对绝大多数人来说，结直肠癌（CRC）风险增加的主要因素是年龄增长。50岁以后风险明显增加；有90%的CRC病例在50岁后才被诊断。与其他种族相比，非裔美国人的发病率和死亡率更高；然而，一项meta分析结果则未发现非裔美国人有更高的癌前期病变发生率。
一级亲属中有CRC病史、年龄小于55岁者，其风险约增加1倍。个人有CRC病史、高危腺瘤或卵巢癌病史也会增加风险。
其他危险因素弱于年龄和家族史。 患有炎症性肠道疾病（如溃疡性结肠炎或克罗恩病）的人，在其发病8年后结直肠癌的风险明显增高，建议定期进行肠镜检查。
一小部分CRC（<5%）发生在有遗传倾向的人群中，包括家族性腺瘤性息肉和遗传性非息肉性结直肠病变的患者。
For the great majority of people, the major factor that increases a person’s risk for colorectal cancer (CRC) is increasing age. Risk increases dramatically after age 50 years; 90% of all CRCs are diagnosed after this age. Incidence and mortality rates are higher in African Americans compared with other races; however, a meta-analysis found no evidence that African Americans have higher rates of precancerous lesions.
The history of CRC in a first-degree relative, especially if before the age of 55 years, roughly doubles the risk. A personal history of CRC, high-risk adenomas, or ovarian cancer also increases the risk.
Other risk factors are weaker than age and family history. People with an inflammatory bowel disease, such as ulcerative colitis or Crohn disease, have a much higher risk of CRC starting about 8 years after disease onset and are recommended to have frequent colonoscopic surveillance.
A small percentage (<5%) of CRCs occur in people with a genetic predisposition, including familial adenomatous polyposis and hereditary nonpolyposis coli.
注：关于结直肠癌筛查、结肠癌治疗和直肠癌治疗，分别在PDQ小结中叙述。
基于观察性研究的确凿证据，过度饮酒与结直肠癌（CRC）风险增加有关。
影响程度：一项对8项队列研究的综合分析结果显示，摄入量超过45g/天的调整相对危险度（RR）为1.41（95%置信区间[CI]，1.16–1.72）
基于确凿的证据，吸烟与结直肠癌发病和死亡风险增加有关。
影响程度：一项对106项观察性研究的综合分析结果显示，目前吸烟者与从未吸烟者相比，CRC的调整RR为1.18（95%CI，1.11-1.25）。
基于确凿的证据，肥胖与结直肠癌发病和死亡风险增加有关。
影响程度：在一项大型队列研究中，体重指数大于29的女性发生结肠癌的调整RR为1.45（95%CI，1.02–2.07）。
在另一项大型队列研究中，发现结直肠癌死亡率也有类似的增加。
基于确凿的证据，一级亲属CRC家族史或个人有CRC病史可增加罹患CRC的风险。
有遗传倾向者，包括家族性腺瘤性息肉和遗传性非息肉性结直肠病变，罹患CRC的风险增高。
影响程度：对于有家族性腺瘤性息肉病患者而言，到40岁时其罹患结直肠癌的风险已高达100%。林奇（ Lynch）综合征的患者一生中罹患结直肠癌的风险约为80%。
有关家族史和遗传性病变的更多信息，请参阅结直肠癌遗传学的PDQ小结。
基于确凿的证据，有规律的体力活动与结直肠癌发病率降低有关。
影响程度：一项对52项观察性研究的meta分析发现，CRC发病率降低了24%，在统计学上有显著意义（RR，0.76；95%CI，0.72-0.81）。
基于确凿的证据，每天服用阿司匹林（乙酰水杨酸[ASA]）可降低10-20年后CRC的发病率和死亡率。这是基于对阿司匹林用于心血管疾病一级和二级预防的试验的三个参与者水平数据meta分析。
影响程度：使用ASA可在约10-19年内降低40%CRC发生的长期风险（风险比[HR]，0.60；95%CI，0.47-0.76）。
每日服用75-1200mg ASA可将20年结直肠癌死亡风险降低约33%（HR，0.67；95%CI，0.52-0.86）。
基于确凿的证据，使用ASA的危害包括过度出血，包括胃肠道出血和出血性卒中。
影响程度：使用超低剂量ASA（即每天或每隔一天不超过100mg）可导致10年内预计每1000人中额外发生14例（95%CI，7-23）严重胃肠道出血事件和3.2例（95%CI，-0.5-0.82）额外出血性卒中事件。这些风险随着年龄的增长而增加。
基于确凿的证据，联合激素治疗（马结合雌激素联合孕激素）可降低浸润性结直肠癌的发病率。
基于确凿的证据，马结合雌激素联合孕激素在降低结直肠癌死亡率方面几乎没有或根本没有益处。来自妇女健康倡议（WHI）的数据，一项评估雌激素联合孕激素的随机、安慰剂对照试验，平均干预时间为5.6年，随访时间为11.6年，结果显示，与服用安慰剂的妇女相比，接受激素联合治疗的妇女在诊断时癌症（病灶处和远处转移）的分期在统计学上显著升高，但结直肠癌死亡数在统计学上没有显著意义。
影响程度：联合激素治疗组的CRC病例比安慰剂组少（0.12% vs 0.16%；HR，0.72；95%CI，0.56-0.94）。队列研究的meta分析观察到，与激素联合治疗相关的结直肠癌发病率的相对风险为0.86（95%CI，0.76-0.97）。
联合激素治疗组有37例CRC患者死亡，而安慰剂组有27例（0.04% vs 0.03%；HR，1.29；95%CI，0.78-2.11）。
基于确凿的证据，绝经后联合使用雌激素和孕激素的危害包括乳腺癌、冠心病和血栓栓塞事件的风险增加。
影响程度：WHI显示联合激素治疗组浸润性乳腺癌增加26%，冠心病事件增加29%，卒中率增加41%，血栓栓塞事件增加2倍。
基于确凿的证据，切除腺瘤性息肉可降低结直肠癌的风险。这种降低大部分可能是由于切除大息肉（即>1.0cm），而切除非常常见的小息肉的获益尚不清楚。一些证据表明，左侧CRC的风险降低可能大于右侧。
基于确凿的证据，息肉切除的主要危害包括结肠穿孔和出血。
影响程度：每1000次操作中发生7到9例次。
没有充分的证据表明使用非甾体抗炎药可以降低结直肠癌的风险。在无遗传倾向但有结肠腺瘤切除病史的人群中，3项RCT发现塞来昔布和罗非昔布降低了复发性腺瘤的发生率，但随访时间太短而无法确定是否会影响CRC发病率或死亡率。
基于确凿的证据，非甾体抗炎药可降低腺瘤的风险，但降低CRC风险的程度尚不确定。
基于确凿的证据，使用非甾体抗炎药的危害相对常见，且可能比较严重，包括上消化道出血、慢性肾脏疾病和严重的心血管事件，如心肌梗死、心力衰竭和出血性卒中。
最近一项报告比较了环氧化酶-2（COX-2）抑制剂塞来昔布（200 mg/d）与非选择性非甾体类药物萘普生（850 mg/d）和布洛芬（2000 mg/d）在严重关节炎患者中的作用（即未使用低剂量作为一级预防）。结果显示，服用非选择性非甾体类药物的患者发生严重心血管事件的几率并不低。然而，该研究未评估较低剂量的相对安全性，也没有评估COX-2抑制剂罗非昔布的安全性。
影响程度：非甾体抗炎药引起的上消化道并发症的平均超额风险估计为每年每1000人中有4至5例。
超额风险因潜在的胃肠道风险而不同，然而，在超过10%的使用者中，其可能超过每1000人每年10个额外病例。
严重心血管事件增加了50%到60%。
没有充分的证据确定补钙是否能降低CRC的风险。
没有可靠的证据表明，从成年开始的低脂肪、少肉、高纤维、高水果和高蔬菜的饮食可以在临床上显著降低CRC风险。
基于一般的证据，马结合雌激素不影响浸润性结直肠癌的发病率或患者生存率。
影响程度：不适用。
基于确凿的证据，他汀类药物不能降低CRC的发病率或死亡率。
基于确凿的证据，他汀类药物的危害很小。
Note: Separate PDQ summaries on Colorectal Cancer Screening; Colon Cancer Treatment; and Rectal Cancer Treatment are also available.
Based on solid evidence from observational studies, excessive alcohol use is associated with an increased risk of colorectal cancer (CRC).
Magnitude of Effect: A pooled analysis of eight cohort studies estimated an adjusted relative risk (RR) of 1.41 (95% confidence interval [CI], 1.16–1.72) for consumption exceeding 45 g/day.
Based on solid evidence, cigarette smoking is associated with increased incidence of and mortality from CRC.
Magnitude of Effect: A pooled analysis of 106 observational studies estimated an adjusted RR (current smokers vs. never smokers) of 1.18 for developing CRC (95% CI, 1.11–1.25).
Based on solid evidence, obesity is associated with increased incidence of and mortality from CRC.
Magnitude of Effect: In one large cohort study, the adjusted RR of developing colon cancer for women with a body mass index greater than 29 was 1.45 (95% CI, 1.02–2.07).
A similar increase in CRC mortality was found in another large cohort study.
Based on solid evidence, a family history of CRC in a first-degree relative or a personal history of CRC increases the risk of CRC.
Having a genetic predisposition, including familial adenomatous polyposis and hereditary nonpolyposis coli, also increases risk of CRC.
Magnitude of Effect: In persons with familial adenomatous polyposis, the risk of CRC by age 40 can be as high as 100%. Persons with Lynch syndrome can have a lifetime risk of CRC of about 80%.
Refer to the PDQ summary on Genetics of Colorectal Cancer for more information about family history and hereditary conditions.
Based on solid evidence, regular physical activity is associated with a decreased incidence of CRC.
Magnitude of Effect: A meta-analysis of 52 observational studies found a statistically significant 24% reduction in CRC incidence (RR, 0.76; 95% CI, 0.72–0.81).
Based on solid evidence, daily aspirin (acetylsalicylic acid [ASA]) reduces CRC incidence and mortality after 10 to 20 years. This is based on three individual participant-level data meta-analyses of trials of aspirin used for the primary and secondary prevention of cardiovascular disease.
Magnitude of Effect: ASA use reduces the long-term risk of developing CRC by 40% about 10 to 19 years after initiation (hazard ratio [HR], 0.60; 95% CI, 0.47–0.76).
Daily doses of 75 to 1,200 mg of ASA reduce the 20-year risk of CRC death by approximately 33% (HR, 0.67; 95% CI, 0.52–0.86).
Based on solid evidence, harms of ASA use include excessive bleeding, including gastrointestinal bleeds and hemorrhagic stroke.
Magnitude of Effect: Very low-dose ASA use (i.e., ≤100 mg every day or every other day) results in an estimated 14 (95% CI, 7–23) additional major gastrointestinal bleeding events and 3.2 (95% CI, -0.5 to 0.82) extra hemorrhagic strokes per 1,000 persons over 10 years. These risks increase with advancing age.
Based on solid evidence, combined hormone therapy (conjugated equine estrogen and progestin) decreases the incidence of invasive CRC.
Based on fair evidence, combination conjugated equine estrogen and progestin has little or no benefit in reducing mortality from CRC. Data from the Women’s Health Initiative (WHI), a randomized, placebo-controlled trial evaluating estrogen plus progestin, with a mean intervention of 5.6 years and a follow-up of 11.6 years showed that women taking combined hormone therapy had a statistically significant higher stage of cancer (regional and distant) at diagnosis but not a statistically significant number of deaths from CRC compared with women taking the placebo.
Magnitude of Effect: There were fewer CRCs in the combined hormone therapy group than in the placebo group (0.12% vs. 0.16%; HR, 0.72; 95% CI, 0.56–0.94). A meta-analysis of cohort studies observed a RR of 0.86 (95% CI, 0.76–0.97) for incidence of CRC associated with combined hormone therapy.
There were 37 CRC deaths in the combined hormone therapy arm compared with 27 deaths in the placebo arm (0.04% vs. 0.03%; HR, 1.29; 95% CI, 0.78–2.11).
Based on solid evidence, harms of postmenopausal combined estrogen-plus-progestin hormone use include increased risk of breast cancer, coronary heart disease, and thromboembolic events.
Magnitude of Effect: The WHI showed a 26% increase in invasive breast cancer in the combined hormone group, a 29% increase in coronary heart disease events, a 41% increase in stroke rates, and a twofold higher rate of thromboembolic events.
Based on fair evidence, removal of adenomatous polyps reduces the risk of CRC. Much of this reduction likely comes from removal of large (i.e., >1.0 cm) polyps, while the benefit of removing smaller polyps—which are much more common—is unknown. Some but not all observational evidence indicates that this reduction may be greater for left-sided CRC than for right-sided CRC.
Based on solid evidence, the major harms of polyp removal include perforation of the colon and bleeding.
Magnitude of Effect: Seven to nine events per 1,000 procedures.
There is inadequate evidence that the use of NSAIDs reduces the risk of CRC. In people without genetic predisposition but with a prior history of a colonic adenoma that had been removed, three RCTs found that celecoxib and rofecoxib decreased the incidence of recurrent adenoma, although follow-up was too short to determine whether CRC incidence or mortality would have been affected.
Based on solid evidence, NSAIDs reduce the risk of adenomas, but the extent to which this translates into a reduction of CRC is uncertain.
Based on solid evidence, harms of NSAID use are relatively common and potentially serious, and include upper gastrointestinal bleeding, chronic kidney disease, and serious cardiovascular events such as myocardial infarction, heart failure, and hemorrhagic stroke.
A recent report compared the cyclooxygenase-2 (COX-2) inhibitor celecoxib (200 mg/d) with the nonselective nonsteroidals naproxen (850 mg/d) and ibuprofen (2,000 mg/d) in individuals with severe arthritis (i.e., not using lower doses as for primary prevention). The results showed that serious cardiovascular events were not less common for those taking the nonselective nonsteroidals. However, this study did not assess the comparative safety of lower doses or the safety of the COX-2 inhibitor rofecoxib.
Magnitude of Effect: The estimated average excess risk of upper gastrointestinal complications in average-risk people attributable to NSAIDs is 4 to 5 per 1,000 people per year.
The excess risk varies with the underlying gastrointestinal risk, however, it likely exceeds ten extra cases per 1,000 people per year in more than 10% of users.
Serious cardiovascular events are increased by 50% to 60%.
The evidence is inadequate to determine whether calcium supplementation reduces the risk of CRC.
There is no reliable evidence that a diet started in adulthood that is low in fat and meat and high in fiber, fruits, and vegetables reduces the risk of CRC by a clinically important degree.
Based on fair evidence, conjugated equine estrogens do not affect the incidence of, or survival from, invasive CRC.
Magnitude of Effect: N/A.
Based on solid evidence, statins do not reduce the incidence or mortality from CRC.
Based on solid evidence, the harms of statins are small.
结直肠癌（CRC）是全球第三常见的恶性肿瘤，也是美国男性和女性中第三大癌症死亡原因。结直肠癌也是中国第三常见的恶行肿瘤，是中国男性因癌症死亡的第五大原因，女性的第四大原因。
估计2020年美国将有147950例新诊断病例，53200例死亡病例。据估计，2015年中国结直肠癌新发病例38.8万例，死亡18.7万例。
在2007年至2016年期间，美国55岁及以上成年人的CRC发病率每年下降3.6%。过去20年来，中国结直肠癌的发病率有所上升。在2003~2007年，CRC中国人口标化发病率为14.41/10万，2015年为18.02/10万。
从2007年到2016年，55岁以下的成年人中，CRC的发病率每年增加2%。
过去20年来，男女死亡率均有所降低。2008年至2017年间，55岁及以上成年人的死亡率每年下降2.6%，而55岁以下成年人的死亡率每年上升1%。男女死亡率也均有所升高。在2003~2007年，CRC死亡率为6.27/10万，而2015年为8.21/10万。
与其他种族相比，非裔美国人的发病率和死亡率更高；然而，meta分析未发现非裔美国人有更高的癌前病变率。
CRC患者的5年总生存率为64%。预计约4.4%的美国人在有生之年会发展成CRC患者。
罹患CRC的风险在40岁后开始增加，在50至55岁时急剧上升；随后每十年风险增加一倍，并继续呈指数增长。尽管在外科技术和辅助治疗方面取得了进展，但晚期肿瘤患者的生存率仅略有提高。
因此，必须制定有效的一级和二级预防措施，以减少CRC的发病率和死亡率。
一级预防包括在临床出现CRC之前使用药物或其他干预措施，旨在预防临床CRC发生和死亡。
遗传学、流行病学和实验性研究提示，CRC是遗传因素和环境因素之间复杂交互作用的结果。CRC的自然史和相关风险因素对发病率和死亡率的影响的量化研究一直是CRC领域研究的重点。
有证据表明CRC与饮酒有关。一项纳入了8个队列研究的meta分析显示，与非饮酒者相比，饮酒者每日饮酒45g（即每日大约3杯标准量）罹患CRC的相对危险度（RR）为1.41（95%置信区间[CI]：1.16–1.72）。
病例-对照研究提示，饮酒与大肠癌之间存在中度至高度的正相关关系。
一项meta分析发现，这种相关性在男女性别及肿瘤部位上不存在明显差异。
有5项研究报道，饮酒与结直肠腺瘤之间存在正相关关系。
在法国勃艮第开展的一项饮食、遗传因素和腺瘤-癌变序贯现象的病例-对照研究中，
对直径小于10.0mm的腺瘤和直径大于10.0mm的腺瘤进行了单独分组。酒精摄入量与腺瘤之间的正相关性仅存在于较大的腺瘤中，这表明酒精摄入可能参与腺瘤-癌变序贯进程。
一项大型队列研究发现，酒精摄入量与CRC死亡之间存在剂量-反应关系，与非饮酒者相比，每日饮用4杯或更多者的RR为1.2（95%CI：1.0–1.5）。
大多数关于吸烟和腺瘤的病例-对照研究发现吸烟者的患病风险明显增加。
此外，无论男性还是女性，吸烟与息肉切除术后腺瘤复发的风险显著相关。
护士健康研究表明，癌症的诱导期至少为35年。
同样地，卫生专业人员随访研究显示，吸烟史与大、小腺瘤的风险都显著相关，至少需35年的诱导期才能恶变为CRC。
美国的一项大规模全国性队列研究——癌症预防研究II（CPS II）显示，多变量校正的CRC死亡率在当前吸烟者中最高，在既往吸烟者中居中，在非吸烟者中最低。同时观察到，在吸烟20年或以上的男性和女性人群中，CRC死亡风险增加。
基于CPS II的数据，估计1997年美国人口中12%的CRC死亡是由吸烟引起的。一项针对瑞典双胞胎的大型人群队列研究发现，重度吸烟35年或更长时间可使结肠癌发病风险增加近3倍，尽管按肿瘤部位分组分析后发现，此效应仅在直肠癌而非结肠癌中具有统计学意义。
另一项大型人群病例-对照研究也支持这一种观点，即当前和过去10年内的烟草使用与结肠癌风险相关。与从不吸烟者相比，每日吸烟超过一包者患病风险增加50%。
然而，一项针对57,000例芬兰人的28年随访研究显示，尽管持续吸烟者罹患CRC的风险增加了57%至71%，但是CRC发生发展与基线吸烟状态无关。
对首次结肠镜检查的人群进行4年的随访后，未发现吸烟，甚至长时间吸烟与腺瘤的复发相关。
一项纳入了106项观察性研究的meta分析发现，CRC发病率的RR（既往吸烟者相较于非吸烟者）为1.18（95%CI：1.11-1.25），绝对风险增加10.8例/100000人年（95%CI：7.9-13.6）。剂量-效应关系具有统计学意义。在综合了17项有关CRC死亡率的研究中，吸烟与CRC死亡相关，RR（既往吸烟者相较于非吸烟者）为1.25（95%CI：1.14-1.37），死亡率的绝对增加值为6.0例/100000人年。对于发病率和死亡率，吸烟与直肠癌的相关性强于结肠癌。
至少有三项大型队列研究表明肥胖与CRC发病率或死亡率相关。
护士健康研究发现，与身体质量指数（BMI）小于21的女性相比，BMI大于29的女性CRC发病率的校正RR为1.45（95%CI：1.02–2.07）。
CPS II发现，
与BMI在18.5到24.9之间的人相比，BMI在30到34.9之间的男性和女性的CRC死亡率校正RR为1.47（95%CI：1.30-1.66），同时存在明显的剂量-反应关系。
男性和女性中有相似效应。
最早的一些来自美国犹他州家族的关于CRC家族史的研究报告，那些有一级亲属死于CRC的人，其CRC死亡率（3.9%）高于性别和年龄匹配的对照组（1.2%）。这一差异在随后的许多研究中得到重复，这些研究一致发现，一级亲属中有CRC相关病史的人群，其自身患CRC的风险增加了两到三倍。尽管研究设计（病例-对照研究、队列研究）、抽样框架、样本量、数据验证方法、分析方法和研究对象人群来源各不相同，但风险的大小是一致的。
一项系统综述和meta分析针对家族性CRC风险进行了研究。
在纳入分析的24项研究中，除一项研究外，其余研究均发现，如果一级亲属中有CRC相关病史，个体自身罹患CRC的风险会增加。合并分析发现如果一级亲属有CRC病史，CRC发病率的RR为2.25（95%CI：2.00–2.53）。11项研究中有8项研究发现，一级亲属先证癌发生在结肠的个体，患结直肠癌的风险略高于一级亲属先证癌发生在直肠的个体。合并分析结果显示结肠癌和直肠癌患者亲属患CRC的RR分别为2.42（95%CI：2.20-2.65）和1.89（95%CI：1.62-2.21）。该分析未发现肿瘤部位（右侧或左侧）结肠癌的RR存在明显差异。
遗传性CRC包括两种：由于APC基因胚系突变导致的家族性腺瘤性息肉病（FAP）（包括衰减型息肉病），
以及由于DNA错配修复基因突变导致的遗传性非息肉病性结直肠癌（林奇综合征）。
许多其他家系表现有CRC和/或腺瘤的聚集性，但与可识别的遗传综合征无明显关联，统称为家族性CRC。
有关CRC遗传风险因素的更多信息，请参阅结直肠癌遗传学PDQ小结。
一些研究表明，久坐的生活方式与CRC风险增加相关，
但不是全部研究都显示这样的结果。
大量观察性研究对体力活动与结肠癌风险的相关性进行了研究。
大多数研究显示体力活动水平与结肠癌发病率呈负相关，平均RR降低了40%至50%。美国的大型队列研究发现，将平均能量消耗高的与消耗低的人群进行比较，校正后的RR存在统计学差异，RR为0.54（95%CI：0.33–0.90）
和0.53（95%CI：0.32-0.88）。
一项纳入了52项观察性研究的meta分析发现，总校正RR为0.76（95%CI：0.72-0.81），男性和女性的结果相似。
纳入基于个体参与者数据的随机对照试验（RCT）和观察性研究的meta分析，
在研究阿司匹林在心血管疾病预防中的使用时发现，乙酰水杨酸（ASA）可降低CRC的发病率，但至少在接受阿司匹林治疗10年后才有效（开始治疗后10年内CRC发病率的合并RR为0.99 [95%CI：0.85–1.15] ，开始治疗后10–19年内的RR为0.60 [95%CI：0.47–0.76]）。
在妇女健康研究中，一项有关ASA使用的2×2因素随机试验显示，每隔一天服用100mg的ASA，且平均治疗时间为10年者，其17.5年发生CRC的风险降低约20%（HR：0.80；95%CI：0.67–0.97）。
护士健康研究的一份报告对82,911名女性进行20年随访后，发现与未常规服用ASA者相比，常规服用者（每周≥2片，标准规格为325mg/片）患结肠癌的多变量RR为0.77（95%CI：0.67-0.88）。但只在服用超过10年者中，才观察到有显著意义的RR。
有一项纳入了635例接受根治性切除术的既往CRC患者（T1-T2 N0 M0）的随机研究，结果显示在接受中位时间为31个月的治疗后，与安慰剂组相比，每日服用325mg ASA的个体，其任何腺瘤复发的校正RR均降低（0.65；95%CI：0.46-0.91）。ASA组新发结肠病变的检出可能性低于安慰剂组（新发息肉检出的HR为0.54；95%CI：0.43-0.94，P = 0.022）。
一项纳入了1121例近期罹患结直肠腺瘤的病人的研究显示，在平均接受33个月治疗后，与安慰剂组相比，ASA 81mg/天组和ASA 325mg/天组的各类腺瘤未校正RR分别为0.81（95%CI：0.69–0.96）和0.96（95%CI：0.81–1.13）。对于晚期新生物患者（腺瘤直径≥10.0 mm或有管绒毛状或绒毛状特征，重度异型增生或浸润性癌），ASA 81mg/天组的RR为0.59（95%CI：0.38–0.92）， ASA 325mg/天组的RR为0.83（95%CI：0.55–1.23）。
同时评估了ASA对CRC患者死亡率的潜在影响。2010年一项基于个体参与者数据的meta分析，在分析了4项心血管疾病一级和二级预防RCT的长期（中位随访时间为18.3年）数据后发现，与对照组相比，每日使用75-1200mg ASA且至少持续一年的个体，其结肠癌的累积死亡风险下降（HR：0.67；95%CI：0.52–0.86）。阿司匹林的使用在随机分组后10到20年内降低了CRC患者的死亡率，但短于10年时未观察到该效应。
2011年一项基于受试者个体水平数据的meta分析，在分析了6项心血管疾病一级或二级预防RCT的数据后发现，与对照组相比，接受ASA治疗至少5年的患者CRC死亡风险下降，风险比为0.41（95%CI：0.71-1.00）。而在随机分组后前5年内未观察到明显的统计学意义。
一项meta分析纳入了6项RCT，其中5项来自英国，研究将患者随机分配至服用阿司匹林组或安慰剂组，平均治疗时长为4年或更长。研究者收集了所有在试验中死于癌症的个体数据。其中3项英国试验在随机分组后随访20年，并在试验完成后，通过死亡证明和癌症登记获得癌症死亡资料。该meta分析基于每项试验的比值比（OR），而非对个体患者数据进行精算分析，发现分配至阿司匹林组的患者，在20年期间因CRC死亡的风险降低。阿司匹林最大剂量组死于CRC的OR为0.55（95%CI：0.41-0.76），阿司匹林其他剂量组的OR为0.58（95%CI：0.44-0.78）。
妇女健康研究是迄今为止最大规模的阿司匹林随机试验（N=39,876），该试验发现在随访的前10年内，每隔一天低剂量服用阿司匹林的患者其CRC死亡率未降低。该研究未报告CRC患者死亡率的长期风险。
阿司匹林存在一些与其使用相关的重要潜在危害，在将其作为疾病预防策略时，应将这些危害纳入考虑范围。常规低剂量服用阿司匹林会增加胃肠道大出血和包括出血性卒中在内的颅内出血风险。一项研究阿司匹林用于心血管疾病一级预防的系统综述发现，每日或每隔一日服用100mg或以上的阿司匹林，可使患者发生严重胃肠道出血的风险增加58%（OR：1.58；95%CI：1.29–1.95），或使颅内出血的风险增加30%（OR：1.30；95%CI：1.00–1.68）。老年人、男性和那些伴有促出血合并危险因素的人群，可能有更高风险。
几项观察性研究提示，绝经后女性激素补充剂使用者患结肠癌的风险降低。
对于直肠癌，大多数研究并未观察到相关性，或风险仅略微增加。
妇女健康倡议（WHI）试验将雌激素联合孕激素治疗和仅雌激素治疗对CRC发病率和死亡率的影响作为次要结局进行了研究。在进行长期随访（平均11.6年）后，发现与安慰剂组相比，雌孕激素联合治疗组中确诊CRC的患者更少（HR：0.72；95%CI：0.56-0.94）；但更容易发生淋巴结转移（50.5% vs 28.6%；P < 0.001），且肿瘤分期更高（病灶处和远端转移处）（68.8% vs 51.4%；P = 0.003）。联合治疗组CRC死亡人数高于安慰剂组（37 vs 27），但无统计学上显著意义（HR：1.29；95%CI：0.78-2.11）。
一项综合了美国国家息肉研究（NPS）数据和外部、历史对照比较的研究发现，结肠镜下息肉切除术后CRC的发病率比三个非同期的历史对照组减少了76%到90%。
这项研究可能在某些方面存在偏倚，夸大了息肉切除的效果；；最主要问题是，NPS将在基线检查时患有CRC的潜在入选者排除。而在三个对照组中未采取同样的排除标准（或未做基线结肠镜检查），基线时已患CRC的病人在随后的随访中将被记为新发CRC。虽然进行了校正，但由于CRC无症状期存在的时长无从得知，因此无法估计该问题对结果的影响程度。
NPS队列的另一项长期随访研究（中位随访时长为15.8年；最长23年）提示，息肉切除术使CRC的死亡率降低了约53%（不仅是由于在初次检查时排除了CRC患者）。然而，必须谨慎看待降低的程度，因为这项研究没有直接的对照组，主要依赖于与美国国家癌症研究所的监测、流行病学和最终结果计划的预期数据进行比较。此外，关于可能使死亡率下降的因素，其详细信息尚不清楚。NPS研究中患者在第1年和第3年接受结肠镜检查；同时在第1年为两组对照组中的其中一组安排结肠镜检查；所有受试者在第6年接受结肠镜检查。然而，在随访6年后，对患者可能接受的确切监测以及该监测如何降低CRC死亡率的描述并不充分。
预计英国乙状结肠镜筛查试验的进一步随访将提供更多关于息肉切除术长期效果的详细信息，至少是有关左侧结肠的信息。
其他关于乙状结肠镜筛查（此时息肉和早期癌症都可以被切除）的证据提示，内镜筛查是有益的，至少对于左侧结肠，其影响切实而长远。在一项RCT中，170,000人随机分配接受一次乙状结肠镜检查或常规医疗护理。在乙状结肠镜检查中，息肉被切除，一旦发现癌症，患者将接受进一步治疗。根据乙状结肠镜检查结果，检查结果正常或仅有一个或两个小（<1cm）管状腺瘤的个体被认定为患CRC的风险较低，这些个体不会被转诊接受结肠镜相关检查或结肠镜监测。在随后10年的随访中，低风险组（约95%参与者为低风险组）左侧CRC的发病率为每年0.02%至0.04%，与平均风险相比，处于非常低的风险水平。风险的降低是由于大、小息肉的检出和切除，还是由风险较低个体的选择性所致，目前尚不清晰。
大息肉的自然史尚不清楚，但一些证据提示，这种病变每年约有1%的比例发展为CRC。
有强有力的数据支持内镜检查对降低左半结肠癌死亡率有效的研究结果，也有多项研究对内镜检查降低右半结肠癌死亡率的能力提出了疑问。
因此，目前尚不清楚内镜检查（如结肠镜筛查）的总体效果，以及其对结肠左侧和右侧的影响是否有很大差异。
其他研究提示，较大的息肉（即>1.0cm）最有可能发展成CRC，其中包括大多数具有绒毛或高级别组织学特征的息肉。回顾性队列研究则显示了包括出血在内的息肉切除术的危害。
一项大型队列研究（301,240人中有3894例CRC病例）发现，每日或每周服用非阿司匹林（non-ASA）非甾体抗炎药（NSAID）与近端和远端结肠癌（而非直肠癌）10年发病率的降低有关，每日服用NSAID的结肠癌风险（HR）为0.67（95%CI：0.58-0.77）。由于对非ASA非甾体抗炎药暴露的评估仅进行了一次研究，且是通过自我报告的方式进行，没有关于服用剂量或服用时长的信息，因此这项单一研究的准确性较低。还需要进一步研究来支持这一结果。
虽然目前尚无足够证据来确定非甾体抗炎药是否能降低结直肠癌的发病率，但支持者认为非甾体抗炎药可以通过抑制环氧化酶（COX）的活性发挥抑癌作用。COX在花生四烯酸转化为类前列腺素、前列腺素和血栓素A2过程中起重要作用。非甾体抗炎药不仅包括阿司匹林（ASA，这里单独考虑）和其他第一代药物（非选择性地抑制COX的两种亚型：COX-1和COX-2），还包括主要抑制COX-2的第二代新型药物。一般来说，COX-1在大多数组织中都有表达，主要起维持正常生理功能的作用（如参与胃肠粘膜保护和调节血小板凝集）。COX-2活性在应激反应以及介导和传递关节炎特有的疼痛和炎症中至关重要。
非选择性COX抑制剂包括：吲哚美辛（吲哚美辛）、舒林酸（克林霉素）、吡罗昔康（费尔丁）、二氟尼柳（多洛比德）、布洛芬（阿维特，布洛芬）、酮洛芬（奥鲁地斯）、萘普生（萘普生）、萘普生钠（阿列夫，萘普生）。选择性COX-2抑制剂包括塞来昔布（西乐葆）、罗非昔布（万络）和戊地昔布（伐地考昔）。罗非昔布和戊地昔布会增加严重心血管事件的风险，已停止在市场销售。
塞来昔布和罗非昔布都有可能造成严重心血管事件，包括剂量相关的心血管原因的死亡、心肌梗死、卒中或心力衰竭。
表1总结的4项试验证明了这两种药物与严重心血管事件高风险相关。此外，一项网络meta分析整合了当时所有大规模、比较任一种非甾体抗炎药与其他非甾体抗炎药或安慰剂的随机对照试验研究，结果发现几乎无证据支持所研究的任何一种非甾体抗炎药有心血管方面的安全性。萘普生的心血管风险似乎最小。
| 剂量/试验药物 | 风险 | 研究类型 |
|---|---|---|
| 罗非昔布<25 mg/qd；罗非昔布>25 mg/qd | OR：1.47（0.99-2.17）vs. 3.58（1.27-10.17） | 巢式病例-对照研究（所有受试者） |
| 塞来昔布200 mg/qd vs. 400 mg bid | 3.4%；HR：3.4（95%CI：1.4–7.8） | 散发性腺瘤预防试验（N=2035） |
| 罗非昔布25 mg/qd | RR：1.92（95%CI：1.19-3.11；P=0.008） | 散发性腺瘤的化学预防 |
| 罗非昔布25 mg/qd | RR（估值）：2.66（95%CI：1.03–6.86；P=0.04） | 散发性腺瘤的化学预防；Rx时长中位数为7.4月 |
| bid：一天两次；qd：每天一次；CI：置信区间；HR：风险比；OR：优势比；RR：相对风险；Rx：处方。 | ||
非甾体抗炎药的主要危害还包括胃肠道出血和肾损伤。根据研究报道，大部分消化道出血事件的发生率具有剂量相关性。
塞来昔布可降低腺瘤的发病率，但在降低散发性CRC风险方面无临床意义。由于其导致心血管事件风险增加，且已有其他有效降低CRC死亡率的方法（例如筛检），塞来昔布预防CRC的长期效应尚未得到证实。
一项基于人群的回顾性队列研究显示，65岁及以上人群服用非阿司匹林非甾体抗炎药与CRC风险降低相关，尤其是长时间服用的人群。
几项研究已经证明舒林酸能有效减少家族性息肉病的腺瘤数量，并缩小腺瘤的大小。
在一项对77例FAP患者进行的随机双盲对照试验中，每天服用两次400mg塞来昔布的患者结直肠腺瘤的平均数量减少了28.0%（与安慰剂相比，P=0.003），息肉负荷（息肉直径之和）减少了30.7%（P=0.001）；而安慰剂组分别降低4.5%和4.9%。每天两次服用100mg塞来昔布组的降幅分别为11.9%（与安慰剂组相比，P=0.33）和14.6%（P=0.09）。两组不良事件发生率相似。
非甾体抗炎药吡罗昔康（剂量为20mg/天）可使有腺瘤病史的患者的直肠前列腺素平均浓度降低50%
一些研究正在评估ASA或其他非甾体类药物对息肉切除后复发的影响，
其中部分研究检测了粘膜前列腺素的水平。
研究者正在研究NSAID作为一级预防措施的预期效果。然而，以下几个问题不利于其作为预防的推荐用药：缺乏对这些药物的适当剂量和服用时长的了解，以及担心潜在的预防益处（减少筛查或监测的频率或强度）是否可以抵消长期服用的危害（胃肠道溃疡和出血性卒中）。
一项随机安慰剂对照试验评估了补钙（每天3g碳酸钙[1200mg钙元素]）对复发性腺瘤风险的影响，
主要结局是在前两次复查时内镜检查发现至少一个腺瘤的患者比例（其中72%为男性）。至少有一个复发性腺瘤（校正风险比[ARR]：0.81；95%CI，0.67-0.99）和平均腺瘤数量（ARR：0.76；95%CI，0.60-0.96）的风险均有一定程度降低。研究发现钙的效果不受年龄、性别和基线钙、脂肪或纤维的摄入类别的影响。这项研究仅纳入近期患有结直肠腺瘤的患者，无法确定钙对初发腺瘤风险的影响，研究时长也不足以评估补钙对浸润性CRC风险的影响。停止补钙后，低风险可持续至多5年。
其他正在进行的关于腺瘤复发的研究同样值得关注。值得注意的是，钙摄入量可能十分重要；试验中的日摄入量从1250mg到2000mg不等。
在一项纳入36282例绝经后女性的随机双盲安慰剂对照试验中，平均7年每天两次服用500mg钙元素和200IU维生素D3与浸润性CRC的减少无关（HR：1.08；95%CI：0.86–1.34；P=0.051）。
导致该研究出现阴性结果的原因，虽然有种种因素，但可能是随访时间较短（CRC的潜伏期为10-15年）、钙和维生素D的剂量欠佳等。
相较于脂肪摄入量低的人群，脂肪摄入量高的人群具有较高的结肠癌发病率。
在发病率高的西方国家，脂肪占膳食热量的40%至45%；在低风险人群中，脂肪仅占膳食热量的10%。
一些病例-对照研究探讨了肉类或脂肪、蛋白质以及能量摄入与结肠癌风险的关系。
有研究发现肉类或脂肪摄入与结肠癌风险正相关，也有研究结果与之不同。
美国和其他国家开展了若干前瞻性队列研究，在纳入包含爱荷华州妇女健康研究和美国护士健康研究在内的13项研究进行系统综述后发现，肉类摄入与CRC发病率之间存在正相关关系。然而，作者指出，由于只有少数研究评估了肉类摄入对癌症风险的独立效应，上述研究结果可能完全归因于混杂效应。
与此类似，2019年一项对观察性研究的系统综述评估了加工或未加工红肉摄入与CRC发病率和死亡率之间的关系，研究发现：每周减少三份肉食，对发病率和死亡率几乎没有降低，但该发现的准确性评级为低到很低。
一项随机对照研究对已纳入WHI的48835例50-79岁绝经后女性进行了饮食干预，干预目标是减少20%总脂肪摄入量，同时增加蔬菜、水果和谷物的每日摄入量。在8.1年的随访中，干预组的脂肪摄入量比对照组减少了约10%。与对照组相比，无证据显示干预组的浸润性CRC减少（HR：1.08，95%CI：0.90–1.29）。
同样，低脂饮食对各类癌症死亡率、总死亡率或心血管疾病也没有改善。
这一结果在2019年的一项随机对照试验的系统综述中得到了验证，该试验研究了各类红肉消耗对癌症结局的影响。该研究在很大程度上依赖于WHI得出结论，即红肉摄入对CRC发病率几乎没有影响，但由于现有研究的局限性，该结论的准确性为低。
造成膳食脂肪或肉类摄入与CRC风险相关研究的矛盾结果可能
包括：
6项病例对照研究和2项队列研究探讨了结直肠腺瘤的潜在饮食危险因素。
上述8项研究中有3项发现，高脂肪摄入与结直肠腺瘤风险增加有关。高脂肪摄入增加了息肉切除后腺瘤复发的风险。
一项多中心的随机对照试验结果显示，低脂肪（占总热量的20%）、高纤维、水果和蔬菜的膳食结构并不能降低结肠腺瘤复发的风险。
因此，现有证据不足以确定减少饮食中的脂肪和肉类是否会降低CRC发病率。
WHI的雌激素干预治疗在子宫切除的女性中进行，CRC发病率是研究的次要结局。经过中位时间为7.1年的随访，雌激素组发生了58例浸润性癌症，而安慰剂组发生了53例浸润性癌症（HR：1.12；95%CI：0.77-1.63）。两组的肿瘤分期和分级相似。雌激素组患CRC后的死亡率为34%，安慰剂组为30%（HR：1.34；95%CI：0.58-3.19）。
总的来说，现有证据表明他汀类药物的服用既不会增加也不会降低CRC发病率或死亡率。尽管一些病例-对照研究显示风险降低，但一项大型队列研究
和包含4项随机对照试验的meta分析都未
发现服用他汀类药物有任何作用。
Colorectal cancer (CRC) is the third most common malignant neoplasm worldwide and the third leading cause of cancer deaths in men and women combined in the United States.
It is estimated that there will be 147,950 new cases diagnosed in the United States in 2020 and 53,200 deaths due to this disease.
Between 2007 and 2016, incidence rates for CRC in the United States declined by 3.6% per year among adults aged 55 years and older.
Between 2007 and 2016, in adults younger than 55 years, incidence rates for CRC increased by 2% per year.
For the past 20 years, the mortality rate has been declining in both men and women. Between 2008 and 2017, the mortality rate declined by 2.6% per year among adults aged 55 years and older but increased by 1% per year among adults younger than 55 years.
Incidence and mortality rates are higher in African Americans compared with other races; however, a meta-analysis found no evidence that African Americans have higher rates of precancerous lesions.
The overall 5-year survival rate is 64% for CRC. About 4.4% of Americans are expected to develop CRC within their lifetimes.
The risk of CRC begins to increase after the age of 40 years and rises sharply at ages 50 to 55 years; the risk doubles with each succeeding decade, and continues to rise exponentially. Despite advances in surgical techniques and adjuvant therapy, there has been only a modest improvement in survival for patients who present with advanced neoplasms.
Hence, effective primary and secondary preventive approaches must be developed to reduce the morbidity and mortality from CRC.
Primary prevention involves the use of medications or other interventions before the clinical appearance of CRC with the intent of preventing clinical CRC and CRC mortality.
Genetics, experimental, and epidemiologic studies suggest that CRC results from complex interactions between inherited susceptibility and environmental factors. The exact nature and contribution of these factors to CRC incidence and mortality is the subject of ongoing research.
There is evidence of an association of CRC with alcoholic beverage consumption. In a meta-analysis of eight cohort studies, the relative risk (RR) for consumption of 45 g/day (i.e., about three standard drinks per day) compared with nondrinkers was 1.41 (95% confidence interval [CI], 1.16–1.72).
Case-control studies suggest a modest-to-strong positive relationship between alcohol consumption and large bowel cancers.
A meta-analysis found that the association did not vary by sex or location within the large bowel.
Five studies have reported a positive association between alcohol intake and colorectal adenomas.
A case-control study of diet, genetic factors, and the adenoma-carcinoma sequence was conducted in Burgundy.
It separated adenomas smaller than 10.0 mm in diameter from larger adenomas. A positive association between current alcohol intake and adenomas was found to be limited to the larger adenomas, suggesting that alcohol intake could act at the promotional phase of the adenoma-carcinoma sequence.
A large cohort study found a dose-response relationship between alcohol intake and death from CRC, with a RR of 1.2 (95% CI, 1.0–1.5) for four or more drinks per day compared with nondrinkers.
Most case-control studies of cigarette exposure and adenomas have found an elevated risk for smokers.
In addition, a significantly increased risk of adenoma recurrence following polypectomy has been associated with smoking in both men and women.
In the Nurses’ Health Study, the minimum induction period for cancer appears to be at least 35 years.
Similarly, in the Health Professionals Follow-up Study, a history of smoking was associated with both small and large adenomas and with a long induction period of at least 35 years for CRC.
In the Cancer Prevention Study II (CPS II), a large nationwide cohort study, multivariate-adjusted CRC mortality rates were highest among current smokers, intermediate among former smokers, and lowest in nonsmokers, with increased risk observed after 20 or more years of smoking in men and women combined.
On the basis of CPS II data, it was estimated that 12% of CRC deaths in the U.S. population in 1997 were attributable to smoking. A large population-based cohort study of Swedish twins found that heavy smoking of 35 or more years' duration was associated with a nearly threefold increased risk of developing colon cancer, although subsite analysis found a statistically significant effect only for rectal cancer, but not colon cancer.
Another large population-based case-control study supports the view that current tobacco use and tobacco use within the last 10 years is associated with colon cancer. A 50% increase in risk was associated with smoking more than a pack a day relative to never smoking.
However, a 28-year follow-up of 57,000 Finns showed no association between the development of CRC and baseline smoking status, although there was a 57% to 71% increased risk in persistent smokers.
No relationship was found between cigarette smoking, even smoking of long duration, and recurrence of adenomas in a population followed for 4 years after initial colonoscopy.
A meta-analysis of 106 observational studies found a RR (ever smokers vs. nonsmokers) for CRC incidence of 1.18 (95% CI, 1.11–1.25), with an absolute risk increase of 10.8 cases per 100,000 person-years (95% CI, 7.9–13.6). There was a statistically significant dose-response effect. In 17 studies with data on CRC mortality, cigarette smoking was associated with CRC death, with a RR (ever smokers vs. never smokers) of 1.25 (95% CI, 1.14–1.37), and an absolute increase in the death rate of 6.0 deaths per 100,000 person-years. For both incidence and mortality, the association was stronger for rectal cancer than for colon cancer.
At least three large cohort studies have found an association between obesity and CRC incidence or mortality.
The Nurses’ Health Study found that women with a body mass index (BMI) of more than 29, compared with women with a BMI of less than 21, had an adjusted RR for CRC incidence of 1.45 (95% CI,1.02–2.07).
In the CPS II,
men and women with a BMI of 30 to 34.9 had an adjusted RR for CRC mortality (compared with people with a BMI of 18.5–24.9) of 1.47 (95% CI, 1.30–1.66), with a statistically significant dose-response effect.
The effects were similar in men and women.
Some of the earliest studies of family history of CRC were those of Utah families that reported a higher number of deaths from CRC (3.9%) among the first-degree relatives of patients who had died from CRC than among sex-matched and age-matched controls (1.2%). This difference has since been replicated in numerous studies that have consistently found that first-degree relatives of affected cases are themselves at a twofold to threefold increased risk of CRC. Despite the various study designs (case-control, cohort), sampling frames, sample sizes, methods of data verification, analytic methods, and countries where the studies originated, the magnitude of risk is consistent.
A systematic review and meta-analysis of familial CRC risk was reported.
Of 24 studies included in the analysis, all but one reported an increased risk of CRC if there was an affected first-degree relative. The RR for CRC in the pooled study was 2.25 (95% CI, 2.00–2.53) if there was an affected first-degree family member. In 8 of 11 studies, if the index cancer arose in the colon, the risk was slightly higher than if it arose in the rectum. The pooled analysis revealed an RR in relatives of colon and rectal cancer patients of 2.42 (95% CI, 2.20–2.65) and 1.89 (95% CI, 1.62–2.21), respectively. The analysis did not reveal a difference in RR for colon cancer based on location of the tumor (right side vs. left side).
Hereditary CRC has two well-described forms: Familial adenomatous polyposis (FAP) (including an attenuated form of polyposis), due to germline mutations in the APC gene,
and Lynch syndrome, which is caused by germline mutations in DNA mismatch repair genes.
Many other families exhibit aggregation of CRC and/or adenomas, but with no apparent association with an identifiable hereditary syndrome, and are known collectively as familial CRC.
Refer to the PDQ summary on Genetics of Colorectal Cancer for more information about genetic risk factors for CRC.
A sedentary lifestyle has been associated with an increased risk of CRC in some
but not all
studies. Numerous observational studies have examined the relationship between physical activity and colon cancer risk.
Most of these studies have shown an inverse relationship between level of physical activity and colon cancer incidence. The average RR reduction is reportedly 40% to 50%. Large U.S. cohort studies have found statistically significant adjusted RRs of 0.54 (95% CI, 0.33–0.90)
and 0.53 (95% CI, 0.32–0.88)
when comparing people with high versus low average energy expenditure. A meta-analysis of 52 observational studies found an overall adjusted RR of 0.76 (95% CI, 0.72–0.81), with similar results for men and women.
Evidence from individual participant-level data meta-analyses of randomized controlled trials (RCTs) and observational studies
investigating the use of aspirin for the prevention of cardiovascular disease indicates that acetylsalicylic acid (ASA) use reduces the incidence of CRC, but not until at least 10 years after initiation of therapy (pooled RR of CRC incidence within 10 years of initiation, 0.99 [95% CI, 0.85–1.15] vs. RR, 0.60 [95% CI, 0.47–0.76] at 10–19 years after initiation).
In the Women's Health Study, a randomized 2 x 2 factorial trial of 100 mg of ASA every other day for an average of 10 years, CRC incidence was reduced by about 20% after 17.5 years (HR, 0.80; 95% CI, 0.67–0.97).
In a report from the Nurses’ Health Study involving 82,911 women followed for 20 years, the multivariate RR for colon cancer was 0.77 (95% CI, 0.67–0.88) among women who regularly used ASA (≥2 standard 325-mg tablets per week) compared with nonregular use. Significant RR was not observed, however, until more than 10 years of use.
In a randomized study of 635 patients with prior CRC (T1–T2 N0 M0) who had undergone curative resection, ASA intake at 325 mg/day was associated with a decrease in the adjusted RR of any recurrent adenoma as compared with the placebo group (0.65; 95% CI, 0.46–0.91) after a median duration of treatment of 31 months. The likelihood of detection of a new colonic lesion was lower in the ASA group than in the placebo group (HR for the detection of a new polyp, 0.54; 95% CI, 0.43–0.94, P = .022).
In a study of 1,121 patients with a recent history of colorectal adenomas, after a mean duration of treatment of 33 months, the unadjusted RRs of any adenoma (as compared with the placebo group) were 0.81 in the 81 mg/day ASA group (95% CI, 0.69–0.96) and 0.96 in the 325 mg/day ASA group (95% CI, 0.81–1.13). For advanced neoplasms (adenomas ≥10.0 mm in diameter or with tubulovillous or villous features, severe dysplasia, or invasive cancer), the RRs were 0.59 (95% CI, 0.38–0.92) in the 81 mg/day ASA group, and 0.83 (95% CI, 0.55–1.23) in the 325 mg/day ASA group, respectively.
ASA has also been evaluated for its potential effects on CRC mortality. A 2010 individual patient level data meta-analysis analyzed long-term (median follow-up, 18.3 years) data from four RCTs of primary and secondary cardiovascular disease prevention; it found that allocation to use of 75 to 1,200 mg of daily ASA for at least one year reduced the cumulative risk of colon cancer death compared with controls (HR, 0.67; 95% CI, 0.52–0.86). Aspirin reduced CRC mortality beginning 10 to 20 years after randomization, but not before.
A 2011 individual participant level data meta-analysis examined data from six RCTs of primary or secondary cardiovascular disease prevention. In trials with allocation to ASA after at least 5 years of in-trial follow-up, the hazard ratio for CRC mortality was 0.41 (95% CI, 0.71–1.00). There was no statistically significant effect during the first five years after randomization.
Six RCTs, including five from the United Kingdom, were included in a meta-analysis in which patients were randomly assigned to receive either aspirin or placebo, and the mean scheduled duration of trial treatment was 4 years or more. Individual patient data for all in-trial cancer deaths were obtained. In the three United Kingdom trials, cancer deaths after completion of the trials were obtained via death certification and cancer registration, taking the follow-up to 20 years after randomization. Based on meta-analysis of odds ratios (ORs) from each trial rather than on more sensitive actuarial analysis of the individual patient data, allocation to aspirin in the RCTs reduced the 20-year risk of death due to CRC. ORs for maximum aspirin use were 0.55 for CRC risk (95% CI, 0.41–0.76) and for any aspirin use were 0.58 for CRC risk (95% CI, 0.44–0.78).
The Women's Health Study, the largest randomized trial of aspirin to date (N = 39,876), found no reduction in CRC mortality rates with the use of every other day low-dose aspirin during the first 10 years of follow-up. The study did not report on longer-term risk for CRC mortality.
Aspirin has several important potential harms associated with its use that should be a part of any consideration of its use as a disease prevention strategy. Regular low-dose aspirin use increases the risks for major gastrointestinal bleeding and intracranial bleeding events, including hemorrhagic strokes. A systematic review of studies of aspirin use for primary cardiovascular disease prevention found that use of 100 mg or more of aspirin daily or every other day increased a person’s risk for a major gastrointestinal bleed by 58% (OR, 1.58; 95% CI, 1.29–1.95) or an intracranial hemorrhage by 30% (OR, 1.30; 95% CI, 1.00–1.68). These risks may be greater among older individuals, men, and those individuals with comorbid risk factors that promote a risk of bleeding.
Several observational studies have suggested a decreased risk of colon cancer among users of postmenopausal female hormone supplements.
For rectal cancer, most studies have observed no association or a slightly elevated risk.
The Women’s Health Initiative (WHI) trial examined, as a secondary endpoint, the effect of combined estrogen-plus-progestin therapy and estrogen-only therapy on CRC incidence and mortality. Among women in the combined estrogen-plus-progestin group of the WHI, an extended follow-up (mean, 11.6 years) confirmed that fewer CRC were diagnosed in the combined hormone therapy group than in the placebo group (HR, 0.72; 95% CI, 0.56–0.94); the CRCs in women in the combined group were more likely to have lymph node involvement than the CRCs in women in the placebo group (50.5% vs. 28.6%; P < .001) and were classified at higher stages (regional and distant) (68.8% vs. 51.4%; P = .003). The number of CRC deaths in the combined group was higher than in the placebo group (37 vs. 27 deaths), but the difference was not statistically significant (HR, 1.29; 95% CI, 0.78–2.11).
An analysis of data from the National Polyp Study (NPS), with external, historical controls, has commonly been cited to show a reduction of 76% to 90% in the subsequent incidence of CRC after colonoscopic polypectomy compared with three nonconcurrent, historical control groups.
This study may be biased in several ways that inflate the apparent efficacy of polyp removal; the main problem is that potential enrollees in the NPS were excluded if they had CRC at their baseline examination. Because no such exclusions (or baseline colonoscopy examinations) were done in the three comparison groups, persons who had CRC at baseline would be counted as having incident CRC in subsequent follow-up. Although adjustments were attempted, it is not possible to know the magnitude of the impact of this problem on the result because it is not known how long CRC may be present without causing symptoms.
An additional long-term follow-up study (median follow-up, 15.8 years; maximum, 23 years) of the NPS cohort suggested an approximately 53% reduction in CRC mortality due to polypectomy (not just exclusion of persons with CRC at initial exam). However, the degree of reduction must be viewed with caution because this study did not have a direct comparison group, relying mainly on comparison to expected data from the National Cancer Institute's Surveillance, Epidemiology and End Results Program. Further, details are not clear regarding factors that may have led to decreased mortality. Patients in the NPS were assigned to colonoscopy at years 1 and 3; colonoscopy was also offered to one of the two comparison groups at year 1; all participants were offered colonoscopy at year 6. However, following year 6, the exact surveillance that patients may have undergone and how that surveillance might have been associated with decreased CRC mortality were not well described.
It is expected that further follow-up in the United Kingdom Flexible Sigmoidoscopy Screening Trial will be able to provide more detail about the long-term effect of polypectomy, at least on the left side of the colon.
Other evidence about the benefit of sigmoidoscopy screening (at which time both polyps and early cancer would be removed) suggests that the impact of endoscopic screening, at least on the left side of the colon, is substantial and prolonged. In an RCT, 170,000 persons were randomly assigned to one-time sigmoidoscopy versus usual care. At sigmoidoscopy, polyps were removed, cancer was detected, and patients were referred for treatment. Based on sigmoidoscopy findings, persons were considered to have low risk if they had normal exams or only one or two small (<1 cm) tubular adenomas; such persons were not referred either for colonoscopy workup, or for colonoscopic surveillance. In a follow-up of 10 years, the left-sided CRC incidence in the low-risk group (about 95% of attendees were low risk) was 0.02% to 0.04% per year—a very low risk of CRC compared with average risk. The cause of reduced risk—whether due to detection and removal of large polyps or small ones, or selection of individuals at lower risk—is yet unclear.
The natural history of large polyps is not well known, but some evidence suggests that such lesions become clinical CRC at a rate of approximately 1% per year.
As a result of the strong data about the impact of endoscopy on the left colon, evidence from multiple studies has raised questions about the ability of endoscopy to reduce CRC mortality in the right colon.
Thus, it is unclear what the overall impact of endoscopy (e.g., colonoscopy screening) is, and whether there may be a large difference in impact on the left side of the colon compared with the right side.
Other studies suggest that the polyps with the greatest potential to progress to CRC are larger polyps (i.e., >1.0 cm), which include most of those with villous or high-grade histologic features. Retrospective cohort studies also show the harms associated with polypectomy, including bleeding.
One large cohort study (301,240 people with 3,894 CRC cases) found an association between daily or weekly nonaspirin (non-ASA) nonsteroidal anti-inflammatory drug (NSAID) use and reduced 10-year incidence of proximal and distal colon cancer, but not rectal cancer, with an HR of 0.67 (95% CI, 0.58–0.77) for daily use for colon cancer. Because exposure to non-ASA NSAIDs was assessed only once, assessment was by self-report, and there is no information on dose or duration of use, the certainty of this single study must be rated low. Further research is needed before this finding can be accepted.
Although evidence is currently inadequate to determine whether NSAIDs reduce CRC incidence, proponents suggest that any effect of these drugs results from their ability to inhibit the activity of cyclooxygenase (COX). COX is important in the transformation of arachidonic acid into prostanoids, prostaglandins, and thromboxane A2. NSAIDs include not only aspirin (ASA, which is considered separately here) and other, first-generation nonselective inhibitors of the two functional isoforms of COX, termed COX-1 and COX-2, but also newer second-generation drugs that inhibit primarily COX-2. Normally, COX-1 is expressed in most tissues and primarily plays a housekeeping role (e.g., gastrointestinal mucosal protection and platelet aggregation). COX-2 activity is crucial in stress responses and in mediating and propagating the pain and inflammation that are characteristic of arthritis.
Nonselective COX inhibitors include, indomethacin (Indocin); sulindac (Clinoril); piroxicam (Feldene); diflunisal (Dolobid); ibuprofen (Advil, Motrin); ketoprofen (Orudis); naproxen (Naprosyn); and naproxen sodium (Aleve, Anaprox). Selective COX-2 inhibitors include celecoxib (Celebrex), rofecoxib (Vioxx), and valdecoxib (Bextra). Rofecoxib and valdecoxib are no longer marketed because of an associated increased risk of serious cardiovascular events.
Both celecoxib and rofecoxib have been associated with serious cardiovascular events including dose-related death from cardiovascular causes, myocardial infarction, stroke, or heart failure.
Four trials that demonstrated this increased risk are summarized in the Table 1. In addition, a network meta-analysis of all large scale RCTs comparing any NSAID to any other NSAID or placebo found that there is little evidence to suggest that any of the investigated drugs are safe in terms of cardiovascular effects. Naproxen seemed least harmful.
| Dose/Trial Drug | Risk | Study Type |
|---|---|---|
| Rofecoxib <25 mg/qd; rofecoxib >25 mg/qd | OR, 1.47 (0.99–2.17) vs. 3.58 (1.27–10.17) | Nested case-control study all users |
| Celecoxib 200 mg/qd vs. 400 mg bid | 3.4%; HR, 3.4 (95% CI, 1.4–7.8) | Sporadic adenoma prevention trial (N = 2,035) |
| Rofecoxib 25 mg/qd | RR, 1.92 (95% CI, 1.19–3.11; P = .008) | Chemoprevention of sporadic adenoma |
| Rofecoxib 25 mg/qd | RR (estimated), 2.66 (95% CI, 1.03–6.86; P = .04) | Chemoprevention of sporadic adenoma; median study Rx 7.4 months |
| bid = twice a day; qd = every day; CI = confidence interval; HR = hazard ratio; OR = odds ratio; RR = relative risk; Rx = prescription. | ||
Other major harms from all NSAIDs are gastrointestinal bleeding and renal impairment. The incidence of reported major gastrointestinal bleeding events appears to be dose-related.
Celecoxib reduces the incidence of adenomas; however, celecoxib does not have a clinical role in reducing the risk of sporadic CRC. Its long-term efficacy in preventing CRC has not been shown because of increased risk of cardiovascular events, and because there are other effective ways, such as screening to reduce CRC mortality.
A population-based retrospective cohort study of nonaspirin NSAID use among individuals aged 65 years and older was associated with lower risk of CRC, particularly with longer durations of use.
Several rigorous studies have demonstrated the effectiveness of sulindac in reducing the size and number of adenomas in familial polyposis.
In a randomized, double-blind, placebo-controlled study of 77 patients with FAP, patients receiving 400 mg of celecoxib twice a day had a 28.0% reduction in the mean number of colorectal adenomas (P = .003 for the comparison with placebo) and a 30.7% reduction in the polyp burden (sum of polyp diameters; P = .001) as compared with reductions of 4.5% and 4.9%, respectively, in the placebo group. The reductions in the group receiving 100 mg of celecoxib twice a day were 11.9% (P = .33 for the comparison with placebo) and 14.6% (P = .09), respectively. The incidence of adverse events was similar among the groups.
The NSAID piroxicam, at a dose of 20 mg/day, reduced mean rectal prostaglandin concentration by 50% in individuals with a history of adenomas.
Several studies assessing the effect of ASA or other nonsteroidals on polyp recurrence following polypectomy are in progress.
In several of these studies, mucosal prostaglandin concentration is being measured.
The potential for use of NSAIDs as a primary prevention measure is being studied. There are, however, several unresolved issues that preclude making general recommendations for their use. These include a paucity of knowledge about the proper dose and duration for these agents, and concern about whether the potential preventive benefits such as a reduction in the frequency or intensity of screening or surveillance could counterbalance long-term risks such as gastrointestinal ulceration and hemorrhagic stroke for the average-risk individual.
A randomized placebo-controlled trial tested the effect of calcium supplementation (3 g calcium carbonate daily [1,200 mg elemental calcium]) on the risk of recurrent adenoma.
The primary endpoint was the proportion of patients (72% of whom were male) in whom at least one adenoma was detected following a first and/or second follow-up endoscopy. A modest decrease in risk was found for both developing at least one recurrent adenoma (adjusted risk ratio [ARR], 0.81; 95% CI, 0.67–0.99) and in the average number of adenomas (ARR, 0.76; 95% CI, 0.60–0.96). The investigators found the effect of calcium was similar across age, sex, and baseline dietary intake categories of calcium, fat, or fiber. The study was limited to individuals with a recent history of colorectal adenomas and could not determine the effect of calcium on risk of the first adenoma, nor was it large enough or of sufficient duration to examine the risk of invasive CRC. After calcium supplementation is stopped, the lower risk may persist up to 5 years.
The results of other ongoing adenoma recurrence studies are awaited with interest. It is important to note that the dose of calcium salt administered may be important; the usual daily doses in trials have ranged from 1,250 to 2,000 mg of calcium.
In a randomized, double-blind, placebo-controlled trial involving 36,282 postmenopausal women, the administration of 500 mg of elemental calcium and 200 IU of vitamin D3 twice daily for an average of 7.0 years was not associated with a reduction in invasive CRC (HR, 1.08; 95% CI, 0.86–1.34; P = .051).
The relatively short duration of follow-up, considering the latency period of CRC of 10 to 15 years, and suboptimal doses of calcium and vitamin D, may account for the negative effects of this trial, although other factors may also be responsible.
Colon cancer rates are high in populations with high total fat intakes and are lower in those consuming less fat.
On average, fat comprises 40% to 45% of total caloric intake in high-incidence Western countries; in low-risk populations, fat accounts for only 10% of dietary calories.
Several case-control studies have explored the association of colon cancer risk with meat or fat consumption, as well as protein and energy intake.
Although positive associations with meat consumption or with fat intake have been found, the results have been inconsistent.
A number of prospective cohort studies have been conducted in the United States and abroad; a systematic review of 13, including the Iowa Women’s Health Study and the Nurses’ Health Study, concluded that there appeared to be a positive association between meat consumption and CRC incidence. However, the authors noted that because only a few studies tried to investigate the independent effect of meat intake on cancer risk, the observed relationship might be attributed entirely to confounding.
Similarly, a 2019 systematic review of observational studies, evaluating the association between processed or unprocessed red meat consumption and CRC incidence and mortality, concluded that a reduction of three servings per week resulted in very small to no decreases in those outcomes, although the certainty around these findings was judged low to very low.
A randomized controlled dietary modification study was undertaken among 48,835 postmenopausal women aged 50 to 79 years who were also enrolled in the WHI. The intervention promoted a goal of reducing total fat intake by 20%, while increasing daily intake of vegetables, fruits, and grains. The intervention group accomplished a reduction of fat intake of approximately 10% more than did the comparison group during the 8.1 years of follow-up. There was no evidence of reduction in invasive CRCs between the intervention and comparison groups with a HR of 1.08 (95% CI, 0.90–1.29).
Likewise, there was no benefit of the low-fat diet on all-cancer mortality, overall mortality, or cardiovascular disease.
This last observation was echoed in a 2019 systematic review of randomized controlled trials of the effect of variable red meat consumption on cancer outcomes. This review relied heavily on the WHI to reach the conclusion that there appears to be little to no effect of red meat intake on CRC incidence, although the certainty around this finding is low because of limitations in available studies.
Explanations for the conflicting results regarding whether dietary fat or meat intake affects the risk of CRC
include:
Six case-control studies and two cohort studies have explored potential dietary risk factors for colorectal adenomas.
Three of the eight studies found that higher fat consumption was associated with increased risk. High fat intake has been found to increase the risk of adenoma recurrence following polypectomy.
In a multicenter RCT, a diet low in fat (20% of total calories) and high in fiber, fruits, and vegetables did not reduce the risk of recurrence of colorectal adenomas.
Thus, the evidence is inadequate to determine whether reducing dietary fat and meat would reduce CRC incidence.
The estrogen-only intervention component of the WHI was conducted among women who had a hysterectomy, with CRC incidence included as a secondary trial endpoint. CRC incidence was not decreased among women who had taken estrogens; after a median of 7.1 years of follow-up, 58 invasive cancers occurred in the estrogen arm compared with 53 invasive cancers in the placebo arm (HR, 1.12; 95% CI, 0.77–1.63). Tumor stage and grade were similar in the two groups; deaths after CRC were 34% in the hormone group compared with 30% in the placebo group (HR, 1.34; 95% CI, 0.58–3.19).
Overall, evidence indicates that statin use neither increases nor decreases the incidence or mortality of CRC. Although some case-control studies have shown a reduction in risk, neither a large cohort study
nor a meta-analysis of four RCTs
found any effect of statin use.
作者会定期审核PDQ癌症信息总结，并在获得新信息后进行更新。本节介绍截至上述日期对此总结所做的更新。
2020年的估计新发病例和死亡病例的崭新统计数据（引自美国癌症协会数据[参考2]）。修订后的文本指出，2007年至2016年期间，美国55岁及以上成年人结直肠癌（CRC）的发病率每年下降3.6%，在55岁以下的成年人中，CRC的发病率每年上升2%；在2008年至2017年期间，55岁及以上成年人的死亡率每年下降2.6%，55岁以下成年人的死亡率每年上升1%。
修订后的文本指出，CRC 5年总生存率为64%（引自Howlader等人的报道[参考6]）。
修订后的文本指出，在美国和其他国家进行的若干前瞻性队列研究中，纳入包含爱荷华州妇女健康研究和美国护士健康研究在内的13项研究进行系统综述后发现，肉类摄入与CRC发病率之间存在正相关关系。然而，作者指出，由于只有少数研究评估了肉类摄入对癌症风险的独立影响，观察到的相关性可能完全归因于混杂效应。同样，修订后的文本还指出，2019年一项对观察性研究的系统综述评估了加工或未加工红肉摄入与CRC发病率和死亡率之间的关系，研究发现：每周减少三份肉食，对发病率和死亡率几乎没有降低，但该发现的准确性评级为低到很低。
在2019年对各类红肉摄入对癌症结局影响的随机对照试验进行的系统综述中补充说明了，观察到低脂饮食不能降低各类癌症死亡率、总死亡率或心血管疾病风险；该研究在很大程度上依赖于WHI得出结论，即红肉摄入对CRC发病率几乎没有影响，但由于现有研究的局限性，该结论的准确性很低。（引用Zeraatkar等人的报道[参考114]）。
本小结由独立于NCI的PDQ筛查和预防编辑委员会编写和维护。本小结是对既往文献报道的独立回顾，并不代表NCI或NIH的政策声明。更多关于小结中提及的政策和PDQ编辑委员会维护PDQ小结中的作用，详见PDQ总结和PDQ® -NCI的癌症综合数据库网站主页。
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 2). Also revised text to state that between 2007 and 2016, incidence rates for colorectal cancer (CRC) in the United States declined by 3.6% per year among adults aged 55 years and older; however, in adults younger than 55 years, incidence rates for CRC have been increasing by 2% per year. Also revised text to state that between 2008 and 2017, the mortality rate declined by 2.6% per year among adults aged 55 years and older but increased by 1% per year among adults younger than 55 years.
Revised text to state that the overall 5-year survival rate is 64% for CRC (cited Howlader et al. as reference 6).
Revised text to state that a number of prospective cohort studies have been conducted in the United States and abroad; a systematic review of 13, including the Iowa Women's Health Study and the Nurses' Health Study, concluded that there appeared to be a positive association between meat consumption and CRC incidence. However, the authors noted that because only a few studies tried to investigate the independent effect of meat intake on cancer risk, the observed relationship might be attributed entirely to confounding. Also added text to state that similarly, a 2019 systematic review of observational studies, evaluating the association between processed or unprocessed red meat consumption and CRC incidence and mortality, concluded that a reduction of three servings per week resulted in very small to no decreases in those outcomes, although the certainty around these findings was judged low to very low.
Added text to state that the observation of no benefit of the low-fat diet on all-cancer mortality, overall mortality, or cardiovascular disease was echoed in a 2019 systematic review of randomized controlled trials of effect of variable red meat consumption on cancer outcomes; this review relied heavily on the Women's Health Initiative to reach the conclusion that there appears to be little to no effect of red meat intake on CRC incidence, although the certainty around this finding is low because of limitations in available studies (cited Zeraatkar et al. as reference 114).
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 colorectal 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.
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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 Colorectal 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 colorectal 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 Colorectal 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.