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PubMed2006

[Current concepts in the genetics of hereditary and sporadic colorectal cancer and the role of genetics in patient management. Hereditary colorectal cancers].

Colorectal cancer (CRC) is the second leading cause of mortality of malignant diseases in Hungary and according to the incidence and prevalence of CRC Hungary is second among European countries. Hence, it is of outstanding interest to know the current concepts on pathogenesis and genetical background of CRC, as well as incorporate this knowledge in the everyday practice. In the first part of the review authors address the genetic background of hereditary colorectal cancer syndromes. In fact, a positive family history may be found in 20-30% and genetically defined trait (e.g. familial adenomatous polyposis (FAP), hereditary nonpolyposis colorectal cancer (HNPCC) and Peutz-Jeghers-syndrome (PJS)) is responsible for 3-5% of all colon cancers. Germline mutations of tumor suppressor gene, APC (5q21) are found in 70-90% of the cases. Until now more than 300 mutations were identified. Though a typical mutation was not found, the location of the mutation is associated to the clinical phenotype and prognosis. Of note, beside APC mutations, biallelic mutations of the MYH gene may be found in a subset of individuals with FAP. The diagnosis of HNPCC is based on family history and the presence of Amsterdam I-Il or Bethesda criteria. The genetic background and clinical phenotype of the syndrome is heterogeneous. Mutations of different mismatch repair genes (mainly hMLH1 or hMSH2) may be identified in most cases. Genetic testing is advised in first degree relatives of FAP patients, if genetic testing is not available colonoscopic surveillance should be done starting at the age of 10-12 years. Due to the high number of mutation genetic testing is difficult in HNPCC families and colonoscopic screening should be advised to affected families.

Adaptor Proteins, Signal Transducing↗

PubMed1993

Laxative use not a risk for colorectal cancer: data from the Melbourne Colorectal Cancer Study.

Commercial laxative use as a risk factor in colorectal cancer was investigated as one part of a large population based epidemiological study of colorectal cancer incidence, aetiology and survival "The Melbourne Colorectal Cancer Study", conducted in Melbourne, Australia. Commercial laxative use was similar in 685 colorectal cancer patients and 723 age/sex matched community based controls. Also, when laxatives were subdivided into various groups containing anthraquinones, phenolphthalein, mineral salts and others, previous laxative intake was similar between cases and controls. Previous use of anthraquinone laxatives and of phenolphthalein containing laxatives was not associated with the risk of colorectal cancer.

Anthraquinones↗

PubMed2000

Cyclin D1 protein expression and gene polymorphism in colorectal cancer. Aberdeen Colorectal Initiative.

Cyclin D1 is a key cell cycle regulatory protein, the expression and subcellular localization of which is often altered in human tumor cells. A common A/G single nucleotide polymorphism (A870G) in exon 4 of the cyclin D1 gene, CCND1, is associated with the presence of 2 distinct mRNA transcripts for this G1/S regulatory protein, and CCND1 genotype has been related to prognosis in lung cancer and head and neck carcinoma. We have investigated both the expression of cyclin D1 protein and the CCND1 A870G polymorphism in 100 colorectal cancer patients. Immunohistochemistry demonstrated cyclin D1 protein expression in 55% of tumors, and while the absence of cyclin D1 protein was not associated with outcome (p=0.81), high levels of protein expression (>50% of tumor cells expressing cyclin D1) correlated with significantly shortened overall survival (p=0.01). Using polymerase chain reaction restriction fragment length polymorphism analysis, we determined the frequency of each genotype and found that CCND1 genotype was not related to overall survival (p>0.05). In addition, genotype was unrelated to the level of expression and localization of cyclin D1 protein, as well as other key G1/S checkpoint proteins (p21, p27, p53, retinoblastoma) and tumor proliferation markers (proliferating cell nuclear antigen). However, higher levels of p27, and to a lesser extent p21, were associated with reduced cytoplasmic cyclin D1 protein (p=0.029 and p=0.054, respectively). In conclusion, we have demonstrated that high levels of cyclin D1 protein expression are related to outcome in colorectal cancer; however, the CCND1 A870G polymorphism is unrelated to either cyclin D1 protein expression or patient survival.

Adenocarcinoma↗

PubMed1998

Mp colorectal cancer should be defined as early colorectal cancer.

Little is known about the clinicopathologic features of mp colorectal cancer, defined as a cancer where the depth of invasion is limited to within the mucosa, the submucosa and the proper muscle. This study was designed to determine the clinicopathologic features of mp colorectal cancers. From 1973 to 1993, 83 mp colorectal cancer and 66 sm colorectal cancer patients were treated in our department and were enrolled in this study. During the same period, 66 patients with sm colorectal cancer defined as a cancer where the depth of invasion is limited to within the mucosa and the submucosa, were treated. The clinicopathologic findings of these patients were determined retrospectively from their hospital records. Clinicopathologic differences in sm and mp colorectal cancers were compared with sm and mp gastric cancers. The incidence of mp colorectal cancer increased from 7.9% in 1973-1977 to 16.2% in 1988-1993. An advanced macroscopic appearance, a larger tumor size, lymph node metastasis and lymph vessel invasion were more predominant in mp than sm colorectal cancer. Multivariate analysis demonstrated that these clinicopathologic factors were not statistically independent prognostic factors for mp colorectal cancer patients. There was no statistical difference in postoperative survival between sm and mp colorectal cancer patients. Mp colorectal cancer should be defined as early colorectal cancer, because the postoperative survival rate does not differ between mp and sm colorectal cancers, and the clinicopathologic differences between these two are negligible.

Colorectal Neoplasms↗

PubMed1986

Heterogeneous expression of two oncodevelopmental antigens, CEA and SSEA-1, in colorectal cancer.

Colorectal carcinomas are composed of heterogeneous cell subpopulations which may be instrumental in conferring metastatic potential and therapeutic refractoriness to these tumours. To assess cellular heterogeneity, the expression has been examined of two oncodevelopmental antigens, carcinoembryonic antigen (CEA) and stage-specific embryonic antigen 1 (SSEA-1), by double immunofluorescence microscopy on 11 human colorectal carcinomas. Although both antigens were expressed in each tumour, their regional and cellular locations differed considerably. SSEA-1 expression was rarely expressed in poorly differentiated cancers but was enhanced with increasing degrees of differentiation. CEA expression was independent of histological differentiation. SSEA-1 was expressed with similar frequency in cell membranes, cytoplasm, and glandular contents regardless of degree of differentiation. Cytoplasmic staining with CEA however, was limited to more poorly differentiated tumours. In normal mucosa remote from the tumours and transitional mucosa adjacent to them, SSEA-1 stained only a few lower crypts whereas CEA stained a majority of both upper and lower crypts. Although biochemical studies have indicated that the SSEA-1 epitope may reside on CEA molecules, the fact that colon cancer tissues express these two antigens quite heterogeneously suggests differences in antigenic processing which may be dependent upon the degree of cellular differentiation.

Adenocarcinoma↗

PubMed1979

Adjuvant cytotoxic liver perfusion for colorectal cancer.

Colorectal liver metastases develop by malignant cells entering the portal venous circulation. A randomized prospective clinical trial was commenced in 1975 to assess the value of adjuvant umbilical vein cytotoxic perfusion (with 5-fluorouracil) following colorectal resection. One hundred and fifty-four patients without macroscopic liver secondaries have so far entered the trial. The mean age, sex, site and stage of the disease were similar in the control and perfusion groups and there was no statistically significant difference in postoperative complications or hospital stay (17.1 +/- 7.9 days control, 15.8 +/- 7.4 days perfusion group). So far, 23 deaths have occurred in the control group (20 due to recurrent disease) and 7 in the perfusion group (5 due to recurrent disease). Liver metastases were present in 13 control patients and 2 perfusion patients. These results show an encouraging trend and suggest that adjuvant cytotoxic liver perfusion may reduce the development of colorectal liver metastases and hence improve the subsequent prognosis.

Adenocarcinoma↗

PubMed2005

AP-1 and colorectal cancer.

Activator protein-1 (AP-1) is a transcription factor that consists of either a Jun-Jun homodimer or a Jun-Fos heterodimer. AP-1 regulates the expression of multiple genes essential for cell proliferation, differentiation and apoptosis. Numerous reports suggest that AP-1 plays an important role in various human diseases. Among them, the roles relating to human cancers have been strongly suggested for a long time. In human cancers, colorectal cancer is still a leading cause of morbidity and mortality in the world. Since there are some reports about the role of AP-1 in colorectal cancer response to a number of stimuli, such as cytokines and growth factors, and oncogenictransformation, therapeutic inhibition of AP-1 activity has attracted considerable interest. Here, we demonstrate the biological properties of AP-1 and its role in colorectal cancer, and discuss a possibility of an AP-1 inhibitor, an adenovirus dominant-negative mutant of c-Jun, as a therapeutic agent for gene therapy.

Animals↗

PubMed2003

[The role of surgery in the treatment of hepatic metastases from colorectal cancer].

Colorectal neoplasms are a common and frequently fatal illness. Presence of distance metastases from colorectal neoplasm does not preclude therapeutic treatments. Surgical resection is the standard treatment for hepatic colorectal metastasis. Some good results in hepatic metastasectomy are due to the progress of radiology which allows not only early findings of metastatic pathology but defines a surgical technique planning. Patients who are candidates for surgical resection are those with no extrahepatic pathology, resectable hepatic metastases with 1 cm of disease free margin and adequate residual parenchyma. Recurren-ces are shown in two thirds of surgical patients; this suggests that microscopic pathology persists commonly even after resection and that adjuvant therapy is critical. In recent years, many palliative techniques for hepatic cancers have been developed. Potentially useful role of these techniques is ablation of small lesions in patients with contraindications to hepatic resection, small recurrences not resectable, and not resectable neoplasms diffuse in both lobes. Accurate follow-up is essential after hepatic metastasectomy. In conclusion, patients with hepatic potentially resectable colorectal metastases should be evaluated by an expert surgeon, because better long-term outcome is derived from surgical resection.

Adenocarcinoma↗

PubMed2002

Are there two sides to colorectal cancer?

Colorectal carcinomas (CRC) that arise proximal (right) or distal (left) to the splenic flexure exhibit differences in incidence according to geographic region, age and gender. Together with observations that tumours in the hereditary cancer syndromes HNPCC and FAP occur predominantly in the right and left colon, respectively, the existence of 2 categories of CRC based on site of origin in the large bowel was proposed more than a decade ago. Differences between normal right and left colonic segments that could favour progression through different tumourigenic pathways are summarized in this review. Accumulating evidence suggests that the risk of CRC conferred by various environmental and genetic factors is different for proximal and distal tumours. Right- and left-sided tumours also exhibit different sensitivities to fluorouracil-based chemotherapy. Such differences are probably related to the molecular characteristics of the tumours, with the microsatellite instability and CpG island methylator phenotypes being associated with right-sided tumours and chromosomal instability with left-sided tumours. Future molecular-based classification systems for CRC that rely upon distinctive gene expression patterns may allow a clearer discrimination of subgroups than that provided by tumour site alone. Until then however, the existence of 2 broadly different groups of cancer defined by site of origin in the colon should be considered in the design of future epidemiologic studies as well as in the design of new clinical trials aimed at testing novel adjuvant therapies.

Colonic Neoplasms↗

PubMed2003

[Prevention of colorectal cancer in families with hereditary nonpolyposis colorectal cancer].

INTRODUCTION: Hereditary non-polyposis colorectal cancer (HNPCC) is a dominant inherited colorectal cancer syndrome, with lifetime risk up to 90% of developing colorectal cancer (CRC) for carriers of the genes. Screening with colonoscopy can reduce the CRC-rate by 62% and prevent CRC-deaths. The HNPCC-Register was established with the aim of identification and registration of Danish HNPCC-families and coordination of surveillance. MATERIALS AND METHODS: The results of 703 colonic screenings in 396 asymptomatic individuals from 150 HNPCC-families were analysed and related to the family diagnosis. RESULTS: In 112 asymptomatic individuals, 31, colorectal cancers and 140 adenomas were diagnosed. Neoplasia was found in one fifth of the examinations and almost one third of the individuals developed an asymptomatic neoplasia which was detected by screening. At the time of the diagnosis, 77% of the colorectal cancers were localized (Dukes stage A or B). DISCUSSION: In Finland, screening for colorectal cancers in HNPCC-families prevents 25-45-fold more CRC-deaths compared to general population screening for colorectal cancer. The results of the Danish colonic HNPCC-screening reveal neoplasia in 21% of the examinations and the colorectal cancers found by screening were at a more favourable Dukes stage compared to sporadic CRC, and probably also CRC found by general population screening. The HNPCC-Register initiates surveillance together with the clinical genetic departments, but the results of the recommended colonic examinations are not automatically reported to the HNPCC-Register. To enable an in-depth investigation of the effect of CRC-screening in all Danish HNPCC-families, further financial resources should be allocated to the HNPCC-Register to collect the results.

Adenocarcinoma↗

PubMed2001

The role of irinotecan and oxaliplatin in the treatment of advanced colorectal cancer.

Colorectal carcinoma is one of the most common malignancies in the western world, and although fluorouracil (5-FU) has been used in its treatment for almost 40 years, new agents with significant activity have been introduced recently. Irinotecan (CPT-11, Camptosar), a topoisomerase I inhibitor, administered at 300 to 350 mg/m2 every 3 weeks is significantly more active than continuous-infusion 5-FU in patients who have experienced disease progression after conventional therapy with 5-FU. In comparison to best supportive care, irinotecan improves survival and preserves quality of life despite treatment-related toxicity. Moreover, the combination of irinotecan and 5-FU has been explored in a number of different schedules. In previously untreated patients, overall response rates are high. Irinotecan can also be combined with mitomycin (mitomycin-C [Mutamycin]), oxaliplatin, or raltitrexed (Tomudex). Oxaliplatin is a new-generation platinum compound that has demonstrated activity against colorectal carcinoma in preclinical trials. It has been evaluated as a single agent against advanced colorectal carcinoma in the salvage setting and also in combination with 5-FU as initial therapy for metastatic disease (where it shows significant activity). The toxicity profile of oxaliplatin (chiefly characterized by neurotoxicity) differs from that of irinotecan (primarily producing diarrhea) and the potential, therefore, exists for combining these agents or for exploiting their possible synergy with 5-FU. The introduction of these two new active agents of different pharmacologic classes promises to enable significant improvements in the treatment of patients with colorectal carcinoma.

Antineoplastic Agents↗

PubMedDate not supplied

[Epidemiology and prevention of colorectal cancer].

Colorectal carcinoma is very common in western countries. It is in the front line of malignant pathology in France. The estimated number of new cases is almost 26,000 per year. The role played by diet in the onset of colorectal carcinomas is well established. The majority of studies indicate the protective role played by green vegetables. The role of other factors remains controversial: protective role of fibres, calcium and vitamins and favorizing role of fats, proteins, red meat, alcohol and calorie intake. The role of bile salts in increasing the size of adenomas and their malignant change is accepted. A number of therapeutic trials have involved modifications in bile salt concentrations. These should enable the proposal of a primary prevention strategy. The early detection of carcinomas and the secondary prevention of colorectal carcinoma (by detection of the adenomas which precede a high proportion of carcinomas) are areas of great interest. Detection of occult blood in stools as a mass screening test is currently being evaluated. Methods used to obtain a high participation rate among the population vary from one country to another, but are now well-defined. It will be necessary to wait for 2 years before being able to determine the effect on mortality and an even longer period to evaluate the effect on the incidence of colorectal carcinoma.

Adenoma↗

PubMed1989

Expression of the myc gene family in different stages of human colorectal cancer.

Colorectal carcinoma serves as a model system for the study of changes in gene expression and structure relating to tumorigenesis. In this study, the levels of c-myc, N-myc and L-myc mRNAs were assessed in normal human colonic mucosa in 33 cases representing different stages of adenocarcinoma and in 36 adenomatous polyps, the presumed premalignant stage. Consistent with the findings of Erisman et al. (1985), we found that the c-myc gene was overexpressed (3-24-fold) in approximately two-thirds of the tumors examined. Amplification of the gene (3-4-fold) was observed in 2 of 12 tumors examined and did not correlate with the level of expression. Greater amounts of c-myc-specific mRNA than occur in normal tissue was also found in about two-thirds of the polyps examined demonstrating that premalignant lesions also overexpress the gene. N-myc and L-myc specific transcripts can be detected at low abundance in normal colonic mucosa. These genes were found to be frequently overexpressed in tumors and polyps, but in most cases the level of overexpression was modest. A single case of adenocarcinoma showed an approximately 30-fold increase in the level of N-myc mRNA without gene amplification. Adenomatous polyps more frequently overexpressed the L-myc gene than tumors.

Adenocarcinoma↗

PubMed1990

Primary prevention of colorectal cancer. The WHO Collaborating Centre for the Prevention of Colorectal Cancer.

Colorectal cancer is the third most common malignant neoplasm worldwide. Epidemiological and laboratory animal studies have established a link between various nutritional factors and the etiology of this cancer. Recent studies in genetic epidemiology and molecular biology have shown that inherited genetic factors also play an important role in colorectal carcinogenesis. Thus, genetic-nutritional interactions may form the basis for the development of this cancer. Nutritional factors that appear to promote or attenuate the carcinogenic process in the colon include fat, excess calories, fibre, calcium, selenium, and various vitamins. Strategies for primary prevention of colorectal cancer should therefore be targeted to all populations who are at risk because of dietary and hereditary predisposition. Based on current knowledge, recommended nutrition guidelines for reducing the risk of colon cancer include decreased fat consumption, adequate amounts of fruits, vegetables, and calcium, and avoidance of overweight. Research to further elucidate the role of diet in colorectal carcinogenesis should include randomized studies in humans, testing of various nutritional regimens, and the use of colonic adenomas and markers of cell proliferation and differentiation as end-points.

Colorectal Neoplasms↗

PubMed1999

Histologic comparison of hereditary nonpolyposis colorectal cancer associated with MSH2 and MLH1 and colorectal cancer from the general population.

PURPOSE: Hereditary nonpolyposis colorectal cancer is reported to have special histologic features. This study compares the histologic features of hereditary nonpolyposis colorectal cancer to colorectal cancers from the general population when hereditary nonpolyposis colorectal cancer cases are restricted to families with known MSH2 and MLH1 mutations. METHODS: Thirty-seven cancers from kindreds carrying MSH2 mutations, 27 cancers from kindreds carrying MLH1 mutations, and 37 colorectal cancers from the general population were reviewed by a pathologist blinded to hereditary nonpolyposis colorectal cancer gene status. Tumor grade, growth pattern, Crohn's-like lymphoid reaction, mucin production, extent of disease in the bowel wall, and lymph node status were evaluated. RESULTS: Poor differentiation and Crohn's-like reaction were a feature of 44 and 49 percent of hereditary nonpolyposis colorectal cancer compared with 14 percent (P = 0.002) and 27 percent (P = 0.049) of colorectal cancers from the general population, respectively. There was no difference in growth pattern, mucin production, lymph node involvement, or local extent of disease between hereditary nonpolyposis colorectal cancer and colorectal cancers from the general population. Poor differentiation and lymph node metastases were found in 57 and 49 percent of MSH2 compared with 26 percent (P = 0.002) and 10 percent (P = 0.03) of MLH1-associated cancers, respectively. There was no difference in growth pattern, mucin production, Crohn's-like lymphoid reaction, or local extent of disease between subgroups of hereditary nonpolyposis colorectal cancer. CONCLUSIONS: Poor differentiation and Crohn's-like reaction are more common in hereditary nonpolyposis colorectal cancer than colorectal cancers from general population. Poor differentiation and lymph node metastases are more commonly seen in MSH2-associated cancers than MLH1. Evaluation of the natural history, pathogenesis, and prognosis of colorectal cancer in hereditary nonpolyposis colorectal cancer should include consideration of which mismatch repair genes are mutated and what the specific mutations are.

Adaptor Proteins, Signal Transducing↗

PubMed1998

Germline mutations of hMLH1 and hMSH2 genes in patients with suspected hereditary nonpolyposis colorectal cancer and sporadic early-onset colorectal cancer.

PURPOSE: The present study was designed to determine the frequency of germline mutations in the hMLH1 and hMSH2 genes in 31 families suspected of having hereditary nonpolyposis colorectal cancer who do not fulfill the criteria of the International Collaborative Group on Hereditary Nonpolyposis Colorectal Cancer but in whom a genetic basis for colon cancer is strongly suspected and 45 patients with sporadic early-onset colorectal cancer who developed colorectal cancer before the age of 40 years without any family history of colorectal cancer. METHODS: Genomic DNAs were prepared from peripheral blood samples of patients who were tested. All coding exons and exon-intron borders of these two genes were screened, first with the polymerase chain reaction-single-strand conformation polymorphism method, followed by sequencing of the DNA fragments displaying an abnormal single-strand conformation polymorphism pattern. RESULTS: In 31 families with suspected hereditary nonpolyposis colorectal cancer, we found six different germline mutations in seven unrelated families, including one missense mutation and three frame-shift mutations in the hMLH1 gene and one missense mutation and one frame-shift mutation in the hMSH2 gene. Totally, frequency of mutation was 23 percent, 16 percent and 7 percent in the hMLH1 and hMSH2, respectively. Only one missense mutation of the hMSH2 gene was identified in 45 patients (2 percent) with sporadic early-onset colorectal cancer. The mutation detection rate in families with suspected hereditary nonpolyposis colorectal cancer was significantly higher than that of patients with sporadic early-onset colorectal cancer (P < 0.05). CONCLUSION: Our definition of suspected hereditary nonpolyposis colorectal cancer is useful in the diagnosis of hereditary nonpolyposis colorectal cancer and for identifying those families who need genetic presymptomatic diagnosis. Our results indicate that it may be important to perform DNA testing in families suspected of having hereditary nonpolyposis colorectal cancer. On the other hand, we only detected a low mutation rate (2 percent) in 45 patients with sporadic early-onset colorectal cancer.

Adaptor Proteins, Signal Transducing↗

PubMed2000

Mutational analysis of the transforming growth factor beta receptor type II gene in hereditary nonpolyposis colorectal cancer and early-onset colorectal cancer patients.

Somatic mutations in the transforming growth factor beta receptor type II (TGF-beta RII) gene have been observed in various human cancers showing microsatellite instability. Most of the mutations observed were additions or deletions of the mononucleotide repeat sequence present in TGF-beta RII coding region, suggesting that the TGF-beta RII may be a target gene of genomic instability in tumorigenesis. Recently, we reported germ-line frameshift mutations in the mononucleotide repeat sequence of the hMSH6 gene, which is believed to be one of the target genes of genomic instability in tumorigenesis, suggesting the possibility of germ-line mutation in mononucleotide repeat sequences. Moreover, one case of germ-line mutation in the TGF-beta RII gene was identified in a hereditary nonpolyposis colorectal cancer (HNPCC) kindred, indicating the involvement of TGF-beta RII inactivation in tumorigenesis of HNPCC. However, germ-line mutation analysis of all of the coding sequences and the mononucleotide repeat sequence of the TGF-beta RII in HNPCC patients has not yet been fully elucidated. Therefore, to further investigate the presence of germ-line mutations, we screened all of the coding region sequences and mononucleotide repeat sequence of TGF-beta RII from 35 HNPCC, 44 suspected HNPCC, and 45 sporadic early-onset colorectal cancer patients. However, no pathogenic mutations other than silent mutations, introgenic mutation, and polymorphisms were identified. Two silent mutations at codons 309 (ACG to ACA) and 340 (CAT to CAC) in the kinase domain located in exon 4 were detected. A 1-bp cytidine deletion was observed 6 bases from the 3' end of intron. Two polymorphisms were identified at codon 389 (AAC to AAT) and at the fourth-to-last base in intron 3. The polymorphism at codon 389 was more frequent in HNPCC (20%; 7 of 35) and suspected HNPCC patients (18%; 8 of 44) than in nonmalignant control group (10%; 5 of 50). Moreover, the frequency was significantly higher in early-onset colorectal cancer patients (31%; 14 of 45). This is the first report of a different frequency of polymorphism in HNPCC, suspected HNPCC, early-onset colorectal cancer patients, and healthy normal individuals. This result suggests that: (a) germ-line mutation of the TGF-beta RII gene may be a rare event during tumorigenesis in HNPCC and sporadic early-onset colorectal cancer; (b) the mononucleotide repeat sequence of the TGF-beta RII gene is an apparent target of genomic instability but not of germ-line mutation; and (c) the polymorphism of codon 389 (AAC to AAT) is frequent, especially in early-onset colorectal cancer patients, in which it is more frequent than in control group.

Adult↗

PubMed2003

Excessive alcohol intake enhances the development of synchronous cancerous lesion in colorectal cancer patients.

BACKGROUND AND AIMS: We examined the potential impact of alcohol drinking on the incidence of synchronous colorectal cancer. PATIENTS AND METHODS: This study comprised 191 men with colorectal cancer who had undergone surgical resection. Synchronous colorectal cancer was found in 16 patients (8.4%). The relationship between synchronous colorectal cancer and alcohol intake was analyzed by multivariate methods. Cumulative alcohol intake was assessed by the drinking index (weekly average multiplied by years of drinking). RESULTS: There was higher incidence of associated adenoma in the synchronous cancer group. Heavy cumulative intake (drinking index 9800 or higher) was associated with significantly higher risk synchronous colorectal cancer than in nondrinkers (odds ratio 6.8). The association of alcohol intake with the risk of synchronous colorectal cancer was not affected by the type of alcohol beverages. CONCLUSION: This study demonstrated that excessive alcohol intake might be an independent risk factor for synchronous colorectal cancer. The screening program based on this information may prevent the synchronous lesions being missed.

Adenocarcinoma↗