注：同时提供有关胃癌筛查、胃癌治疗、及癌症筛查和预防研究证据等级的单独PDQ总结。
胃癌的高危人群包括患有萎缩性胃炎或恶性贫血的老年人、散发性胃腺瘤患者、
家族性腺瘤性息肉病患者
或遗传性非息肉性结肠癌患者、
以及来自胃癌高发国家的移民种族人群
橡胶和煤矿行业工人胃癌的发病风险也较高。
胃癌的危险因素包括癌前病变，如慢性萎缩性胃炎和肠上皮化生、恶性贫血、胃腺瘤性息肉病；遗传因素包括胃癌家族史、Li-Fraumeni综合征和A型血型；
环境因素包括果蔬摄入不足、食用盐渍、熏制或变质的食品、吸烟和辐射暴露。
证据一致显示胃幽门螺杆菌感染与胃体、胃窦癌及胃淋巴瘤的发生、进展密切相关。
国际癌症研究机构（IARC）将幽门螺杆菌感染列为非贲门胃癌与胃低度恶性B细胞黏膜相关淋巴组织淋巴瘤（MALT淋巴瘤）的病因之一（即1类人类致癌物）
在幽门螺杆菌根除治疗成功的人群中，那些在治疗过程中使用质子泵抑制剂（PPI）的个体相较于未使用者胃癌的发生率更高。
但是不能忽略混杂偏倚和检测偏倚。
与普通人群相比，十二指肠溃疡患者患胃癌的风险可能更低。
基于确凿的证据，吸烟会增加胃癌的发病风险。
2004年，美国卫生总署报告中将吸烟列为胃癌的病因之一，既往吸烟者患胃癌的平均相对危险度（RR）为1.2，而当前吸烟者的RR为1.6。
与持续吸烟者相比，既往吸烟者的胃癌发病风险自戒烟起随时间不断降低。据此可认为，不吸烟或戒烟可以降低胃癌的发病风险。
影响程度：一项系统性综述与meta分析显示，与不吸烟者相比，男性吸烟者的胃癌发病风险增加60%，女性吸烟者的胃癌发病风险增加20%。
基于确凿的证据，幽门螺杆菌感染者胃癌发病风险增加。在胃癌高发地区开展的7项随机研究中，除1项之外，其余均在亚洲进行。纳入了这7项研究的meta分析结果提示，治疗幽门螺杆菌感染可降低胃癌发病风险（从1.7%降低至1.1%；RR=0.65；95%可信区间为0.43-0.98）
只有两项研究将胃癌的发病率作为主要研究结果，且只有另外两项研究为双盲试验。目前尚不明确这些研究结果对北美人群是否适用。
一项临床试验的首次报告中，对3365名受试者进行随机分组后随访，进行意向治疗分析；报告显示阿莫西林联合奥美拉唑的短期治疗后，在15年随访期内，胃癌发病率下降了39%，胃癌死亡率也呈类似降低，但并无统计学显著性。
影响程度：可能降低癌症的发病风险；对癌症死亡率的影响尚不明确。
有一定的证据显示，高盐饮食和新鲜蔬菜水果摄入不足或高盐饮食都可能增加胃癌的发病风险。从蔬菜水果或其他植物性食物中摄入的维生素C的量与胃癌发病风险降低相关。绿茶、高全麦谷物膳食或膳食中富含类胡萝卜素和葱属植物化合物均可降低胃癌的发病风险。然而目前尚不确定调整膳食模式（如增加蔬菜、水果、全麦谷物摄入）能否降低胃癌的发病风险。
影响程度：小，难以确定。
Note: Separate PDQ summaries on Stomach (Gastric) Cancer Screening, Gastric Cancer Treatment, and Levels of Evidence for Cancer Screening and Prevention Studies are also available.
People at elevated risk for gastric cancer include elderly patients with atrophic gastritis or pernicious anemia, patients with sporadic gastric adenomas,
familial adenomatous polyposis,
or hereditary nonpolyposis colon cancer,
and immigrant ethnic populations from countries with high rates of gastric carcinoma.
Workers in the rubber and coal industries are also at increased risk.
Risk factors for gastric cancer include the presence of precursor conditions such as chronic atrophic gastritis and intestinal metaplasia, pernicious anemia, and gastric adenomatous polyps. Genetic factors include a family history of gastric cancer, Li Fraumeni syndrome, and type A blood type.
Environmental factors include low consumption of fruits and vegetables; consumption of salted, smoked, or poorly preserved foods; cigarette smoking; and radiation exposure.
There is consistent evidence that Helicobacter pylori infection, also known as H. pylori infection, of the stomach is strongly associated with both the initiation and promotion of carcinoma of the gastric body and antrum and of gastric lymphoma.
The International Agency for Research on Cancer classifies H. pylori infection as a cause of noncardia gastric carcinoma and gastric low-grade B-cell mucosa-associated lymphoid tissue or MALT lymphoma (i.e., a Group 1 human carcinogen).
Gastric cancer has been observed to be more common among individuals who use proton pump inhibitors (PPIs), relative to nonusers, after apparent successful H. Pylori eradication therapy,
but confounding and detection bias cannot be ruled out as explanations.
Compared with the general population, people with duodenal ulcer disease may have a lower risk of gastric cancer.
Based on solid evidence, smoking is associated with an increased risk of stomach cancer.
The 2004 Surgeon General’s report identifies cigarette smoking as a cause of stomach cancer, with an average relative risk (RR) in former smokers of 1.2 and in current smokers of 1.6.
Compared with persistent smokers, the risk of stomach cancer decreases among former smokers with time since cessation. This pattern of observations makes it reasonable to infer that cigarette smoking prevention or cessation would result in a decreased risk of gastric cancer.
Magnitude of Effect: A systematic review and meta-analysis showed a 60% increase in gastric cancer in male smokers and a 20% increase in gastric cancer in female smokers compared with nonsmokers.
Based on solid evidence, H. pylori infection is associated with an increased risk of gastric cancer. A meta-analysis of seven randomized studies, all conducted in areas of high-risk gastric cancer and all but one conducted in Asia, suggests that treatment of H. pylori may reduce gastric cancer risk (from 1.7% to 1.1%; RR = 0.65; 95% confidence interval, 0.43–0.98).
Only two studies assessed gastric cancer incidence as the primary study outcome, and two different studies were double blinded. It is unclear how generalizable the results may be to the North American population.
In the initial report from a clinical trial, 3,365 randomized subjects were followed in an intention-to-treat analysis; it was shown that short-term treatment with amoxicillin and omeprazole reduced the incidence of gastric cancer by 39% during a period of 15 years following randomization, with similar but not statistically significant reductions for gastric cancer mortality.
Magnitude of Effect: Risk of cancer may be reduced; effect on cancer mortality is not known.
Based on fair evidence, excessive salt intake and deficient dietary consumption of fresh fruits and vegetables are associated with an increased risk of gastric cancer. Dietary intake of vitamin C contained in vegetables, fruits, and other foods of plant origin is associated with a reduced risk of gastric cancer. Diets high in whole-grain cereals, carotenoids, allium compounds, and green tea are also associated with a reduced risk of this cancer. However, it is uncertain if changing one's diet to include more vegetables, fruits, and whole grains would reduce the risk of gastric cancer.
Magnitude of Effect: Small, difficult to determine.
2004至2008年间，美国年龄校正后的胃癌发病率为7.7/10万，男性发病率为女性的两倍。据估计，2015年中国胃癌发病世标率为18.57/10万，男性发病率约为女性的2.5倍。
近几十年来，世界范围内胃癌的死亡率一直在下降，在美国尤为突出。而中国胃癌死亡率并未出现下降趋势。
1930年，美国白人男性的胃癌死亡率约为40/10万，而2003至2007年间则为4.6/10万。此外在2003至2007年间，美国黑人男性的胃癌死亡率比白人高2.3倍。在2003~2007年，中国胃癌死亡率为12.00/10万，而2015年则为13.08/10万。
近年来，美国每年胃癌新发病例数稳定，据估计，到2020年，美国将有2.76万人被诊断为胃癌，有11010人将因胃癌而死亡。据估计，2015年中国胃癌新发病例40.3万例，死亡29.1万例。
胃癌是世界上第四大最常见的癌症。胃癌是中国第二大最常见癌症。
据估计，2008年全球每年胃癌患者约为98.8万例，因胃癌死亡人数约为73.6万人。不同国家地区的胃癌年龄标化发病率各不相同：男性从3.9/10万到42.4/10万，女性从2.2/10万到18.3/10万。70%以上的胃癌患者在发展中国家，50%在东亚。
美国大多数胃癌患者在确诊时已为晚期，表现在2005年至2011年间胃癌患者的5年总生存率为29.9%。随着大规模胃癌筛查工作的开展，中国胃癌患者的生存率逐渐提高，表现为2002到2005年胃癌患者年龄标化的5年生存率为27.4%；从2012年到2015年5年生存率达35.1%。
局限于黏膜或黏膜下层的肿瘤（“早期”胃癌）预后较好，在日本此类患者的5年总生存率为95%以上，在美国为65%以上。在胃癌的高危人群中，与筛查项目相关的二级预防措施已经确立。
在日本，内窥镜切除技术日臻完善，在胃癌发病率稳定的情况下有望大幅降低死亡率。然而，这一假设尚未经过临床试验证实。（详情请参阅PDQ总结中胃癌的筛查。）
近年来学术界对胃癌发病机制的认识逐渐深入。在正常胃黏膜转变为胃癌的漫长过程中，一系列的癌前变化过程已经得到确认，如：正常的胃黏膜会逐渐转化为慢性胃炎、多灶性萎缩性胃炎，进而进展为不同程度的肠上皮化生、不典型增生，最后发展为浸润性胃癌。
胃黏膜上皮长年接受的各类刺激促进了这一转化过程，如高盐饮食，最为显著的一个因素是幽门螺杆菌感染。
一项系统综述和meta分析显示，与不吸烟者相比，男性吸烟者的胃癌发病风险增加60%，女性吸烟者的胃癌发病风险增加20%。
一项基于吸烟和胃癌关系研究的系统综述分析了不同暴露水平下吸烟和胃癌之间的关联强度，为证实吸烟为胃癌最重要的行为危险因素提供了有力的证据。
与持续吸烟者相比，既往吸烟者胃癌风险自戒烟起随时间不断降低。这些研究结果提示，不吸烟或戒烟可以降低胃癌的发病风险。
幽门螺杆菌感染是胃腺癌的公认病因。
幽门螺杆菌感染的自然史尚待研究，不同人群的传播机制、再次感染率与复发率尚不明确。
一项140例幽门螺杆菌感染者参与的小规模随机临床试验表明，可能存在密切接触的家庭成员间的传播。
其中70例受试者仅本人接受了幽门螺杆菌根除治疗，另外70例受试者与同住的有幽门螺杆菌感染的家人均接受了幽门螺杆菌根除治疗。治疗后9个月，两组的感染阳性率分别为38.6%与7.1%（比值比为8.61；95%可信区间（CI），2.91-22.84），结果提示家庭成员中未经治疗的感染者可能会导致传播。
全球约半数人口有幽门螺杆菌感染，但对所有慢性感染患者进行抗菌治疗难以实现，且可能会产生耐药性。已经在动物实验模型上证实了抗幽门螺杆菌疫苗的有效性，但迄今为止，尚未在人体内开展疫苗的有效性研究。
一项随机对照试验表明，在随机分组后的15年随访期内，阿莫西林联合奥美拉唑的短期治疗后可使胃癌发病率下降了39%，胃癌死亡率也呈类似降低，但并无统计学显著性。
在不同胃癌风险水平的人群中治疗幽门螺杆菌的获益程度尚不清楚。一项基于随机对照试验和观察性的系统综述和meta分析评估了三种不同临床情况下的幽门螺杆菌治疗方案。
作者共纳入 24 项研究（其中22 项来自亚洲），在34万人年的随访中，发现参与随访的48,000 人中有715 例胃癌患者。接受幽门螺杆菌根除治疗的人胃癌发生率较低（合并RR为0.53；95%CI为0.44-0.64）。在无症状感染者（合并RR为0.62；95%CI为0.49-0.79）和行内镜下胃癌切除术后的患者（合并RR为0.46；95%CI为0.35-0.60）中，幽门螺杆菌根除治疗均和胃癌风险显著降低相关。在胃癌发病率最低的人群中，胃癌风险并未降低。该研究的局限性包括未考虑治疗的副作用，例如引起幽门螺杆菌和其他微生物的抗生素耐药性；幽门螺杆菌的根除可能会降低幽门螺杆菌对食管腺癌的保护作用。研究结果可能对某些高危人群的治疗有一定的指导意义，如美国的亚洲移民群体和基础胃黏膜疾病（如萎缩性胃炎）患者；或有助于预防复发性胃癌。
质子泵抑制剂（PPI）的使用与胃萎缩的恶化有关，尤其是在幽门螺杆菌感染的个体中。一项研究分析了全香港地区健康数据库中在2003到2012年间接受过幽门螺旋菌治疗的63397例治愈患者信息。结果表明，与幽门螺杆菌治疗后未使用PPI的患者相比，幽门螺杆菌治疗后使用PPI的患者患胃癌的风险增加了两倍以上。
由于这一结果可能是由残余混杂或检测偏倚所引起，其与临床实际情况的相关性尚不确定。
相关性和病例对照研究已经表明过多的盐摄入是胃癌的一个可能危险因素。
归功于公共卫生系统所开展的高血压疾病的宣传，日本与大多数西方国家居民的每日盐摄入量已经明显降低，这可能与胃癌发病率的下降有一定关系。高盐摄入与胃癌风险之间存在关联的一致性。
病例对照的研究和队列研究的流行病学证据表明，新鲜水果和蔬菜摄入量的增加与胃癌发病率的降低有关。
然而，尚未开展随机对照试验以正式因果关联。
由于有证据表明胃癌与饮食中水果和蔬菜的摄入，尤其是那些富含抗氧化剂的水果和蔬菜的摄入呈负相关，含有抗氧化剂的膳食补充剂引起了研究者的兴趣。
研究者计算了受试者膳食中微量营养素的摄入情况，表明 β 胡萝卜素、维生素 A、维生素 E、硒、维生素 C 或含有这些化合物的食物可能是胃癌的保护因素。中国的一项化学干预试验结果显示，补充β 胡萝卜素、维生素E和硒有助于降低胃癌死亡率，结果具有统计学显著性。
然而，研究人群可能存在营养不良的情况，结果尚不确定是否可以推广到其他人群（例如美国）。此外，实验性的研究设计无法评估β-胡萝卜素、维生素E和硒的相对作用。
同样，在中国山东省栖霞县开展了一项为期3年的随机、安慰剂对照试验，即每天口服 200 mg 大蒜素（大蒜的成分之一）同时每隔一天口服 100 mcg 硒，每年持续 服用1 个月。该地区大蒜摄入量及大蒜中硒含量均低于中国其他地区。
尽管研究设计为双盲试验，但大蒜素可散发大蒜的独特气味，对双盲的实施存在一定影响。研究共招募5033人，入选的受试者应至少符合以下一条标准：（1）胃部疾病病史，（2）肿瘤家族史，（3）吸烟史，（4）饮酒史，这些受试者被随机分配到各组。该研究发表于中国医学期刊，具体不详。随访11年后，大蒜素/硒元素组共出现23例胃癌病例，而安慰剂组则出现30例（基线特征校准后RR= 0.48； 95%CI，0.21-1.06）。这些胃癌病例中仅60%经病理组织学确诊。研究结果的性别差异明显：男性RR= 0.36（95%CI，0.14-0.92）；女性RR= 1.14（95%CI，0.22-5.76）。鉴于此研究的设计缺陷与结果报告问题，获益证据（包括男性）等级较弱，可能无法推广至西方国家。
在委内瑞拉的胃癌高危人群中开展一项随机、双盲、化学干预试验显示抗氧化维生素（维生素 C、E 和 β 胡 萝卜素）联合服用并未改变胃癌前病变的进展或转归。
本试验中维生素补充剂并未产生效果的另一个可能解释是研究人群中晚期癌前病变的患病率和幽门螺杆菌的感染率均偏高。
一项基于芬兰男性吸烟者中α-生育酚 β-胡萝卜素试验的二次研究评价了补充维生素对胃癌发病率的影响。
未观察到这些营养补充剂对胃癌的保护作用。在已报道的一项对976例哥伦比亚患者进行的为期6年的随访研究中，患者被随机分配接受8种不同的治疗方案，包括单独或联合使用维生素补充剂及抗幽门螺杆菌治疗，并与安慰剂组进行对照。接受抗幽门螺杆菌治疗的79例患者与安慰剂对照组相比，其肠上皮化生有一定程度的退行性改变，结果处于统计学显著性的临界值（15%vs6%；RR= 3.1；95%CI，1.0-9.3）。但并未观察到抗生素与维生素联合使用的额外获益。更为重要的是，肠上皮化生的进展率并不随治疗改变。安慰剂组的胃癌进展率为23%，抗生素组则为17%
一项关于抗氧化剂膳食补充剂预防胃肠道癌症（包括胃癌）的随机试验的系统综述，评价了膳食营养补充剂这一干预措施在胃癌预防中的作用。
二十项试验评估了抗氧化补充剂或维生素C对胃肠道癌症的预防作用。对于胃癌，有12项试验是对一种或多种微量营养素联合使用与安慰剂对照进行比较，包括单用β胡萝卜素（4项试验）；单用维生素C（1项试验）；单用维生素E（1项试验）；维生素A联合β胡萝卜素（1项试验）；β胡萝卜素联合维生素C（1项试验）；β胡萝卜素联合维生素E（1项试验）；β胡萝卜素联合维生素C与E（1项试验）；硒联合维生素C与E（1项试验）；β胡萝卜素、维生素C、维生素E和硒联合使用（1项试验）。上述研究结果均未发现抗氧化补充剂对胃癌发病率的影响有统计学显著性。对所有抗氧化剂试验结果的综合评估亦无显著性差异（胃癌RR= 1.14；95%CI，0.97-1.33）。经过2.1-12年的治疗后，联合补充抗氧化剂组中约有0.51%的受试者罹患胃癌，而安慰剂组则为0.38%，随访时间最长的可达14.1年。对20项研究利用固效应模型进行综合分析发现，服用抗氧化剂组总死亡率高于安慰剂组（死亡率RR= 1.04；95%CI，1.02-1.07），但随机效应模型中并未发现这一结果（死亡率RR= 1.02；95%CI：0.97-1.07）。
The age-adjusted incidence rate for gastric cancer in the United States for the years 2004 to 2008 was 7.7 persons per 100,000 population. Incidence among men is twice as high as among women.
Mortality rates for gastric cancer have been declining worldwide in recent decades, most prominently in the United States.
Mortality rates for white males in the United States were approximately 40 deaths per 100,000 population in 1930, compared with 4.6 deaths per 100,000 population for the years 2003 to 2007. The death rate from gastric cancer for black males was 2.3 times higher than for whites for the years 2003 to 2007.
The annual number of new cases seems to be steady in recent years; in 2020, it is estimated that 27,600 Americans will be diagnosed with gastric cancer and 11,010 persons will die of it.
Gastric cancer is the fourth most common cancer in the world.
Worldwide, the estimated number of cases per year in 2008 was 988,000, and the estimated number of deaths was 736,000. Age-standardized annual incidence rates vary widely across the world: from 3.9 to 42.4 cases per 100,000 in men, and from 2.2 to 18.3 cases per 100,000 in women. More than 70% of cases occur in developing countries, and 50% of the cases occur in Eastern Asia.
Most gastric cancers in the United States are advanced at diagnosis, which is reflected in an overall 5-year survival rate of 29.9% from 2005 to 2011.
Carcinomas localized to the mucosa or submucosa (“early” cancers) have a much better prognosis; the 5-year survival rate is more than 95% in Japan and more than 65% in the United States. In high-risk populations, secondary prevention measures linked to screening programs have been instituted.
In Japan, endoscopic resection techniques have been refined and could possibly be responsible for drastic reductions in mortality rates in the presence of steady incidence rates. This hypothesis, however, has not been tested in clinical trials. (Refer to the PDQ summary on Stomach (Gastric) Cancer Screening for more information.)
Understanding the pathogenesis of gastric cancer has advanced over the years. A lengthy precancerous process has been identified in which the gastric mucosa is slowly transformed from normal to chronic gastritis, to multifocal atrophy, to intestinal metaplasia of various degrees, to dysplasia, and then to invasive carcinoma.
The process is apparently driven by forces acting on the gastric epithelium for many years, such as excessive dietary salt and most prominently, infection with Helicobacter pylori.
A systematic review and meta-analysis showed a 60% increase in gastric cancer in male smokers and a 20% increase in gastric cancer in female smokers compared with nonsmokers.
A systematic review of studies addressing the relationship between cigarette smoking and gastric cancer to estimate the magnitude of the association for different levels of exposure to cancer provides solid evidence to classify smoking as the most important behavioral risk factor for gastric cancer.
Compared with persistent smokers, the risk of stomach cancer decreases among former smokers with time since cessation. The pattern that emerges from these observations makes it reasonable to infer that cigarette smoking prevention or cessation would result in a decreased risk of gastric cancer.
H. pylori infection is an accepted cause of gastric adenocarcinoma.
Questions remain concerning the natural history of H. pylori infection; the mechanism of transmission and the rates of reinfection or recrudescence for different populations are unknown.
A small randomized trial of antibiotic eradication in 140 H. pylori-infected people suggests the possibility of transmission among close family members.
In 70 participants, only the participant received eradication therapy; in the other 70 participants, all H. pylori-infected family members living with the primary participant also received the eradication therapy. Nine months after the therapy, the positivity rates in the index participants in each group were 38.6% and 7.1%, respectively (odds ratio = 8.61; 95% confidence interval [CI], 2.91–22.84), suggesting the possibility of transmission from untreated, infected family members.
Because about half of the world population is infected with H. pylori, antibacterial treatment for all people who are chronically infected may be impractical and could trigger antimicrobial resistance. Vaccination against H. pylori has been shown effective in experimental animal models, but thus far, such efficacy has not been studied in humans.
A randomized controlled trial (RCT) showed that short-term treatment with amoxicillin and omeprazole reduced the incidence of gastric cancer by 39% during a period of 15 years following randomization, with similar but not statistically significant reductions for gastric cancer mortality.
The magnitude of benefit of treating H. pylori in populations with different levels of gastric cancer risk has been unclear. A systematic review and meta-analysis of RCTs and observational studies was done to assess the treatment of H. pylori with curative regimens for three different clinical scenarios:
The authors found 24 eligible studies (22 from Asia) with 715 incident gastric cancers among 48,000 individuals in 340,000 person-years of follow-up. Individuals with eradication treatment for H. pylori had a lower incidence of gastric cancer (pooled incidence rate ratio, 0.53; 95% CI, 0.44–0.64). Treatment was associated with substantially lower risk in individuals who had asymptomatic infection (pooled incidence rate ratio, 0.62; 95% CI, 0.49–0.79) and in individuals after endoscopic resection of gastric cancer (pooled incidence rate ratio, 0.46; 95% CI, 0.35–0.60). Risk was not lower in those in the lowest tertile of gastric cancer incidence. Limitations of the study include a lack of consideration of the negative effects of treatment, such as causing antibiotic resistance of H. pylori and other microorganisms; and that eradication of H. pylori might reduce a postulated protective effect of H. pylori for esophageal adenocarcinoma. The results may have implications for the treatment of some subgroups of individuals with particularly high risk, such as Asian immigrant populations in the United States and individuals with underlying gastric mucosal disease (such as atrophic gastritis); or to help prevent recurrent gastric cancer.
Proton pump inhibitor (PPI) use is associated with worsening of gastric atrophy, particularly in H. pylori–infected individuals. One study analyzed 63,397 patients who were included in a territory-wide health database in Hong Kong, who had been treated for H. pylori between 2003 and 2012, and who had appeared to be cleared of the infection. The results suggested more than a twofold increase in risk of gastric cancer for those who used PPIs after H. pylori treatment, relative to those who had not used PPIs after H. pylori treatment.
Because the finding could be caused by residual confounding or detection bias, its relevance to clinical practice is uncertain.
Excessive salt intake has been identified as a possible risk factor for gastric cancer in correlation and case-control studies.
The daily intake of salt has decreased drastically in most western countries and in Japan, in part due to public health campaigns to reduce hypertensive diseases. This may be at least partially responsible for declines in gastric cancer rates. There is a consistent association between high salt intake and the risk of gastric cancer.
Epidemiologic evidence from case-control and cohort studies suggests that increased intake of fresh fruits and vegetables is associated with decreased gastric cancer rates.
However, no RCTs have been done to establish a causal association.
Because of the evidence for an inverse association between gastric cancer and dietary intake of fruits and vegetables, especially those rich in antioxidants, there has been interest in dietary supplementation with antioxidants.
Dietary indices of micronutrient intake have been calculated and indicate possible protective effects of beta carotene, vitamin A, vitamin E, selenium, vitamin C, or foods that contain these compounds. A chemoprevention trial in China reported a statistically significant reduction in the gastric cancer mortality rate after supplementation with beta carotene, vitamin E, and selenium.
The population studied, however, may have been nutritionally deficient, raising questions of generalizability to other populations such as that of the United States. In addition, the experimental design did not permit assessment of the relative effects of beta carotene, vitamin E, and selenium.
Likewise, there was a randomized placebo-controlled trial of 200 mg of oral allitridium (a component of garlic) every day combined with 100 mcg of oral selenium every other day for 1 month of each year over a 3-year period in Qixia County (Shandong Province, China), an area with low intake of garlic and low selenium content in their garlic compared with other areas of China.
Although designed as a double-blinded trial, allitridium causes a distinctive odor of garlic. A total of 5,033 people, who met at least one of the following criteria: (1) medical history of stomach disorder, (2) family history of tumor, (3) history of smoking, or (4) history of alcohol consumption, were randomly assigned. The study, published in a Chinese medical journal, was not well described. After a follow-up for as many as 11 years, there were a total of 23 gastric cancer cases in the allitridium/selenium group and 30 cases in the placebo group (relative risk [RR] after adjustment for a number of baseline characteristics = 0.48; 95% CI, 0.21–1.06). Only 60% of the gastric cancers were diagnosed by histopathology. There was a qualitative difference in outcome by sex: RRmen = 0.36 (95% CI, 0.14–0.92); RRwomen = 1.14 (95% CI, 0.22–5.76). Given the problems with design and reporting of the study, the evidence of benefit (including men) is weak and may not be generalizable to Western countries.
In a randomized, double-blind, chemoprevention trial in Venezuela among a population at increased risk for gastric cancer, a combination of antioxidant vitamins (vitamins C, E, and beta carotene) failed to modify progression or regression of precancerous gastric lesions.
Another potential explanation for the lack of benefit of vitamin supplementation in this trial was the high prevalence of advanced premalignant lesions and the high H. pylori infection rate.
A secondary analysis of the Alpha-Tocopherol Beta Carotene trial conducted in male smokers in Finland evaluated the effect of supplementation on gastric cancer incidence.
No protective effects for these supplements against gastric cancer were observed. Six-year follow-up results of a study of 976 Colombian patients have been reported. Patients were randomly assigned to receive eight different treatments that included vitamin supplements and anti-H. pylori therapy either alone or in combination versus placebo. Among the 79 patients who received anti-H. pylori therapy, a borderline statistically significant regression of intestinal metaplasia when compared with a placebo (15% vs. 6%; RR, 3.1; 95% CI, 1.0–9.3) was noted. However, the combinations of antibiotics and vitamins did not confer additional benefits. More importantly, the progression rate of intestinal metaplasia was comparable irrespective of the treatments received. The progression rate was 23% in the placebo group and 17% in antibiotic recipients.
A systematic review examined randomized trials of antioxidant dietary supplements for the prevention of gastrointestinal cancers, including gastric cancer.
Twenty trials were identified that assessed the preventive effects of antioxidant supplements or vitamin C on gastrointestinal cancer. With regard to gastric cancer, there were 12 comparisons of one or more micronutrients with placebo: beta-carotene alone (4 trials); vitamin C alone (1 trial); vitamin E alone (1 trial); vitamin A plus beta-carotene (1 trial); beta-carotene plus vitamin C (1 trial); beta-carotene plus vitamin E (1 trial); beta-carotene plus vitamins C and E (1 trial); selenium plus vitamins C and E (1 trial); and beta-carotene, vitamins C and E, and selenium (1 trial). None of the comparisons showed a statistically significant effect on the incidence of gastric cancer. The overall summary estimate across all trials of antioxidants showed no statistically significant effect (RR of gastric cancer, 1.14; 95% CI, 0.97–1.33). Approximately 0.51% of participants in the combined antioxidant groups developed gastric cancer versus 0.38% in the placebo groups after treatment of 2.1 to 12 years and follow-up for as many as 14.1 years. In the combined analysis of all 20 trials of antioxidants for the prevention of gastrointestinal cancers, a fixed effects model showed an increase in overall mortality of antioxidants compared with a placebo (RR for mortality, 1.04; 95% CI, 1.02–1.07) but not in a random effects model (RR for mortality, 1.02; 95% CI, 0.97–1.07)
定期对PDQ癌症信息总结进行审核，并在获得新信息时予以更新。本节介绍了截至上述日期对本总结所做的最新更改。
更新了2020年估计新发病例和死亡人数的统计数据（引自美国癌症协会数据—参考文献5）。
本总结由PDQ筛查与预防编辑委员会编写和维护，编辑委员会在编辑方面独立于NCI。本总结反映了对文献的独立审查，并不代表NCI或NIH的政策声明。关于总结政策和PDQ编辑委员会在维护PDQ总结中作用的更多信息，请参见关于本PDQ总结和PDQ®-NCI的综合癌症数据库页面。
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 5).
This summary is written and maintained by the PDQ Screening and Prevention 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.
This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about stomach (gastric) cancer prevention. 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.
This summary is reviewed regularly and updated as necessary by the PDQ Screening and Prevention 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:
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.
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.
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 Screening and Prevention Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.
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® Screening and Prevention Editorial Board. PDQ Stomach (Gastric) Cancer Prevention. Bethesda, MD: National Cancer Institute. Updated
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.
The information in these summaries 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.
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.
This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about stomach (gastric) cancer prevention. 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.
This summary is reviewed regularly and updated as necessary by the PDQ Screening and Prevention 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:
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.
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.
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 Screening and Prevention Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.
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® Screening and Prevention Editorial Board. PDQ Stomach (Gastric) Cancer Prevention. Bethesda, MD: National Cancer Institute. Updated
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.
The information in these summaries 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.
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.