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PubMed1985

[Screening for colorectal cancer based on our experience with early colorectal cancer and adenoma].

In order to establish method of screening for colorectal cancer, we studied clinicopathological features in 116 cases of adenoma, precancerous lesion, and in 80 cases of early colorectal cancer. The incidence of early cancer began to rise at the age of more than 40, reaching a peak in the sixth decade. The risk for men was higher than for women. In relation to the location of these lesions, 71% of the adenoma and 91% of the early cancer were in the left colon and rectum. As symptoms on admission, overt bleeding from the rectum appeared in 35% of the adenoma and in 56% of the early cancer patients, respectively. Therefore, we emphasize that it is extremely important to examine overt and occult bleeding as the first screening for colorectal cancer.

Adenoma↗
PubMed2001

Nonsteroidal antiinflammatory drugs, cyclooxygenase-2, and colorectal cancer prevention.

Colorectal cancer is the second leading cause of cancer deaths in the United States. Despite proven screening strategies, less than 40% of eligible Americans undergo appropriate screening for colorectal cancer. Research evaluating the underlying defects responsible for hereditary nonpolyposis colorectal cancer and familial adenomatous polyposis has provided insight into some of the molecular mechanisms responsible for familial and sporadic colorectal cancer. The signaling pathways involved in the development of colorectal cancer may provide effective targets for prevention and treatment. These targets include cyclooxygenase-2, peroxisome proliferator activated receptor- delta, peroxisome proliferator activated receptor- gamma, transforming growth factor- beta receptors, and the inducible-nitric oxide synthase.

Journal Article↗
PubMed1999

[Genetics of colorectal cancer. II. Hereditary background of sporadic and familial colorectal cancer].

About 15% of patients with colorectal cancer have a positive family history: 5% have hereditary colorectal cancer (hereditary non-polyposis colorectal carcinoma (HNPCC), familial adenomatous polyposis (FAP) or some other hereditary syndrome), while in 10% no clear hereditary pattern can be recognized ('familial colorectal cancer'). In sporadic and in familial intestinal cancer, a demonstrable hereditary predisposition may undoubtedly exist. HNPCC is often characterized by microsatellite instability, i.e. an increased number of short DNA sequences in the DNA indicating a disorder in DNA repair and a mutation in a DNA 'mismatch repair' (MMR) gene. Indicative of hereditary bowel cancer on the basis of such an MMR gene mutation are: (a) presence of bowel cancer in > or = 3 relatives, (b) early age at the time of the diagnosis of 'bowel cancer', (c) multiple primary bowel tumours, (d) uterine cancer in the family and (e) bowel and uterine cancer in a woman. Recent data demand a new subdivision of hereditary bowel cancer, based upon both the clinical picture and the results of DNA-tests. The genetic alterations in colonic adenomas and carcinomas are known to a large extent. In future these insights may be important in clinical practice, such as a more individual determination of the patient's prognosis and accordingly, of the treatment and follow-up.

Adenoma↗
PubMed1994

Crohn's disease and colorectal cancer.

The colorectal cancer risk in Crohn's disease eliminating all known biases was assessed in a cohort of 281 patients with Crohn's disease who resided in the West Midlands at the time of diagnosis, and were first seen within five years of onset of symptoms between 1945-1975. All patients were 15 years of age or more at onset and were followed up from 12-35 years (total 5213 person years at risk (PYR)). The colorectal cancer risk in the series compared with the risk in the general population was computed by applying sex and age specific PYRs to the date of death or end of the study period 31 December 1991. There were six colonic and two rectal cancers. Six of the eight colorectal cancers were diagnosed 20 or more years after the onset of Crohn's disease. The relative risk (RR) of colorectal cancer for the series as a whole was 3.4 (p < 0.001), with a fivefold excess in the colon, but no significant excess in the rectum. Patients with extensive colitis showed an 18-fold increase in risk (RR = 18.2, p < 0.001), which decreased with increasing age at onset. This study shows that there is a statistical excess risk of developing colorectal cancer in patients who develop their Crohn's disease at a young age of onset (less than 30 years of age).

Adolescent↗
PubMed2000

Evaluation of fecal mutagenicity and colorectal cancer risk.

Colorectal cancer is one of the most common internal malignancies in Western society. The cause of this disease appears to be multifactorial and involves genetic as well as environmental aspects. The human colon is continuously exposed to a complex mixture of compounds, which is either of direct dietary origin or the result of digestive, microbial and excretory processes. In order to establish the mutagenic burden of the colorectal mucosa, analysis of specific compounds in feces is usually preferred. Alternatively, the mutagenic potency of fecal extracts has been determined, but the interpretation of these more integrative measurements is hampered by methodological shortcomings. In this review, we focus on exposure of the large bowel to five different classes of fecal mutagens that have previously been related to colorectal cancer risk. These include heterocyclic aromatic amines (HCA) and polycyclic aromatic hydrocarbons (PAH), two exogenous factors that are predominantly ingested as pyrolysis products present in food and (partially) excreted in the feces. Additionally, we discuss N-nitroso-compounds, fecapentaenes and bile acids, all fecal constituents (mainly) of endogenous origin. The mutagenic and carcinogenic potency of the above mentioned compounds as well as their presence in feces, proposed mode of action and potential role in the initiation and promotion of human colorectal cancer are discussed. The combined results from in vitro and in vivo research unequivocally demonstrate that these classes of compounds comprise potent mutagens that induce many different forms of genetic damage and that particularly bile acids and fecapentaenes may also affect the carcinogenic process by epigenetic mechanisms. Large inter-individual differences in levels of exposures have been reported, including those in a range where considerable genetic damage can be expected based on evidence from animal studies. Particularly, however, exposure profiles of PAH and N-nitroso compounds (NOC) have to be more accurately established to come to a risk evaluation. Moreover, lack of human studies and inconsistency between epidemiological data make it impossible to describe colorectal cancer risk as a result of specific exposures in quantitative terms, or even to indicate the relative importance of the mutagens discussed. Particularly, the polymorphisms of genes involved in the metabolism of heterocyclic amines are important determinants of carcinogenic risk. However, the present knowledge of gene-environment interactions with regard to colorectal cancer risk is rather limited. We expect that the introduction of DNA chip technology in colorectal cancer epidemiology will offer new opportunities to identify combinations of exposures and genetic polymorphisms that relate to increased cancer risk. This knowledge will enable us to improve epidemiological study design and statistical power in future research.

Amines↗
PubMed1998

Urinary tract cancer and hereditary nonpolyposis colorectal cancer: risks and screening options.

PURPOSE: We investigate the risk of the different types of urinary tract cancer in hereditary nonpolyposis colorectal cancer families and review screening options. MATERIALS AND METHODS: We retrospectively calculated the relative and cumulative risks of developing urinary tract cancer by comparing tumor occurrence in patients and their first degree relatives in the Dutch hereditary nonpolyposis colorectal cancer registry with those in the general Dutch population. A person-year analysis was used, including data on 1,321 individuals from 50 hereditary nonpolyposis colorectal cancer families. RESULTS: The relative risk of developing transitional cell cancer of the renal pelvis or ureter was 14.04 (95% confidence interval 6.69 to 29.45, p <0.05) and the cumulative risk was 2.6%. The risks of renal (excluding renal pelvis) and bladder cancers were not significantly increased. Urinary tract cancer was diagnosed at a relatively young age and many women were affected. Some familial clustering was observed. CONCLUSIONS: Our findings indicate that hereditary nonpolyposis colorectal cancer is associated with an increased risk of transitional cell cancer of the upper urinary tract. The cumulative risk is relatively low, although a subset of hereditary nonpolyposis colorectal cancer families may be exposed to a much higher risk. As yet nothing is known of the clinical impact of screening for urinary tract cancer in cases of hereditary nonpolyposis colorectal cancer. In a research setting screening by excretory urography of hereditary nonpolyposis colorectal cancer families with a strong history of upper urinary tract cancer should be considered.

Age Factors↗
PubMed2002

Improving colorectal cancer follow-up: the dedicated single-visit colorectal cancer follow-up clinic.

OBJECTIVE: To assess the effectiveness of the dedicated single-visit colorectal cancer follow-up clinic in improving postoperative surveillance. PATIENTS AND METHODS: Data of follow-up of 137 consecutive patients with colorectal cancer treated by the senior author over a 3 year period were obtained. Surveillance over three periods in time were analysed: (i) before the establishment of a protocol; (ii) following the implementation of a protocol for follow-up of colorectal cancer with liver ultrasound and colonoscopy; and (iii) following the establishment of the dedicated single-visit colorectal cancer follow-up clinic. RESULTS: The single-visit colorectal cancer follow-up clinic has reduced the mean time to the interventions (from 12.1 months to 6.0 months for the liver ultrasound and from 8.7 months to 6.4 months for the colonoscopy). In addition, the percentage of patients having their liver ultrasound within the targeted time has increased from 14% to 55%. The percentage of patients having their colonoscopy within the targeted time has also increased from 50% to 77%. The percentage who missed their liver ultrasound has been reduced from 57% to 0%. The percentage of patients who missed their colonoscopy has also been reduced from 36% to 3%. CONCLUSION: The dedicated single-visit colorectal cancer follow-up clinic improves the postoperative surveillance of patients with colorectal cancer.

Adult↗
PubMed2004

Assessment of operative risk in colorectal cancer surgery: the Cleveland Clinic Foundation colorectal cancer model.

INTRODUCTION: Predictive models play a pivotal role in the provision of risk-adjusted, operative mortality rates. The purpose of the study was to describe the development of a dedicated prognostic index for quantifying operative risk in colorectal cancer surgery. METHODS: Data were collected from 5,034 consecutive patients undergoing major surgery in a single center from October 1976 to July 2002. Primary end point was 30-day operative mortality. A multilevel Bayesian logistic regression model was developed to adjust for case-mix and accommodate the variability of outcomes between surgeons. The model was internally validated (split-sample) and tested using measures of discrimination, calibration, and subgroup analysis. RESULTS: The patients' median age was 66 (range, 18-98) years. Operative mortality was 2.3 percent with no significant variability between surgeons or through time. Multivariate analysis identified the following independent risk factors: age (odds ratio = 1.5 per 10-year increase), American Society of Anesthesiologists grade (odds ratio for ASA II, III, IV-V vs. I = 2.6, 4.3, 6.8), TNM staging (odds ratio for Stage IV vs. I-III = 2.6), mode of surgery (odds ratio for urgent vs. nonurgent = 2.1) no-cancer resection vs. cancer resection (odds ratio = 4.5), and hematocrit level. The model offered adequate discrimination (area under receiver operator characteristic curve = 0.801) and excellent agreement between observed and model-predicted outcomes over ten major colorectal procedures (P = 0.191). CONCLUSIONS: The colorectal cancer model provided an accurate means of estimating risk for individual patients in the preoperative setting. It has important implications in everyday practice, because it may be used as an adjunct in the process of informed consent and for monitoring surgical performance through time.

Adolescent↗
PubMed2006

Profiling markers of prognosis in colorectal cancer.

PURPOSE: Colorectal cancer is one of the most common forms of cancer in developed nations and the incidence of this disease is increasing. There is a need to further stratify prognostically distinct groups of colorectal cancer, and the purpose of this study was to identify prognostically significant immunohistochemical marker profiles in colorectal cancer. EXPERIMENTAL DESIGN: In this study, a range (n = 23) of markers [pRb, p16, p21, p27, p53, proliferating cell nuclear antigen, cyclin D1, bcl-2, epidermal growth factor receptor, C-erb-B2, topoisomerase-I, liver fatty acid-binding protein, matrix metalloproteinases (MMP) 1-3, 7, 9, and 13, MT1-MMP, MT2-MMP, and tissue inhibitors of MMP 1-3] of putative prognostic significance have been investigated by immunohistochemistry on formalin-fixed, wax-embedded sections in a series (n = 90) of stage III (Dukes C) colorectal cancers. An immunohistochemical score based on the intensity of immunoreactivity and, where relevant, the proportion of immunoreactive cells was established for each marker. RESULTS: Unsupervised two-dimensional hierarchical cluster analysis identified three distinct cluster groups (designated groups 1-3) with different marker profiles. There were significant survival differences between groups 1 and 2 (log rank = 11.48; P = 0.0007) and between groups 1 and 3 (log rank = 8.32; P = 0.0039). Multivariate analysis showed that the complete marker profile was independently the most significant prognostic factor (hazard ratio, 2.27; 95% confidence interval, 1.15-4.48; P = 0.004). CONCLUSIONS: This study has identified an immunohistochemical marker profile of colorectal cancer and showed that it is an independent indicator of prognosis in this type of cancer.

Adult↗
PubMed1992

Progressing toward a molecular description of colorectal cancer development.

During the past decade, the powerful techniques of molecular biology and genetics have been applied to the study of human cancer. Colorectal tumors have proved to be an excellent system in which to search for and study the mutations involved in the development and progression of a common human cancer because of their natural history and several inherited syndromes that strongly predispose to colorectal cancer. A current view is that colorectal cancer results, at least in part, from the accumulation of multiple mutations in oncogenes and tumor suppressor genes in an affected cell. Although the genetic alterations often occur in a preferred sequence, the total accumulation of changes, rather than their order with respect to one another, appears to be a critical determinant of the biological properties of the tumor cell. Study of the inherited and somatic mutations in colorectal tumor cells may provide insights not only into the pathogenesis of cancer, but may also lead to future understanding of the mechanisms of the origin of mutations and the role of environmental and dietary factors in colorectal tumor development.

Adenoma↗
PubMed2005

Impact of a family history of colorectal cancer on age at diagnosis, anatomic location, and clinical characteristics of colorectal cancer.

BACKGROUND: Among the risk factors for colorectal cancer (CRC) is a family history of colorectal cancer. Reliable evidence is needed regarding the clinical characteristics of cancer in patients with this history to determine if a change in the diagnostic approach is needed. AIM OF THE STUDY: This study set out to determine specific clinical outcomes in patients with CRC with a family history of one first-degree relative with sporadic colorectal cancer compared to control patients with colorectal cancer but without the family history. METHODS: We designed a case-control study of colorectal cancer registry data between 1988 and 1999. Patients with a family history of one first-degree relative with colorectal cancer were compared to those without the history with regard to four characteristics: age at cancer diagnosis, anatomic location of the cancer, presence of distal adenomas with proximal cancer, and stage of disease at diagnosis. RESULTS: Nine hundred and twenty-one patients met the inclusion criteria. Family history was positive in 124 patients. The demography of the populations was similar, except for mean age, which was 65 yr for men with a family history and proximal cancer compared to 70 yr for their counterparts without the family history (p = 0.03). The anatomic location of the cancer, presence of distal benign neoplasia when the cancer was proximal, and disease stage at diagnosis were not different between the groups. CONCLUSIONS: Men with a family history of sporadic colorectal cancer and proximal colon cancer were younger than men without the family history and proximal colon cancer. The overall results do not indicate that a change in the diagnostic approach is needed.

Adult↗
PubMed2004

BRAF mutation is frequently present in sporadic colorectal cancer with methylated hMLH1, but not in hereditary nonpolyposis colorectal cancer.

PURPOSE: The BRAF gene encodes a serine/threonine kinase and plays an important role in the mitogen-activated protein kinase signaling pathway. BRAF mutations in sporadic colorectal cancer with microsatellite instability (MSI) are more frequently detected than those in microsatellite stable cancer. In this study, we sought to compare the frequencies of BRAF mutations in sporadic colorectal cancer with MSI with those in hereditary nonpolyposis colorectal cancer (HNPCC). EXPERIMENTAL DESIGN: We analyzed BRAF mutations in 26 colorectal cancer cell lines, 80 sporadic colorectal cancers, and 20 tumors from HNPCC patients by DNA sequencing and sequence-specific PCR. The methylation status of the hMLH1 gene was measured by either sequencing or restriction enzyme digestion after NaHSO(3) treatment. RESULTS: We observed a strong correlation of BRAF mutation with hMLH1 promoter methylation. BRAF mutations were present in 13 of 15 (87%) of the colorectal cell lines and cancers with methylated hMLH1, whereas only 4 of 91 (4%) of the cell lines and cancers with unmethylated hMLH1 carried the mutations (P < 0.00001). Sixteen of 17 mutations were at residue 599 (V599E). A BRAF mutation was also identified at residue 463 (G463V) in one cell line. In addition, BRAF mutations were not found in any cancers or cell lines with K-ras mutations. In 20 MSI+ cancers from HNPCC patients, however, BRAF mutations were not detectable, including a subset of 9 tumors with negative hMLH1 immunostaining and methylated hMLH1. CONCLUSIONS: BRAF mutations are frequently present in sporadic colorectal cancer with methylated hMLH1, but not in HNPCC-related cancers. This discrepancy of BRAF mutations between sporadic MSI+ cancer and HNPCC might be used in a strategy for the detection of HNPCC families.

Adaptor Proteins, Signal Transducing↗
PubMed1994

Do gastroenterologists themselves follow the American Cancer Society recommendations for colorectal cancer screening?

OBJECTIVE: Colorectal cancer is a leading cause of mortality from cancer in the United States. Unfortunately, many patients already have advanced disease by the time symptoms occur. Screening of asymptomatic persons offers the potential of detecting the disease at its early and curable stages. The American Cancer Society (ACS) screening recommendations are the most widely employed in this country. We sought to determine whether gastroenterologists themselves follow the ACS recommendations, and if not, to determine their reasons for not doing so. We also looked at gastroenterologists' use of diets and supplements that might reduce the likelihood of colorectal cancer. METHOD: A questionnaire was mailed out to all gastroenterologists with U.S. addresses listed in the American College of Gastroenterology membership directory. RESULTS: Of 1466 respondents, 330 were excluded because they were at high risk for colorectal cancer or were not gastroenterologists. This left 875 gastroenterologists age 40 years and over and 261 gastroenterologists under age 40 for analysis. Overall, 68% of respondents felt the ACS recommendations were adequate; 32% did not. Of those who disagreed with the ACS recommendations, 58% preferred screening colonoscopy, and 22% preferred flexible sigmoidoscopy without annual fecal occult blood testing. Of gastroenterologists age 40 and over, 38% strictly followed the ACS recommendations themselves, 39% partially, and 23% did not follow them. Fifty percent of those who did not strictly follow the recommendations believed they were adequate but procrastinated or "did not have the time" to follow them. Overall, 82% of gastroenterologists said they used a high fiber diet, 68% used a diet low in fat, 18% used a calcium supplement, and 25% used aspirin regularly. CONCLUSIONS: Although two-thirds of gastroenterologists agreed with the ACS recommendations, only 38% themselves followed them strictly. Of the approximately one-third of gastroenterologists who considered them inadequate, a majority preferred screening colonoscopy. Gastroenterologists were more aggressive in following dietary practices that might help prevent colorectal cancer development than they were in undergoing screening.

Adult↗
PubMed2004

Predictive factors for response to chemotherapy in colorectal cancer patients.

Colorectal cancer represents a major health problem in the western world. A lot of drugs have been employed in treatment of this disease, but only few data are available about predictive factors for response to anticancer treatments in colorectal cancer. Aim of this paper is to review the main data about this investigation field. Using a Medline database search (1966-2003) we reviewed all the relevant papers that investigate clinical and molecular predictors for response to the main drugs used in the treatment of colorectal cancer patients, both in adjuvant and in advanced setting. Moreover we comprehensively reviewed all the data published in abstract form during the most significant international meetings. Our review put in evidence the most important predictive factors for response in colorectal cancer patients treated with anticancer chemotherapy both in adjuvant and in advanced setting. The predictive factors are clustered on the basis of the different anticancer drugs. The results of this review provide the rationale basis for personalizing anticancer treatment in colorectal cancer patients by molecular and clinical features, aiming to improve response rate and reduce toxicities.

Antineoplastic Agents↗
PubMed2000

Palliative chemotherapy for advanced colorectal cancer: systematic review and meta-analysis. Colorectal Cancer Collaborative Group.

OBJECTIVES: To determine the benefits and harms of palliative chemotherapy in patients with locally advanced or metastatic colorectal cancer and to compare the outcomes for elderly and younger patients. DESIGN: Meta-analysis of individual patient data and published summary statistics from trials for which individual patient data could not be obtained from the investigators. STUDIES: All randomised controlled trials comparing palliative chemotherapy with supportive care in patients with advanced colorectal cancer that were identified by computerised and hand searches of the literature, scanning references, and contacting investigators. MAIN OUTCOME MEASURES: Survival, disease progression, quality of life, and toxicity. RESULTS: 13 randomised controlled trials including a total of 1365 patients met the inclusion criteria. Meta-analysis of seven trials that provided individual patient data (866 patients) showed that palliative chemotherapy was associated with a 35% reduction in the risk of death (95% confidence interval 24% to 44%). This translates into an absolute improvement in survival of 16% at both six and 12 months and an improvement in median survival of 3.7 months. No age related differences were found in the effectiveness of chemotherapy, but elderly patients were under represented in trials. The overall quality of evidence relating to treatment toxicity, symptom control, and quality of life was poor. CONCLUSIONS: Chemotherapy is effective in prolonging time to disease progression and survival in patients with advanced colorectal cancer. The survival benefit may be underestimated in this analysis as some patients in the control arms received chemotherapy.

Aged↗
PubMedDate not supplied

From guaiac to immune fecal occult blood tests: the emergence of technology in colorectal cancer screening.

Colorectal cancer is the second leading cause of cancer deaths in the United States for both men and women. Colorectal cancer screening is an important means for reducing morbidity and mortality. The American Cancer Society recommends five different screening regimens for adults of average risk, age 50 years and older. The optimal effectiveness of a screening program is dependent on the accuracy of the screening test used. An accurate screening test would have high sensitivity (positive) when an adenomatous polyp or cancer is present and high specificity (negative) in their absence. In April 2002, the American Cancer Society Colorectal Cancer Advisory Group concluded that the immunochemical fecal occult blood test has some advantages that merit revision of their guideline statement for fecal occult blood testing, to include the immunochemical fecal occult blood test. The advantages cited were the possibility of improved sensitivity and specificity and the lack of required dietary restrictions, which make it a more patient-friendly test. Several types of immunochemical fecal occult blood tests are discussed in this article, including their advantages and disadvantages compared with those of the traditional guaiac fecal occult blood testing.

Age Factors↗
PubMedDate not supplied

Early detection and prevention of colorectal cancer (review).

Colorectal cancer is a leading cause of cancer-related deaths, and the two most important considerations for avoidance of this disease are early detection and prevention. If metastasis has occurred to distant sites, such as the liver and lung, the 5-year survival rate for colorectal cancer is below 10%, but this increases to greater than 90% when the cancer is found early. Early detection can be facilitated by use of the digital rectal exam, fecal occult blood test, sigmoidoscopy, and colonoscopy, but these methods might be supplemented in the future by other screening assays using intermediate biomarkers. One interesting biomarker, the aberrant crypt focus (ACF), has been observed in resected human colons, and is the earliest detectable morphological change in the colons of experimental animals treated with carcinogens such as the cooked meat heterocyclic amines. The ACF can also be used as an end-point to screen for potential inhibitors of colorectal cancer; using this approach, we identified conjugated linoleic acids, indole-3-carbinol, chlorophyllin, and tea polyphenols as promising inhibitors in the colon. These compounds can be added to a growing list of natural and synthetic agents that might be effective against colorectal cancer, including selenium, calcium, and nonsteroidal anti-inflammatory agents. However, results from human clinical trials with several of these compounds have highlighted the need for detailed mechanism data before recommendations can be made for wide-scale use in humans. In the meantime, the best approach to reducing the risk of colorectal cancer would be to increase the dietary intake of fruits, vegetables and cereals, while reducing the overall intake of fat, particularly from animal sources.

Anticarcinogenic Agents↗
PubMed2004

Treatment of Hereditary Colorectal Cancer Syndromes.

Colorectal cancer is the second leading cause of cancer-related death in the United States. Although most colorectal cancers are sporadic, about 25% have a familial predisposition and 5% to 7% are hereditary and occur in genetically distinct high-risk families. Advances in treatment options and management of hereditary colorectal cancer syndromes that have occurred over the past years have been principally due to advances in the understanding of the genetics of these syndromes and in additional options for testing. This has led to the possibility of preclinical diagnosis and early surveillance and treatment. In addition, improvements in medical and surgical management have also occurred. This article focuses on four hereditary colon cancer syndromes: familial adenomatous polyposis, hereditary non-polyposis colorectal cancer, juvenile polyposis syndrome, and Peutz-Jeghers syndrome.

Journal Article↗