结直肠腺瘤切除术后息肉复发及内镜监测的临床分析

目的研究结直肠腺瘤(colorectal adenoma,CRA)切除术后息肉复发的情况,以确定合理的内镜监测间隔时间。方法收录2005年5月-2012年5月于北京朝阳医院消化内科完成结肠镜下息肉切除术、病理组织学确诊为CRA、术后再次入院行肠镜复查的患者共143例,男89例,女54例。统计分析复发息肉的累计复发率,确定影响复发息肉的重要危险因素和中位复发时间。结果息肉总体复发率为72%,患者性别、年龄、息肉大小、息肉数目、息肉发生部位、病理类型等因素中,仅CRA的大小和病理类型对复发有重要影响。初检CRA直径1 cm的患者较CRA直径≤1 cm的患者复发风险高(P=0.02)。CRA病理中含有绒毛成分的患者较仅为管状腺瘤的患者复发风险高(P=0.08)。结论建议含绒毛成分或直径1 cm的CRA患者术后6~12个月复查肠镜,而直径≤1 cm的管状腺瘤患者可在术后2年左右复查肠镜。     

幽门螺旋杆菌感染与结直肠腺瘤复发的相关性分析

背景结直肠腺瘤(colorectal adenoma, CRA)是结直肠癌(colorectalcancer,CRC)的癌前病变,早期切除及预防其复发是预防结肠癌的有效措施.但腺瘤切除后容易复发,有研究显示幽门螺旋杆菌(Helicobacter pylori,H. pylori)感染是CRA发生原因之一,本研究拟分析H.pylori感染及根除H. pylori对CRA复发的影响.目的探讨CRA术后复发的危险因素,尤其是H. pylori感染对CRA复发的影响.方法收集本院门诊及病房行肠镜检查并病理证实为CRA的病例,根据13C呼气试验结果,将其分为A组(H. pylori阴性组)和B组(H. pylori阳性组); B组病例再随机分成两组:C组根除H. pylori, D组未根除H. pylori. 1年后复查肠镜及呼气试验,根据随访肠镜的结果,比较息肉复发病例和未复发病例的一般资料,并对CRA复发的危险因素进行Logistic回归分析.结果共有733例CRA患者纳入本研究,各组中患者的一般资料以及术前息肉的大小、数目、病理类型及手术方式等均无显著差异(P0.05).术后1年复查, H. pylori感染组(B组)患者息肉复发率显著高于A组(23.02%vs15.79%, P 0.05);而根除H. pylori后的C组息肉复发率则显著低于未根除的D组(17.37%vs 28.36%, P0.05).在息肉复发的所有危险因素中,男性患者、BMI≥25kg/m2,息肉个数≥3枚、息肉大小≥20mm及H. pylori感染等因素存在统计学差异(P0.05); Logistic回归分析显示, H. pylori感染是息肉复发的独立危险因素(OR=1.556, P 0.05),而根除H. pylori与息肉的复发呈负相关性(OR=0.509, P0.05).结论H. pylori感染会增加CRA的复发,是CRA术后复发的独立危险因素,根除H. pylori后能显著降低CRA的复发.     

结直肠息肉的临床特征研究

目的 探讨不同类型结直肠息肉分布的临床特征.方法 收集444例结直肠息肉患者的临床资料,分析结直肠息肉与不同性别、年龄、检出部位、病理及直径大小之间的相关性.结果 结直肠息肉患者中男性构成比明显高于女性(男∶女=2.02∶1).检出部位在左半结肠患者比例明显高于右半结肠(64.6％比25.7％).不同病理类型中,腺瘤性...     

结肠息肉临床病理特点分析313例

目的:探讨结肠息肉临床及病理组织学特征为临床诊疗工作提供参考.方法:回顾性分析南京市第一医院2011-09/2014-09共313例结肠息肉病例,所有患者于门诊就诊行电子肠镜检查,考虑为息肉者经患者知情同意后住院行结肠息肉内镜下治疗,镜下及病理组织学均证实为结肠息肉.结果:结肠息肉患者中腺瘤发生率为72.8%腺瘤与非腺瘤病例临床表现无统计学差异,结肠息肉中腺瘤的发生与性别、山田分型、生长部位及息肉数目无关,各年龄层、息肉直径之间腺瘤的发生率有统计学差异(P0.05);腺瘤上皮内瘤变程度与性别、年龄、生长部位、息肉数目无关,而山田分型、各息肉直径之间腺瘤上皮内瘤变程度有统计学差异(P0.05).结论:结肠息肉的临床表现无特异性,以左半结肠多见,腺瘤发生率男女之间无统计学差异,以40岁以上中老年人多见,直径1 cm息肉腺瘤发生率更高,山田分型、生长部位及息肉数目不影响腺瘤发生率;腺瘤性息肉上皮内瘤变程度与山田分型及息肉直径相关,山田Ⅲ、Ⅳ型息肉、直径1 cm息肉高级别上皮内瘤变发生增高.     

内镜下治疗大肠息肉256例的临床分析

目的探讨大肠息肉的分布、病理分型以及高频电切除的疗效及安全性。方法对256例患者结肠息肉采用内镜下高频电切除治疗,观察其分布情况、病理分型、疗效及并发症。结果有效切除率为100%,左半结肠占72.66%右半结肠9.76%横结肠17.58%,腺瘤性息肉占49.6%,术中及术后24 h内出血率3.12.%,手术24 h后出血率0.78%,穿孔发生率0.39%,单发者一年随访复发率16.00%,多发者半年复发率23.66%。结论大肠息肉发生以左半结肠为主,病理分型主要为腺瘤,高频电切除大肠息肉安全、可靠、有效,如术中或术后发生出血,则应积极进行内镜下治疗,该方法值得临床广泛应用。     

幽门螺杆菌感染和胃泌素与结直肠腺瘤性息肉的相关性研究

目的探讨幽门螺杆菌(Helicobacter pylori,H.pylori)感染和血清胃泌素水平与结直肠腺瘤性息肉的相关性。方法经胃、肠镜检查,选取120例结直肠腺瘤性息肉患者为研究组,需描述息肉的部位、大小、数目、黏膜情况、山田分型和组织病理分型。另选取120例结肠无明显异常者为对照组,所有入选者均完成13C-尿素呼气试验和胃泌素17(gastrin 17,G17)检测。结果研究组的年龄、中老年患者比例(≥40岁)和H.pylori阳性率均高于对照组,差异有统计学意义(P0.05);左半结肠、多发性和大息肉(≥10 mm)的H.pylori阳性率明显高于右半结肠、单发性和小息肉(10 mm)(P0.05),而山田分型和病理分型亚组比较,差异无统计学意义(P0.05)。研究组血清G17水平高于对照组,二组中H.pylori阳性者G17水平也分别高于H.pylori阴性者,差异均有统计学意义(P0.05)。结论 H.pylori感染可能通过刺激胃泌素分泌影响结直肠腺瘤性息肉的发生、发展,对于H.pylori阳性,尤其中老年患者,应尽早完善结肠镜检查,降低结直肠癌(colorectal cancer,CRC)的潜在风险。     

十年连续内镜检出1747例大肠息肉分析

目的研究近十年大肠息肉发生部位的变化及与性别、发病年龄及病理类型的关系。方法分析1995～2004年我院内镜中心检出并经病理证实的1747例大肠息肉。息肉发生部位按右半结肠、横结肠、左半结肠、直肠及多发性息肉统计。比较前5年（1995～1999）和后5年（2000～2004）结肠息肉解剖部位的变化。结果1995～1999年检出大肠息肉共591例，以左半结肠、直肠为主（38．6％、25．9％），右半结肠、横结肠和多发性息肉分别为9％、7．8％和18．7％。200～2004年检出大肠息肉明显增加，为l156例。仍以左半结肠和直肠息肉多见（37％、24．6％），右半结肠、横结肠和多发性息肉分别为11．9％、10．2％和16．3％。前后5年相比，大肠息肉解剖部位无明显变化（P〉0．05）。1747例结肠息肉中，男女之比为1．42：1；35～60岁年龄段发病比例高；病理类型以腺瘤性息肉为主（81．2％）。结论大肠息肉内镜检出例数增加迅速。近十年大肠息肉解剖部位无明显变化。息肉好发部位在左半结肠和直肠，以腺瘤性息肉为主。     

代谢综合征组分与结直肠腺瘤临床病理特征的相关性

背景:结直肠癌(CRC)是消化系统常见的恶性肿瘤之一,结直肠腺瘤(CRA)为公认的CRC癌前病变。因此,寻找CRA的危险因素对预防CRC具有重要意义。目的:探讨代谢综合征(MS)组分与CRA临床病理特征的相关性。方法:收集2014年12月—2016年12月内蒙古医科大学附属医院收治的460例CRA患者,记录MS组分和CRA的临床病理特征。MS与CRA临床病理特征相关性的分析采用χ2检验或Spearman秩相关分析。CRA临床病理特征的影响因素分析采用Logistic回归分析。结果:MS与CRA病理类型、CRA带蒂、CRA大小相关(P 0. 001,rp=0. 317; P 0. 001,rp=0. 321; P=0. 001,rs=0. 150),而与CRA部位、数目无关(P 0. 05)。高血压、糖尿病、高三酰甘油(TG)、高腰围可使绒毛状腺瘤发生风险增加(P 0. 05),年龄、高腰围可使管状绒毛状腺瘤发生风险增加(P 0. 05)。高血压、高TG、高腰围可使CRA带蒂的发生风险增加(P 0. 05)。年龄可使全结肠CRA发生风险增加(P 0. 05),其余因素对近端结肠CRA、全结肠CRA均无明显影响(P0. 05)。糖尿病、高腰围为影响CRA大小的危险因素(P 0. 05)。性别、年龄、高血压、糖尿病、高TG、低HDL、高腰围与CRA数目均无关(P 0. 05)。结论:MS与CRA的病理类型、是否带蒂、大小相关。高血压、糖尿病、高TG、高腰围为绒毛状腺瘤的危险因素;年龄、高腰围为管状绒毛状腺瘤的危险因素。高血压、高TG、高腰围为CRA带蒂的危险因素。年龄为全结肠CRA的危险因素。糖尿病、高腰围为CRA大小的危险因素。     

老年人与中青年人大肠息肉临床特点对比研究

目的探索老年人大肠息肉的临床特征。方法收集在上海中医药大学附属曙光医院2006年1月-2019年12月行电子结肠镜检查并且病理证实为大肠息肉的患者1000例,进行回顾性研究,按年龄分为老年组576例,中青年组424例。统计分析老年大肠息肉患者的临床症状、息肉大小、形态、部位、数目、息肉病理分型及其与息肉癌变的相关性,同时与中青年组比较。结果老年组最常见的临床表现为便血或粪隐血阳性(48.1%)及腹胀(45.8%),中青年组主要表现为腹胀(26.7%)和便秘(25.7%);2组患者均以无蒂、多发息肉多见,左半结肠是息肉好发部位;2组均以<2 cm的息肉多见;老年组≥2 cm的息肉多于中青年组(6.2%vs 3.6%,P=0.008);2组病理分型均以管状腺瘤为主,老年组管状绒毛状腺瘤比例高于中青年组(12.6%vs 7.6%,P=0.000);癌变率男女性间无差异;老年组息肉癌变率高于中青年组(9.7%vs 4.7%,P=0.004),左半结肠息肉、无蒂息肉、绒毛状腺瘤、>2 cm息肉癌变率高;老年组<2 cm息肉癌变率高于中青组(2.4%vs 1.0%,P=0.014)。结论腹胀、便血或粪隐血阳性是老年大肠息肉患者常见临床表现,老年患者大肠息肉癌变率高于中青年患者,大肠息肉的癌变率与年龄、息肉大小、部位、病理分型密切相关。     

大肠息肉内镜下形态学特点、病理分型与中医证型的相关性

背景大肠息肉(colorectal polyps, CRP)是临床常见病,多发病,治疗上主要依靠内镜下切除为主,但术后易复发,保守治疗CRP的药物临床应用及相关报道较少,且疗效不理想.本文通过探讨不同中医证型的大肠息肉与内镜下息肉形态学特点、病理分型之间的相关性,再结合中医四诊,从而精准辩证得出某一特定阶段CRP的中医证候类型并拟定出个体化的方药,进而调整患者体质类型从而有效预防CRP术后复发,以期减少腺瘤恶变,临床优势明显.目的探讨大肠息肉内镜下形态学特点、病理分型与中医证型之间的相关性,为中医药防治提供依据.方法收集300例大肠息肉患者临床资料进行调查研究,记录中医四诊及内镜下大肠息肉大小、形态、数目、病变部位等信息,确定中医证型,分析并总结内镜下息肉形态学特点、病理分型与中医证型的相互关系及分布规律.结果 300例大肠息肉病理分型以腺瘤性息肉为主,且腺瘤性息肉发生率与性别、职业、各年龄层、息肉大小、山田分型、息肉数量、发病部位等因素相关,差异有显著性(P0.05).与CRP发生相关的中医证型中脾虚湿蕴证、大肠湿热证、寒湿阻滞证中息肉直径多1 cm,呈光滑形多发息肉为主,多无蒂或亚蒂.气滞血瘀证、血虚肠澡证、肝郁气滞证以1-2cm息肉多见,多呈颗粒形单发息肉,多带蒂.各中医证型与息肉数目多少、形态之间差异有统计学意义(P 0.05).脾虚湿蕴证、大肠湿热证、寒湿阻滞证及肝郁气滞证中病理分型以管状腺瘤和增生性息肉多见,其它证型以增生性息肉为主.并发现腺瘤性息肉与非腺瘤性息肉患者的中医证型分布差异有统计学意义(P0.05).结论不同中医证型与大肠息肉数目多少、形态变化有关,但不会影响息肉的大小及发病部位,同时中医证型与病理类型之间存在一定相关性,临床中可通过中医体质调摄预防大肠息肉的发生率及复发率,为防治大肠息肉提供新思路.     

Early-onset colorectal cancer: A separate subset of colorectal cancer

Colorectal cancer (CRC) has a great impact on the world population. With increasing frequency, CRC is described according to the presenting phenotype, based on its molecular characteristics. Classification of CRC tumors according to their genetic and/or epigenetic alterations is not only important for establishing the molecular bases of the disease, but also for predicting patient outcomes and developing more individualized treatments. Early-onset CRC is a heterogeneous disease, with a strong familial component, although the disease is sporadic in an important proportion of cases. Different molecular alterations appear to contribute to the apparent heterogeneity of the early-onset population and subgroups can be distinguished with distinct histopathologic and familial characteristics. Moreover, compared with late-onset CRC, there are characteristics that suggest that early-onset CRC may have a different molecular basis. The purpose of this review was to analyze the current state of knowledge about early-onset CRC with respect to clinicopathologic, familial and molecular features. Together, these features make it increasingly clear that this subset of CRC may be a separate disease, although it has much in common with late-onset CRC.     

Clinical implications of multiple colorectal carcinomas in hereditary nonpolyposis colorectal carcinoma

PURPOSE: An increased incidence of multiple (synchronous and metachronous) colorectal carcinomas has been reported in hereditary nonpolyposis colorectal cancer. This review was undertaken to determine the clinical implications of multiple colorectal carcinomas in hereditary nonpolyposis colorectal cancer. METHODS: A retrospective review of the records of patients in the hereditary nonpolyposis colorectal cancer registry at Roswell Park Cancer Institute who had either synchronous or metachronous colorectal carcinomas was conducted. RESULTS: Twenty-five of 93 patients with documented pathology were found to have multiple colorectal carcinomas. The mean age at diagnosis of the index colorectal carcinoma was 46.7 (range, 28–65) years. There were 7 (7.5 percent) patients with synchronous colorectal carcinomas and 20 (21.5 percent) patients with metachronous colorectal carcinomas. Two of the seven (28.6 percent) patients with synchronous colorectal carcinomas developed a metachronous colorectal carcinoma. In the patients with metachronous colorectal carcinomas, 29 metachronous events were noted: colon (23) and rectum (6). The mean and median time interval for metachronous colorectal carcinomas were 10.9 and 11.8 (range, 1.5–43.8) years, respectively. The mean times to first, second, and third events were 11.7 (range, 1.5–43.5), 7.9 (range, 2.7–18.7), and 12.3 (range, 11.8–12.7) years, respectively. The majority of patients with metachronous colorectal carcinomas did not have stage progression at the diagnosis of the metachronous colorectal carcinomas: 13 patients had lower or same stage at first event, 4 had lower or same stage at second event, and 2 patients had lower stage at third event. Three of 20 patients with metachronous colorectal carcinomas died of their disease. CONCLUSION: Multiple colorectal cancers are common in hereditary nonpolyposis colorectal cancer. Even though stage progression may not be evident at diagnosis of metachronous colorectal cancer, some of these patients will nevertheless die of their disease.Presented at the annual meeting of the Southeastern Surgical Congress, Atlanta, Georgia, February 2 to 4, 1998.     

Staging of colorectal cancer

A new system, the Australian Clinico-pathological Staging (ACPS) System, has recently been proposed for the recording and reporting of colorectal carcinoma. This system requires the accurate use of precise definitions, cooperation between surgeons and pathologist, and a complete pathology report. It utilizes all information available—clinical, radiologic, operative, pathologic—before a stage is allotted. This contrasts with Dukes' system, which is based solely on the pathologic examination of the resected carcinoma. It allows classifications of all cases of colorectal cancer seen, whether treated by resection, palliative surgery, local excision or not at all. The stage at presentation and the five-year survival of 490 patients with colorectal cancer are compared using the ACPS and Dukes' systems. Eighty-four cases were not classifiable under Dukes' system, and there was a significant difference in survival in one of the comparable groups of patients. Read at the joint meeting of the American Society of Colon and Rectal Surgeons with the Section of Colo-Proctology of the Royal Society of Medicine, and the Section of Colonic and Rectal Surgery of the Royal Australasian College of Surgeons, New Orleans, Louisiana, May 6–11, 1984. The Colorectal Project is supported by the Queensland Cancer Fund.     

Surveillance of colorectal cancer

PURPOSE: The authors evaluate the effectiveness of routine colonoscopy and marker evaluation in diagnosis of intraluminal recurrent cancer. METHODS: Chart review was conducted on 481 patients who underwent curative resection for colorectal cancer between 1980 and 1990. Clinical visits were scheduled and carcinoembryonic antigen evaluation was performed every three months, and colonoscopy was performed preoperatively, 12 to 15 months after surgical treatment, and then with intervals of 12 to 24 months or when symptoms appeared. RESULTS: About 10 percent of patients developed intraluminal recurrences. More than one-half of metachronous lesions arose within the first 24 months, and median time to diagnosis was 25 months. Patients with left-sited tumors in the advanced stage had a higher risk of developing recurrent intraluminal disease. Twenty-nine patients underwent a second surgical operation, of which 17 cases were radical. In this group, the five-year survival was 70.6 percent, although no nonradically treated or nonresected patients survived longer than 31 months. Twenty-two patients were asymptomatic at time of diagnosis of recurrence, and of these, 12 patients underwent radical operation; on the other hand, of the 24 symptomatic patients, only 5 were treated radically. Carcinoembryonic antigen was the first sign of recurrence in eight cases. Colonoscopy must be performed within the first 12 to 15 months after operation, whereas an interval of 24 months between examinations seems sufficient to guarantee early detection of metachronous lesions. CONCLUSION: Serial tumor marker evaluation is of help in earlier diagnosis of local recurrences. Asymptomatic patients more frequently undergo another operation for cure and thus have a better survival rate.     

Pathology of colorectal cancer

The earliest phases of colorectal tumourigenesis initiate in the normal mucosa, with a generalised disorder of cell replication, and with the appearance of clusters of enlarged crypts (aberrant crypts) showing proliferative, biochemical and biomolecular abnormalities. The large majority of colorectal malignancies develop from adenomatous polyps. These can be defined as well demarcated masses of epithelial dysplasia, with uncontrolled crypt cell division. An adenoma can be considered malignant when neoplastic cells pass through the muscularis mucosae and infiltrate the submucosa. Definitions like "carcinoma in situ" or "intramucosal carcinoma" should be abandoned, since they lead to confusion. Although several lines of evidence indicate that carcinomas usually originate from pre-existing adenomas, this does not imply that all polyps undergo malignant changes, and does not exclude "de novo" carcinogenesis. Besides adenomas, other types of polypoid lesions include hyperplastic polyps (showing elongated crypts often with cystic dilatation), serrated adenomas (with a serrated glandular pattern], flat adenomas (flat lesions which are difficult to detect in routine lower endoscopy, but may possess malignant potential), hamartomatous polyps (which show a complex branching pattern of smooth muscle supporting normal lamina propria and glands), and inflammatory polyps. Colorectal carcinomas are one of the most frequent neoplasms in Western society; the macroscopic appearance of these lesions may be that of a polypoid vegetating mass or of a flat infiltrating lesion. Most of these tumours are adenocarcinomas (96%), that, in some cases, show a mucinous component. More rare malignancies of the large bowel include signet-ring cell carcinoma, squamous carcinoma, undifferentiated neoplasms and medullary type adenocarcinoma (solid carcinoma with minimal glandular differentiation or slight cellular pleomorphism). Colorectal carcinoma can be graded into well, moderately and poorly differentiated lesions; there is little evidence, however, that grading may be of help in evaluating prognosis of affected patients. In conclusion, colorectal tumours cover a wide range of premalignant and malignant lesions, many of which can easily be removed at endoscopy. It follows that colorectal neoplasms might be prevented by interfering with the various steps of carcinogenesis, which begins with uncontrolled epithelial cell replication, continues with the formation of adenomas of various dimensions, and eventually evolves into malignancy.     

Ordinary colorectal adenocarcinomavs. primary colorectal signet-ring cell carcinoma

PURPOSE: This study contributes to the characterization of primary colorectal signet-ring cell cancer in contrast to ordinary colorectal carcinoma. Primary colorectal signet-ring cell cancer is a rare but distinctive primary neoplasm of the large bowel with still-controversial clinicopathologic features. METHODS: Clinicopathologic features and survival data are evaluated in comparison with those of the ordinary colorectal adenocarcinoma (non-signet colorectal carcinoma) in a retrospective study matched for age, gender, grade, and stage. RESULTS: In a series of 1,600 consecutive colorectal cancer patients since 1979, 14 patients (0.88 percent) with a signet-ring cell cancer were identified. Gender ratio was balanced, and mean age was 67.5 years. The majority of patients had an advanced tumor stage at the time of diagnosis (57.1 percent Stage IV and 35.7 percent Stage III). Median survival time was only 16 months. In a study matched for age, gender, grade, and stage, a lower survival rate was found for patients with signet-ring cell cancer, but the difference did not reach statistical significance. In contrast to non-signet colorectal carcinoma, signet-ring cell cancer was characterized by a significantly higher incidence of peritoneal tumor spread (64.3 percent) and a lower incidence of hepatic metastases (14.3 percent). CONCLUSIONS: Signet-ring cell cancer represents a rare but distinctive primary neoplasm of the large bowel. It is frequently diagnosed in an advanced tumor stage, thus showing an overall poorer prognosis than nonsignet colorectal carcinoma. Usually only palliative surgery is possible. A high incidence of peritoneal seeding and a low incidence of hepatic metastasis is characteristic of signet-ring cell cancer.     

Follow-up of colorectal cancer

PURPOSE: The value of intensive follow-up for patients after resection of colorectal cancer remains controversial. This study reviews all randomized and prospective cohort studies to assess the value of aggressive follow-up. METHODS: The literature was searched from the years 1972 to 1996 for studies reporting on the follow-up of patients with colorectal cancer. Randomized and comparative-cohort studies that included history, physical examination, and carcinoembrionic antigen values at least three times a year for at least two years were included in a meta-analysis. Single-cohort studies with intensive follow-up and traditional follow-up were also included in a two-group comparative analysis for each outcome indicator. Outcome indicators were 1) curative resection rates after recurrent cancer, 2) survival rates of curative re-resections, 3) length of survival after recurrence, and 4) cumulative five-year survival. RESULTS: Two randomized and three comparative-cohort studies met these criteria and included 2,005 patients, which were evaluated in the meta-analysis. The cumulative five-year survival was 1.16 times higher in the intensively followed group (P=0.003). Two and one-half times more curative re-resections were performed for recurrent cancer in those patients undergoing intensive follow-up (P=0.0001). Those patients in the intensive follow-up group with a recurrence had a 3.62-times higher survival rate than the control (P=0.0004). Fourteen single-cohort studies were also included in the comparative analysis of 6,641 patients. The findings from these aggregated studies support the results of the meta-analysis. CONCLUSION: Our study concludes that intensive follow-up detects more recurrent cancers at a stage amenable to curative resection, resulting in an improvement in survival of recurrences and an increased overall five-year cumulative rate of survival.     

Pathogenesis of colorectal cancer

The development of colorectal cancer has been viewed as an ordered process in which three main phases can be identified: initiation, promotion and progression. There is definite proof that stable alterations of the structure or sequence of DNA (mutations) represent the initiating event; these are followed by an uncontrolled expansion of the neoplastic clones which characterizes tumoural growth. Several classes of genes have been identified (oncogenes, tumour suppressor genes and “mutator” genes) the alterations of which are important in the initiation as well as in the promotion and progression of tumours. Colorectal cancer, therefore, results from a series of genetic changes which lead to the progressive and irreversible loss of normal control of cell growth and differentiation. Available evidence is consistent with the hypothesis that there are several molecular pathways underlying the passage from normal mucosa to colorectal carcinoma, thus explaining the existence of intestinal tumours with a different biological nature, which may represent specific targets for prevention and cure. Well-defined molecular pathways have been identified for: A) sporadic colorectal cancer (“Loss of heterozygosity pathway”); B) familial adenomatous polyposis and related polyposis syndromes; C) hereditary non-polyposis colorectal cancer (“mutator genesimicrosatellite instability pathway”); D) cancer developing in inflammatory bowel diseases; E) familial colorectal cancer. Thus, there is consistent and considerable evidence suggesting the existence of several biological pathways leading to the same phenotypical expression (i.e., colorectal cancer), and it is likely that additional pathways will be clarified in the future. From a practical point of view, tumours with a diverse biology might offer different and more effective preventive and curative approaches.