMMR或MSI-H肿瘤患者的二线治疗

    证据（dMMR或MSI-H肿瘤患者的二线治疗）：

  • 一项评价帕博利珠单抗在伴或不伴dMMR的结肠癌患者及伴dMMR的非结直肠癌患者中的疗效的II期研究表明，免疫相关客观缓解率达71%（7例患者中的5例）。基于这些数据，帕博利珠单抗已获批用于治疗既往治疗后疾病进展且对替代治疗方案不满意的dMMR实体瘤患者。

    • PD-L1阳性肿瘤患者的三线治疗

    帕博利珠单抗

    证据（帕博利珠单抗）：

  • 在II期KEYNOTE-059临床试验（NCT02335411）中，259例既往接受过至少两种化疗方案后疾病进展的复发性或转移性胃癌/胃食管交界部腺癌患者接受了帕博利珠单抗治疗（200 mg，每3周一次）。
  • 在这些患者中，57.1%患者肿瘤呈PD-L1阳性（使用PD-L1 IHC 22C3 pharmDx试剂盒[Dako]进行评价，联合阳性评分≥1）。
  • 所有肿瘤的总体客观缓解率为11.6%，完全缓解（CR）率为2.3%。 PD-L1阳性肿瘤中，客观缓解率为15.5%，CR为2.0%。
  • [证据等级：2Div]

    • 基于这些数据，美国食品药品监督管理局已给予了帕博利珠单抗快速审批，同意其用于PD-L1阳性肿瘤的治疗。

    纳武利尤单抗

    证据（纳武利尤单抗）：

  • 一项设置了安慰剂对照的随机双盲III期临床试验（ONO-4538-12[ATTRACTION-2] [NCT02267343]）入组了来自日本、韩国和中国台湾地区的493例难治性胃食管交界部癌/胃癌患者。
  • 患者按2:1比例随机接受纳武利尤单抗（3 mg/kg，每2周一次）或安慰剂治疗。
  • 纳武利尤单抗治疗组的中位OS为5.26个月（95%CI，4.60-6.37），而安慰剂组为4.14个月（95%CI，3.42-4.86）。
  • 严重治疗相关不良事件的发生率达10%。
  • [证据等级：1iA]

    • 基于这些数据，日本厚生劳动省批准纳武利尤单抗用于治疗既往接受化疗后疾病进展的晚期胃癌。

    临床评价中无法手术的复发性IV期胃癌治疗方案

    临床评价中无法手术的复发性IV期胃癌治疗方案如下所示：

  • 使用FLOT方案（多西他赛、奥沙利铂和 5-FU/甲酰四氢叶酸）的姑息性化疗。
  • 瑞戈非尼。
  • 肿瘤细胞减灭术和腹腔热灌注化疗（HIPEC）。

    • 目前，使用聚ADP核糖聚合酶（PARP）抑制剂和肝细胞生长因子抑制剂的治疗方案尚未显示出疗效。

    当前临床试验

    使用高级临床试验检索工具查找NCI支持的癌症临床试验（当前正在招募患者）。可通过试验地点、治疗类型、药物名称和其他标准缩小检索范围。还可获得关于临床试验的基本信息。

    参考文献

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  • Glimelius B, Ekström K, Hoffman K, et al.: Randomized comparison between chemotherapy plus best supportive care with best supportive care in advanced gastric cancer. Ann Oncol 8 (2): 163-8, 1997.
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  • Kang JH, Lee SI, Lim do H, et al.: Salvage chemotherapy for pretreated gastric cancer: a randomized phase III trial comparing chemotherapy plus best supportive care with best supportive care alone. J Clin Oncol 30 (13): 1513-8, 2012.
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    • Gastric Cancer Treatment (PDQ®)

    Stage IV, Inoperable, and Recurrent Gastric Cancer

    Standard Treatment Options for Stage IV, Inoperable, and Recurrent Gastric Cancer

    Standard treatment options for stage IV, inoperable, and recurrent gastric cancer, including medically or surgically unresectable patients, include the following:

  • First-line palliative systemic therapy with:
  • Palliative chemotherapy.
  • Fluorouracil (5-FU).
  • Epirubicin, cisplatin, and 5-FU (ECF).
  • Epirubicin, oxaliplatin, and capecitabine (EOX).
  • Cisplatin and 5-FU (CF).
  • 5-FU, leucovorin, and oxaliplatin.
  • Docetaxel, cisplatin, and 5-FU.
  • Etoposide, leucovorin, and 5-FU (ELF).
  • 5-FU, leucovorin, and irinotecan.
  • Trastuzumab with chemotherapy in patients with HER2-positive tumors (3+ on immunohistochemistry [IHC] or fluorescence in situ hybridization [FISH]-positive).
  • Second-line palliative systemic therapy.
  • Palliative chemotherapy.
  • Ramucirumab with or without chemotherapy.
  • Immunotherapy.
  • Second-line treatment for patients with defective mismatch repair (dMMR) or microsatellite instability-high (MSI-H) tumors.
  • Third-line treatment for patients with programmed death ligand 1 (PD-L1)‒positive tumors.
  • Pembrolizumab.
  • Nivolumab.
  • Endoluminal laser therapy, endoluminal stent placement, or gastrojejunostomy, may be helpful to patients with gastric obstruction.
  • Palliative radiation therapy may alleviate bleeding, pain, and obstruction.
  • Palliative resection is reserved for patients with continued bleeding or obstruction.

    • First-line palliative systemic therapy

    Palliative chemotherapy

    Standard chemotherapy versus best supportive care for patients with metastatic gastric cancer has been tested in several clinical trials, and there is general agreement that patients who receive chemotherapy live for several months longer on average than patients who receive supportive care.

    [Level of evidence: 1iiA] During the last 20 years, multiple randomized studies evaluating different treatment regimens (monotherapy vs. combination chemotherapy) have been performed in patients with metastatic gastric cancer with no clear consensus emerging as to the best management approach. A meta-analysis of these studies demonstrated a hazard ratio (HR) of 0.83 for overall survival (OS) (95% confidence interval [CI], 0.74–0.93) in favor of combination chemotherapy.

    Evidence (palliative chemotherapy):

  • Of all the combination regimens, ECF is often considered the reference standard in the United States and Europe. In one European trial, 274 patients with metastatic esophagogastric cancer were randomly assigned to receive either ECF or 5-FU, doxorubicin, and methotrexate (FAMTX).
  • The group who received ECF had a significantly longer median survival (8.9 vs. 5.7 months, P = .0009) than the FAMTX group.
  • [Level of evidence: 1iiA]
  • In a second trial that compared ECF with mitomycin, cisplatin, and 5-FU (MCF), there was no statistically significant difference in median survival (9.4 vs. 8.7 months, P = .315).
  • [Level of evidence: 1iiA]
  • Oxaliplatin and capecitabine are often substituted for cisplatin and 5-FU within the ECF regimen on the basis of results from the REAL-2 trial (ISRCTN51678883).
  • This randomized trial of 1,002 patients with advanced esophageal, gastroesophageal junction, or gastric cancer utilized a 2 × 2 design to demonstrate noninferior median OS in patients treated with capecitabine rather than 5-FU (HRdeath = 0.86; 95% CI, 0.82–0.99) and in patients treated with oxaliplatin in place of cisplatin (HRdeath = 0.92; 95% CI, 0.80–1.10).
  • An international collaboration of investigators randomly assigned 445 patients with metastatic gastric cancer to receive docetaxel, cisplatin, and 5-FU (DCF) or CF.
  • Time-to-treatment progression (TTP) was the primary endpoint.
  • Patients who received DCF experienced a significantly longer TTP (5.6 months; 95% CI, 4.9–5.9; vs. 3.7 months; 95% CI, 3.4–4.5; HR, 1.47; 95% CI, 1.19–1.82; log-rank P < .001; risk reduction 32%).
  • The median OS was significantly longer for patients who received DCF compared with patients who received CF (9.2 months; 95% CI, 8.4–10.6; vs. 8.6 months; 95% CI, 7.2–9.5; HR, 1.29; 95% CI, 1.0–1.6; log-rank P = .02; risk reduction = 23%).
  • [Level of evidence: 1iiA]
  • There were high toxicity rates in both arms.
  • Febrile neutropenia was more common in patients who received DCF (29% vs. 12%), and the death rate on the study was 10.4% for patients on the DCF arm and 9.4% for patients on the CF arm.
  • Whether the CF regimen should be considered as an index regimen for the treatment of patients with metastatic gastric cancer is the subject of debate.
  • The results of a study that randomly assigned 245 patients with metastatic gastric cancer to receive CF, FAMTX, or ELF demonstrated no significant difference in response rate, progression-free survival, or OS between the arms.
  • Grades 3 and 4 neutropenia occurred in 35% to 43% of patients on all arms, but severe nausea and vomiting was more common in patients in the CF arm and occurred in 26% of those patients.
  • [Level of evidence: 1iiDiv]

    • Phase II studies evaluating irinotecan-based or oxaliplatin-based regimens demonstrate similar response rates and TTP to those found with ECF or CF, but the former may be less toxic.

    There are conflicting data regarding relative efficacy of any one regimen. Ongoing studies are evaluating these newer regimens.

    Trastuzumab

    Trastuzumab may be combined with first-line chemotherapy agents in treatment of HER2-positive metastatic gastric adenocarcinomas. HER2 testing is recommended for those with metastatic disease.

    Evidence (trastuzumab):

  • In the open-label, international phase III Trastuzumab for Gastric Cancer trial (ToGA [NCT01041404]) , patients with HER2-positive metastatic, inoperable locally advanced, or recurrent gastric or gastroesophageal junction cancer were randomly assigned to chemotherapy with or without the anti-HER2 monoclonal antibody trastuzumab.
  • HER2 positivity was defined as either 3+ staining by IHC or a HER2 to CEP17 ratio of two or more using FISH. Tumors from 3,665 patients were HER2 tested; of the patients, 810 were positive (22%) and 594 met eligibility criteria for randomization. Chemotherapy consisted of cisplatin plus 5-FU or capecitabine chosen at the investigator’s discretion. The study treatment was administered every 3 weeks for six cycles, and trastuzumab was continued every 3 weeks until disease progression, unacceptable toxicity, or withdrawal of consent. Crossover to trastuzumab at disease progression was not permitted.
  • Median OS was 13.8 months (95% CI, 12–16) in patients assigned to trastuzumab and 11.1 months (95% CI, 10–13) in patients assigned to chemotherapy alone (HR, 0.74; 95% CI, 0.60–0.91; P = .0046).
  • [Level of evidence: 1iiA]
  • There was no significant difference in rates of any adverse event, and cardiotoxic effects were equally rare in both arms.

    • Second-line palliative systemic therapy

    Palliative chemotherapy

    When patients develop progression of disease after first-line palliative chemotherapy, there is no standard treatment option. Accepted regimens include irinotecan with or without 5-FU/leucovorin, docetaxel, and paclitaxel with or without ramucirumab. (Refer to the Ramucirumab section of this summary for more information.)

    Evidence (palliative chemotherapy):

  • Investigators in Korea randomly assigned patients with advanced gastric cancer who had received one or two chemotherapy regimens previously that involved both a fluoropyrimidine and a platinum agent to either salvage chemotherapy or best supportive care in a 2:1 fashion.
  • Salvage chemotherapy consisted of either docetaxel (60 mg/m2 every 3 weeks) or irinotecan (150 mg/m2 every 2 weeks) and was left to the discretion of the treating physicians. Of the 202 patients enrolled, 133 received salvage chemotherapy and 69 received best supportive care.
  • Median OS was 5.3 months in the group that received salvage chemotherapy and 3.8 months in the group that received best supportive care (HR, 0.657; P = .007).
  • There was no difference in median OS between docetaxel and irinotecan (5.2 months vs. 6.5 months, P = .116).
  • [Level of evidence: 1iiA]

    • Ramucirumab

    Ramucirumab is a fully humanized monoclonal antibody directed against the vascular endothelial growth factor receptor-2.

    Evidence (ramucirumab):

  • In the international, phase III, placebo-controlled, REGARD trial (NCT00917384), 355 patients with stage IV gastric or gastroesophageal junction cancer who had progressed on a first-line 5-FU‒ or platinum-containing regimen were randomly assigned in a 2:1 fashion to ramucirumab or placebo.
  • Patients who were assigned to ramucirumab had a significantly improved median OS of 5.2 months compared with patients assigned to the placebo who had a median OS of 3.8 months (HR, 0.776; P = .047).
  • Rates of hypertension were higher in the ramucirumab group than in the placebo group.
  • [Level of evidence: 1iiA]

    • Ramucirumab is an acceptable treatment in cisplatin- or 5-FU‒refractory, stage IV, gastric cancer.

  • In the international, double-blinded, phase III RAINBOW trial (NCT01170663), 665 patients were randomly assigned to receive paclitaxel (80 mg/m2) on days 1, 8, and 15 every 28 days with ramucirumab (8 mg/kg) added on days 1 and 15 or a placebo added on days 1 and 15.
  • Patients assigned to ramucirumab had a significant improvement in median OS of 9.6 months compared with patients assigned to a placebo who had a median OS of 7.4 months (HR, 0.807; P = .017).
  • Grade 3 or higher neutropenia, fatigue, hypertension, and abdominal pain were more common in the ramucirumab group.
  • [Level of Evidence: 1iA]

    • The combination of paclitaxel and ramucirumab is an acceptable second-line chemotherapy regimen in patients with stage IV gastric or gastroesophageal junction cancer.

    Immunotherapy

    Checkpoint inhibitors, particularly programmed death 1 (PD-1) inhibitors, are actively being investigated in the management of gastric and gastroesophageal cancers. Testing for dMMR (IHC staining) or MSI polymerase chain reaction, along with PD-L1 combined positive score (CPS score in the United States) is recommended for patients with metastatic gastric adenocarcinoma.

    Second-line treatment for patients with dMMR or MSI-H tumors

    Evidence (second-line treatment for patients with dMMR or MSI-H tumors):

  • In a phase II study of pembrolizumab in patients with colon cancer with or without dMMR, and noncolorectal cancer with dMMR, immune-related objective response rate was 71% (5 of 7 patients). Based upon these data, pembrolizumab has been approved for patients with dMMR solid tumors that have progressed after prior treatment and who have no satisfactory alternative treatment options.

    • Third-line treatment for patients with PD-L1–positive tumors

    Pembrolizumab

    Evidence (pembrolizumab):

  • In the phase II KEYNOTE-059 trial (NCT02335411), 259 patients with recurrent or metastatic gastric/gastroesophageal adenocarcinomas who had progressed on at least two prior chemotherapy regimens were treated with pembrolizumab (200 mg every 3 weeks).
  • Of these patients, 57.1% had PD-L1–positive tumors (evaluated by the PD-L1 IHC 22C3 pharmDx Kit [Dako] with combined positive score ≥1).
  • Overall objective response rate for all tumors was 11.6%, with 2.3% complete response (CR). Among PD-L1–positive disease tumors, the objective response rate was 15.5%, with a 2.0% CR.
  • [Level of evidence: 2Div]

    • On the basis of these data, the U.S. Food and Drug Administration has granted pembrolizumab accelerated approval for PD-L1–positive tumors.

    Nivolumab

    Evidence (nivolumab):

  • A randomized, double-blinded, placebo-controlled, phase III trial (ONO-4538-12 [ATTRACTION-2] [NCT02267343]), enrolled 493 patients with refractory gastroesophageal/gastric cancer from Japan, South Korea, and Taiwan.
  • Patients were randomly assigned 2:1 to receive nivolumab (3mg/kg every 2 weeks) or placebo.
  • The median OS in the nivolumab group was 5.26 months (95% CI, 4.60–6.37) compared with 4.14 months with a placebo (95% CI, 3.42–4.86).
  • Serious treatment–related adverse events occurred in 10% of the patients.
  • [Level of evidence: 1iA]

    • On the basis of these data, the Japanese Ministry of Health, Labor, and Welfare approved nivolumab for treatment of advanced gastric cancer that has progressed on previously received chemotherapy.

    Treatment Options Under Clinical Evaluation for Stage IV, Inoperable, and Recurrent Gastric Cancer

    Treatment options under clinical evaluation for stage IV, inoperable, and recurrent gastric cancer include the following:

  • Palliative chemotherapy with FLOT (docetaxel, oxaliplatin, and 5-FU/leucovorin).
  • Regorafenib.
  • Cytoreductive surgery and heated intraperitoneal chemotherapy (HIPEC).

    • Treatment with poly (ADP-ribose) polymerase (PARP) inhibitors and hepatocyte growth factor inhibitors have not shown efficacy at this time.

    Current Clinical Trials

    Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available.

    ReferenceSection

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  • Ohtsu A, Shimada Y, Shirao K, et al.: Randomized phase III trial of fluorouracil alone versus fluorouracil plus cisplatin versus uracil and tegafur plus mitomycin in patients with unresectable, advanced gastric cancer: The Japan Clinical Oncology Group Study (JCOG9205). J Clin Oncol 21 (1): 54-9, 2003.
  • Waters JS, Norman A, Cunningham D, et al.: Long-term survival after epirubicin, cisplatin and fluorouracil for gastric cancer: results of a randomized trial. Br J Cancer 80 (1-2): 269-72, 1999.
  • Ross P, Nicolson M, Cunningham D, et al.: Prospective randomized trial comparing mitomycin, cisplatin, and protracted venous-infusion fluorouracil (PVI 5-FU) With epirubicin, cisplatin, and PVI 5-FU in advanced esophagogastric cancer. J Clin Oncol 20 (8): 1996-2004, 2002.
  • Cunningham D, Starling N, Rao S, et al.: Capecitabine and oxaliplatin for advanced esophagogastric cancer. N Engl J Med 358 (1): 36-46, 2008.
  • Vanhoefer U, Rougier P, Wilke H, et al.: Final results of a randomized phase III trial of sequential high-dose methotrexate, fluorouracil, and doxorubicin versus etoposide, leucovorin, and fluorouracil versus infusional fluorouracil and cisplatin in advanced gastric cancer: A trial of the European Organization for Research and Treatment of Cancer Gastrointestinal Tract Cancer Cooperative Group. J Clin Oncol 18 (14): 2648-57, 2000.
  • Al-Batran S-E, Homann N, Schmalenberg H, et al.: Perioperative chemotherapy with docetaxel, oxaliplatin, and fluorouracil/leucovorin versus epirubicin, cisplatin, and fluorouracil or capecitabine for resectable gastric or gastroesophageal junction adenocarcinoma (FLOT4-AIO): a multicenter, randomized phase 3 trial. [Abstract] J Clin Oncol 35: (Suppl 15): A-4004, 2017.
  • Van Cutsem E, Moiseyenko VM, Tjulandin S, et al.: Phase III study of docetaxel and cisplatin plus fluorouracil compared with cisplatin and fluorouracil as first-line therapy for advanced gastric cancer: a report of the V325 Study Group. J Clin Oncol 24 (31): 4991-7, 2006.
  • Ajani JA, Ota DM, Jackson DE: Current strategies in the management of locoregional and metastatic gastric carcinoma. Cancer 67 (1 Suppl): 260-5, 1991.
  • Guimbaud R, Louvet C, Ries P, et al.: Prospective, randomized, multicenter, phase III study of fluorouracil, leucovorin, and irinotecan versus epirubicin, cisplatin, and capecitabine in advanced gastric adenocarcinoma: a French intergroup (Fédération Francophone de Cancérologie Digestive, Fédération Nationale des Centres de Lutte Contre le Cancer, and Groupe Coopérateur Multidisciplinaire en Oncologie) study. J Clin Oncol 32 (31): 3520-6, 2014.
  • Ell C, Hochberger J, May A, et al.: Coated and uncoated self-expanding metal stents for malignant stenosis in the upper GI tract: preliminary clinical experiences with Wallstents. Am J Gastroenterol 89 (9): 1496-500, 1994.
  • Murad AM, Santiago FF, Petroianu A, et al.: Modified therapy with 5-fluorouracil, doxorubicin, and methotrexate in advanced gastric cancer. Cancer 72 (1): 37-41, 1993.
  • Pyrhönen S, Kuitunen T, Nyandoto P, et al.: Randomised comparison of fluorouracil, epidoxorubicin and methotrexate (FEMTX) plus supportive care with supportive care alone in patients with non-resectable gastric cancer. Br J Cancer 71 (3): 587-91, 1995.
  • Glimelius B, Ekström K, Hoffman K, et al.: Randomized comparison between chemotherapy plus best supportive care with best supportive care in advanced gastric cancer. Ann Oncol 8 (2): 163-8, 1997.
  • Wagner AD, Grothe W, Haerting J, et al.: Chemotherapy in advanced gastric cancer: a systematic review and meta-analysis based on aggregate data. J Clin Oncol 24 (18): 2903-9, 2006.
  • Webb A, Cunningham D, Scarffe JH, et al.: Randomized trial comparing epirubicin, cisplatin, and fluorouracil versus fluorouracil, doxorubicin, and methotrexate in advanced esophagogastric cancer. J Clin Oncol 15 (1): 261-7, 1997.
  • Ajani JA, Moiseyenko VM, Tjulandin S, et al.: Clinical benefit with docetaxel plus fluorouracil and cisplatin compared with cisplatin and fluorouracil in a phase III trial of advanced gastric or gastroesophageal cancer adenocarcinoma: the V-325 Study Group. J Clin Oncol 25 (22): 3205-9, 2007.
  • Ilson DH: Docetaxel, cisplatin, and fluorouracil in gastric cancer: does the punishment fit the crime? J Clin Oncol 25 (22): 3188-90, 2007.
  • Ilson DH, Saltz L, Enzinger P, et al.: Phase II trial of weekly irinotecan plus cisplatin in advanced esophageal cancer. J Clin Oncol 17 (10): 3270-5, 1999.
  • Beretta E, Di Bartolomeo M, Buzzoni R, et al.: Irinotecan, fluorouracil and folinic acid (FOLFIRI) as effective treatment combination for patients with advanced gastric cancer in poor clinical condition. Tumori 92 (5): 379-83, 2006 Sep-Oct.
  • Pozzo C, Barone C, Szanto J, et al.: Irinotecan in combination with 5-fluorouracil and folinic acid or with cisplatin in patients with advanced gastric or esophageal-gastric junction adenocarcinoma: results of a randomized phase II study. Ann Oncol 15 (12): 1773-81, 2004.
  • Bouché O, Raoul JL, Bonnetain F, et al.: Randomized multicenter phase II trial of a biweekly regimen of fluorouracil and leucovorin (LV5FU2), LV5FU2 plus cisplatin, or LV5FU2 plus irinotecan in patients with previously untreated metastatic gastric cancer: a Federation Francophone de Cancerologie Digestive Group Study--FFCD 9803. J Clin Oncol 22 (21): 4319-28, 2004.
  • Ajani JA, Baker J, Pisters PW, et al.: CPT-11 plus cisplatin in patients with advanced, untreated gastric or gastroesophageal junction carcinoma: results of a phase II study. Cancer 94 (3): 641-6, 2002.
  • Cavanna L, Artioli F, Codignola C, et al.: Oxaliplatin in combination with 5-fluorouracil (5-FU) and leucovorin (LV) in patients with metastatic gastric cancer (MGC). Am J Clin Oncol 29 (4): 371-5, 2006.
  • Bang YJ, Van Cutsem E, Feyereislova A, et al.: Trastuzumab in combination with chemotherapy versus chemotherapy alone for treatment of HER2-positive advanced gastric or gastro-oesophageal junction cancer (ToGA): a phase 3, open-label, randomised controlled trial. Lancet 376 (9742): 687-97, 2010.
  • Kang JH, Lee SI, Lim do H, et al.: Salvage chemotherapy for pretreated gastric cancer: a randomized phase III trial comparing chemotherapy plus best supportive care with best supportive care alone. J Clin Oncol 30 (13): 1513-8, 2012.
  • Fuchs CS, Tomasek J, Yong CJ, et al.: Ramucirumab monotherapy for previously treated advanced gastric or gastro-oesophageal junction adenocarcinoma (REGARD): an international, randomised, multicentre, placebo-controlled, phase 3 trial. Lancet 383 (9911): 31-9, 2014.
  • Wilke H, Muro K, Van Cutsem E, et al.: Ramucirumab plus paclitaxel versus placebo plus paclitaxel in patients with previously treated advanced gastric or gastro-oesophageal junction adenocarcinoma (RAINBOW): a double-blind, randomised phase 3 trial. Lancet Oncol 15 (11): 1224-35, 2014.
  • Fuchs CS, Doi T, Jang RW, et al.: Safety and Efficacy of Pembrolizumab Monotherapy in Patients With Previously Treated Advanced Gastric and Gastroesophageal Junction Cancer: Phase 2 Clinical KEYNOTE-059 Trial. JAMA Oncol 4 (5): e180013, 2018.
  • Kang YK, Boku N, Satoh T, et al.: Nivolumab in patients with advanced gastric or gastro-oesophageal junction cancer refractory to, or intolerant of, at least two previous chemotherapy regimens (ONO-4538-12, ATTRACTION-2): a randomised, double-blind, placebo-controlled, phase 3 trial. Lancet 390 (10111): 2461-2471, 2017.
    • 胃癌治疗(PDQ®)

    本总结中的变更（01/23/2020）

    PDQ癌症信息总结会被定期审核和更新，让最新的信息得以从中体现。本章节描述了截至上述日期对本总结所做的最新变更。

    更新了2020年估计的新发病例和死亡病例的统计数据（引用美国癌症协会的数据作为参考文献1）。

    本总结由PDQ成人治疗编辑委员会撰写并维护。该委员会在编辑权限上独立于NCI。本总结反映了对文献的独立审核观点，并不代表NCI或NIH的政策声明。如需了解更多关于本总结的政策信息，以及PDQ编辑委员会在维护PDQ总结方面作用的信息，请参见有关“本PDQ总结”和“PDQ®-NCI综合癌症数据库”页面。

    Gastric Cancer Treatment (PDQ®)

    Changes to This Summary (01/23/2020)

    The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.

    Updated statistics with estimated new cases and deaths for 2020 (cited American Cancer Society as reference 1).

    This summary is written and maintained by the PDQ Adult Treatment Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ® - NCI's Comprehensive Cancer Database pages.

    胃癌治疗(PDQ®)

    About This PDQ Summary

    Purpose of This Summary

    This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the treatment of gastric cancer. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.

    Reviewers and Updates

    This summary is reviewed regularly and updated as necessary by the PDQ Adult Treatment Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).

    Board members review recently published articles each month to determine whether an article should:

  • be discussed at a meeting,
  • be cited with text, or
  • replace or update an existing article that is already cited.

    • Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.

    The lead reviewer for Gastric Cancer Treatment is:

  • Valerie Lee, MD（约翰霍普金斯大学）

    • Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website's Email Us. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.

    Levels of Evidence

    Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Adult Treatment Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.

    Permission to Use This Summary

    PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as “NCI’s PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary].”

    The preferred citation for this PDQ summary is:

    PDQ® Adult Treatment Editorial Board. PDQ Gastric Cancer Treatment. Bethesda, MD: National Cancer Institute. Updated . Available at: https://www.cancer.gov/types/stomach/hp/stomach-treatment-pdq. Accessed . [PMID: 26389209]

    Images in this summary are used with permission of the author(s), artist, and/or publisher for use within the PDQ summaries only. Permission to use images outside the context of PDQ information must be obtained from the owner(s) and cannot be granted by the National Cancer Institute. Information about using the illustrations in this summary, along with many other cancer-related images, is available in Visuals Online, a collection of over 2,000 scientific images.

    Disclaimer

    Based on the strength of the available evidence, treatment options may be described as either “standard” or “under clinical evaluation.” These classifications should not be used as a basis for insurance reimbursement determinations. More information on insurance coverage is available on Cancer.gov on the Managing Cancer Care page.

    Contact Us

    More information about contacting us or receiving help with the Cancer.gov website can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the website’s Email Us.

    Gastric Cancer Treatment (PDQ®)

    About This PDQ Summary

    Purpose of This Summary

    This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the treatment of gastric cancer. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.

    Reviewers and Updates

    This summary is reviewed regularly and updated as necessary by the PDQ Adult Treatment Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).

    Board members review recently published articles each month to determine whether an article should:

  • be discussed at a meeting,
  • be cited with text, or
  • replace or update an existing article that is already cited.

    • Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.

    The lead reviewer for Gastric Cancer Treatment is:

  • Valerie Lee, MD (Johns Hopkins University)

    • Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website's Email Us. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.

    Levels of Evidence

    Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Adult Treatment Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.

    Permission to Use This Summary

    PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as “NCI’s PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary].”

    The preferred citation for this PDQ summary is:

    PDQ® Adult Treatment Editorial Board. PDQ Gastric Cancer Treatment. Bethesda, MD: National Cancer Institute. Updated . Available at: https://www.cancer.gov/types/stomach/hp/stomach-treatment-pdq. Accessed . [PMID: 26389209]

    Images in this summary are used with permission of the author(s), artist, and/or publisher for use within the PDQ summaries only. Permission to use images outside the context of PDQ information must be obtained from the owner(s) and cannot be granted by the National Cancer Institute. Information about using the illustrations in this summary, along with many other cancer-related images, is available in Visuals Online, a collection of over 2,000 scientific images.

    Disclaimer

    Based on the strength of the available evidence, treatment options may be described as either “standard” or “under clinical evaluation.” These classifications should not be used as a basis for insurance reimbursement determinations. More information on insurance coverage is available on Cancer.gov on the Managing Cancer Care page.

    Contact Us

    More information about contacting us or receiving help with the Cancer.gov website can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the website’s Email Us.

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    目录
    章 节
    胃癌基本信息 胃癌的细胞学分类 胃癌分期信息 治疗方案概述 0期胃癌 I期胃癌 II期和III期胃癌 无法手术的复发性IV期胃癌 本总结中的变更（01/23/2020） About This PDQ Summary
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