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PubMedDate not supplied

Guidelines for colonoscopy surveillance after cancer resection: a consensus update by the American Cancer Society and US Multi-Society Task Force on Colorectal Cancer.

Patients with resected colorectal cancer are at risk for recurrent cancer and metachronous neoplasms in the colon. This joint update of guidelines by the American Cancer Society (ACS) and US Multi-Society Task Force on Colorectal Cancer addresses only the use of endoscopy in the surveillance of these patients. Patients with endoscopically resected Stage I colorectal cancer, surgically resected Stage II and III cancers, and Stage IV cancer resected for cure (isolated hepatic or pulmonary metastasis) are candidates for endoscopic surveillance. The colorectum should be carefully cleared of synchronous neoplasia in the perioperative period. In nonobstructed colons, colonoscopy should be performed preoperatively. In obstructed colons, double contrast barium enema or computed tomography colonography should be done preoperatively, and colonoscopy should be performed 3 to 6 months after surgery. These steps complete the process of clearing synchronous disease. After clearing for synchronous disease, another colonoscopy should be performed in 1 year to look for metachronous lesions. This recommendation is based on reports of a high incidence of apparently metachronous second cancers in the first 2 years after resection. If the examination at 1 year is normal, then the interval before the next subsequent examination should be 3 years. If that colonoscopy is normal, then the interval before the next subsequent examination should be 5 years. Shorter intervals may be indicated by associated adenoma findings (see Postpolypectomy Surveillance Guideline). Shorter intervals are also indicated if the patient's age, family history, or tumor testing indicate definite or probable hereditary nonpolyposis colorectal cancer. Patients undergoing low anterior resection of rectal cancer generally have higher rates of local cancer recurrence, compared with those with colon cancer. Although effectiveness is not proven, performance of endoscopic ultrasound or flexible sigmoidoscopy at 3- to 6-month intervals for the first 2 years after resection can be considered for the purpose of detecting a surgically curable recurrence of the original rectal cancer.

American Cancer Society↗

PubMed1999

Colorectal cancer in hereditary breast cancer kindreds.

PURPOSE: This study compared characteristics of colorectal cancer between families with dominant breast cancer inheritance and the general population. The cumulative incidence of colorectal cancer was also studied in genetically determined breast cancer syndrome subjects with BRCA1 and BRCA2 mutations and compared with the general population. METHODS: Subjects included 42 patients with colorectal cancer from 32 clinically determined hereditary breast cancer kindreds based on the autosomal dominant inheritance of breast cancers and early age of onset. The general population colorectal cancer cohort was composed of 755 patients from a tumor registry. Lifetime risk of colorectal cancer was determined in 164 BRCA1 and 88 BRCA2 gene mutation carriers and compared with the general population. Mean age of colorectal cancer onset, anatomic site distribution, histologic stage at presentation, and five year stage-stratified survival rates were compared between clinically determined hereditary breast cancer family members and the general population. RESULTS: The lifetime risk of colorectal cancer in male BRCA1 and BRCA2 mutation carriers was 5.6 percent, which was not different from 6 percent in males from the general population. Likewise, the lifetime colorectal cancer risk in female BRCA1 and BRCA2 mutation carriers was 3.2 percent, which was not different from 5.9 percent in females from the general population. Mean age of onset +/- standard error for patients with colorectal cancer was 60 +/- 2 years for hereditary breast cancer kindreds compared with 67 +/- 0.4 years for the general population (P = 0.0004). Colorectal cancer site distribution did not vary between hereditary breast cancer and the general population. Overall colorectal cancer stage distribution was significantly different, with more Stage I and fewer Stage IV cancers in subjects with hereditary breast cancer compared with the general population (P = 0.01). Overall five year stage-stratified colorectal cancer survival rate +/- standard error was 66 +/- 8 percent for hereditary breast cancer kindreds and 46 +/- 2 percent for the general population (P = 0.023). CONCLUSION: Lifetime cumulative colorectal cancer incidence in subjects with BRCA1 and BRCA2 gene mutations was not different from the general population. However, significant differences in colorectal cancer were noted between hereditary breast cancer family members and the general population. Hereditary breast cancer-associated colorectal cancer had an earlier age of onset, lower tumor stage, and better survival rate than the general population. Except for age of onset, colorectal cancer in hereditary breast cancer kindreds exhibited more favorable characteristics than colorectal cancer in the general population.

Adult↗

PubMed2005

Dendritic cells fused with allogeneic colorectal cancer cell line present multiple colorectal cancer-specific antigens and induce antitumor immunity against autologous tumor cells.

The aim of antitumor immunotherapy is to induce CTL responses against autologous tumors. Previous work has shown that fusion of human dendritic cells and autologous tumor cells induce CTL responses against autologous tumor cells in vitro. However, in the clinical setting of patients with colorectal carcinoma, a major difficulty is the preparation of sufficient amounts of autologous tumor cells. In the present study, autologous dendritic cells from patients with colorectal carcinoma were fused to allogeneic colorectal tumor cell line, COLM-6 (HLA-A2(-)/HLA-24(-)), carcinoembryonic antigen (CEA)(+), and MUC1(+) as an alternative strategy to deliver shared colorectal carcinoma antigens to dendritic cells. Stimulation of autologous T cells by the fusion cells generated with autologous dendritic cells (HLA-A2(+) and/or HLA-A24(+)) and allogeneic COLM-6 resulted in MHC class I- and MHC class II-restricted proliferation of CD4(+) and CD8(+) T cells, high levels of IFN-gamma production in both CD4(+) and CD8(+) T cells, and the simultaneous induction of CEA- and MUC1-specific CTL responses restricted by HLA-A2 and/or HLA-A24. Finally, CTL induced by dendritic cell/allogeneic COLM-6 fusion cells were able to kill autologous colorectal carcinoma by HLA-A2- and/or HLA-A24-restricted mechanisms. The demonstration of CTL activity against shared tumor-associated antigens using an allogeneic tumor cell line, COLM-6, provides that the presence of alloantigens does not prevent the development of CTL with activity against autologous colorectal carcinoma cells. The fusion of allogeneic colorectal carcinoma cell line and autologous dendritic cells could have potential applicability to the field of antitumor immunotherapy through the cross-priming against shared tumor antigens and provides a platform for adoptive immunotherapy.

Antigens, Neoplasm↗

PubMed2001

Cancer risk in young women at risk of hereditary nonpolyposis colorectal cancer: implications for gynecologic surveillance.

OBJECTIVES: The lifetime risk of endometrial and ovarian cancers in hereditary nonpolyposis colorectal cancer (HNPCC) is up to 60 and 12%, respectively, in addition to the high risk of colorectal cancer. International guidelines recommend surveillance of those at risk with colonoscopy every 1--2 years from age 20--25 years and annual gynecologic surveillance from 25--35 years for women. We reviewed our own experience to see whether these recommendations were appropriate. METHODS: Pedigrees of 120 HNPCC families registered with the Familial Bowel Cancer Service at The Royal Melbourne Hospital were reviewed. Ninety families met our criteria for HNPCC and were included in the study. Pedigrees were analyzed to identify early-age onset colorectal and gynecologic cancers and to calculate cumulative incidence of both cancer types for at-risk women (HNPCC-affected and first-degree female relatives of affected family members) for comparison with the general population. RESULTS: Colorectal cancer occurred in 434 individuals, endometrial cancer in 43, and ovarian cancer in 24. Gynecologic and colorectal cancers were diagnosed at similar ages (mean 49.3 versus 51.8 years; P = 0.25), with 5 (7.1%) gynecologic cancers diagnosed by 35 years. Cumulative incidences of gynecologic and colorectal cancers to ages 25, 30, 35, and 40 years were substantially higher among at-risk women than in the general population. CONCLUSIONS: Consideration should be given to offering gynecologic cancer surveillance from the age of 25 years, as for colorectal cancer. However, this approach should be individualized as it has yet to be demonstrated that surveillance reduces the mortality of gynecologic cancer in HNPCC.

Adult↗

PubMed1990

Body weight and physical activity as predictors of colorectal cancer risk.

The associations between colorectal cancer and body weight (expressed as body mass index) and between colorectal cancer and physical activity were examined in 715 histologically confirmed cases of colorectal adenocarcinoma and 727 age- and sex-matched controls. The data were obtained from a large, population-based study, The Melbourne Colorectal Cancer Study, which was conducted in Melbourne, Australia. There was a statistically significant increase in the risk of rectal cancer but not of colon cancer in overweight and obese males but not in females. This association for males remained statistically significant after adjustment was made for dietary risk factors previously established for this study (Nutr Cancer 9, 21-42, 1987), with the exception of sodium intake, which produced a downward modification of the relative risk close to unity. The increased risk of rectal cancer in overweight and obese males was modified by beer intake, which was previously found to be a risk for rectal cancer in males in this study. Various levels of physical activity were not statistically significantly associated with the risk of colorectal cancer in either males or females. Also, the colorectal cancer risks associated with the body mass index were not significantly altered by adjustment for the physical activity level.

Adult↗

PubMed2002

Expression of lumican in human colorectal cancer cells.

Lumican is a member of a small leucine-rich proteoglycan family and its overexpression in human breast cancer tissues is reported to influence the growth of cancer cells. In the present study, we aimed to clarify the expression of lumican mRNA and its protein in human colorectal cancer cell lines and their localization in normal and cancerous colorectal tissues. Reverse transcription-polymerase chain reaction and western blot analysis revealed lumican mRNA and its protein expression in COLO 205, DLD-1, HCT-15, SW 480 and WiDr colorectal cancer cell lines. The lumican in colorectal cancer cells had non-sulfated or poorly sulfated polylactosamine side chains. Based on its immunoreactivity, the lumican protein was found to be localized in fibroblasts and stromal tissues of normal colorectal tissues, but not in colorectal epithelial cells. In colorectal cancer tissues, the lumican was strongly localized in cancer cells in eight of 12 cancer cases. The lumican protein was also localized in epithelial cells with mild reactive dysplasia and fibroblasts adjacent to cancer cells. Lumican mRNA was expressed in cancer cells and adjacent fibroblasts, and epithelial cells. These findings may indicate that the lumican protein synthesized by cancer cells, fibroblasts and epithelial cells with mild reactive dysplasia found adjacent to cancer cells may affect the growth of human colorectal cancer cells.

Blotting, Western↗

PubMed2005

A scoring system for the strength of a family history of colorectal cancer.

BACKGROUND: Family history of colorectal cancer is associated with an increased risk for the disease, although there are many combinations of family history that are hard to correlate with risk status. A scoring system for family history of colorectal cancer was designed to make risk more readily quantifiable. METHODS: A colonoscopy database was used to test the following points system: each first-degree relative with colorectal cancer = 3 points; each second-degree relative with colorectal cancer = 1 point. Families with one or more first-degree relative affected under 50 years of age = an extra 3 points. Families with one or more second-degree relative affected under 50 years of age = an extra 1 point. Families with multiple relatives on the same side of the family = an extra 3 points (first-degree relatives), 1 point (second-degree relatives), or 2 points (first-degree and second-degree relatives). Points were added and categories defined as follows: low risk, 1 to 4 points; medium risk, 5 to 7 points; high risk, 8 to 10 points; very high risk, >10 points. A control group of average-risk patients having screening colonoscopy was used. Categories were compared in number of adenomas, hyperplastic polyps, and cancers. RESULTS: The records of 992 patients were used to test the system. Mean adenomas per patient per group were 0.4 for controls, 1.0 for low risk, 1.0 for medium risk, 1.7 for high risk, and 1.7 for very high risk. Cancers per group were 2 of 196 for controls, 8 of 513 for low risk, 3 of 171 for medium risk, 3 of 84 for high risk, and 1 of 28 for very high risk. The score categories were combined to produce revised risk levels of low (score 1 to 7) and high (>7). Average adenomas per patient in the revised categories were 0.4 (control), 1.0 (low risk), and 1.7 (high risk). The odds ratio of having one to two adenomas was 1.73 (1.19-2.50, 95% confidence limits) in the low-risk group and 2.39 (1.41-4.01) in the high-risk group. Odds ratios for having three or more adenomas were 5.70 (2.44-13.32) in the low-risk group and 10.35 (3.97-26.97) in the high-risk group. CONCLUSION: In the two-category system proposed here of quantifying familial risk of colorectal cancer, patients having less than 8 points were at low risk and those with 8 or more were at high risk. Surveillance and chemoprevention protocols can be designed through use of these risk categories. A scoring system for family history of colorectal cancer can make risk assessment easier and facilitate both collaborative studies and patient triage into appropriate screening programs.

Adenoma↗

PubMed1998

Possible role of telomerase activation in the cancer predisposition of patients with hereditary nonpolyposis colorectal cancers.

BACKGROUND: Hereditary nonpolyposis colorectal cancer syndrome (HNPCC syndrome; also called Lynch syndrome) is one of the most common cancer predisposition syndromes. Most cases of cancer associated with this syndrome are due to the inheritance of germline mutations in genes that encode proteins required for DNA mismatch repair; defects in these proteins allow mutations to accumulate more rapidly in the DNA and influence the rate of cancer development. Recent studies indicate that the reactivation of the activity of telomerase, an enzyme involved in the synthesis of chromosomal ends, in somatic cells may play a role in carcinogenesis. In this study, we evaluated the expression of telomerase in normal and cancerous colorectal tissue specimens from HNPCC and non-HNPCC patients. METHODS: The polymerase chain reaction-based telomeric repeat amplification protocol was used to assay telomerase activity in colorectal tissue specimens from 33 non-HNPCC patients (23 normal, 26 polyps, and 37 cancer specimens) and from 24 HNPCC patients (24 normal, 0 polyps, and 28 cancer specimens). RESULTS: Thirty-one of 37 carcinoma samples from 18 non-HNPCC patients and 27 of 28 carcinoma samples from 24 HNPCC patients were found to be positive for telomerase activity. Whereas only one of 23 normal mucosa samples from 23 non-HNPCC patients was found to have (weak) telomerase activity, eight of 24 normal mucosa samples from 24 HNPCC patients were positive for telomerase; the difference between the two groups was statistically significant (two-sided P = .0226). IMPLICATION: This study generates the hypothesis that genetic defects in individuals with HNPCC syndrome facilitate the reactivation of telomerase activity, a process which may be associated with their predisposition to develop cancer.

Adult↗

PubMed2005

Expression of granulocyte colony stimulating factor receptor in human colorectal cancer.

AIMS: To discover if human colorectal cancer expresses granulocyte colony stimulating factor receptor (G-CSFR) and if granulocyte colony stimulating factor (G-CSF) plays an important part in the development and progression of human colorectal cancer. METHODS: Forty two specimens of colorectal cancer and normal colorectal mucosa were investigated, taken from the colon or rectum in group of colorectal cancer patients. Immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR) technique were used to show G-CSFR expression. The relation between expression of G-CSFR and clinical or pathological factors was analysed. RESULTS: Immucohistochemical analyses showed that G-CSFR was expressed in the human colorectal cancer (25 of 42, 59.52%) and seemed to be up-regulated compared with the normal mucosa (14 of 42, 33.33%, p<0.001). In pronounced contrast with mostly strongly positive tumours, corresponding normal colorectal mucosa was negative or weakly positive. A significant correlation was found between G-CSFR expression and tumour stage (p = 0.001), tumour differentiation (p<0.001), but there was no significant relation between the expression of G-CSFR and the age, sex, and tumour size (p = 0.346, p = 0.686, p = 0.459). In RT-PCR, 21 of all 42 tumours had G-CSFR mRNA expression, while only 11 of 42 normal colorectal mucosa had such expression. CONCLUSIONS: These data show that G-CSFR is commonly expressed in human colorectal cancers, thus supporting a possible role for G-CSF in colorectal cancer physiology.

Adolescent↗

PubMed2004

A prospective study of plasma C-peptide and colorectal cancer risk in men.

BACKGROUND: Colorectal cancer and type 2 diabetes share many risk factors, and hyperinsulinemia appears to be associated with an increased risk of colorectal cancer. We used the concentration of plasma C-peptide (an indicator of insulin production) to determine whether insulin and insulin resistance are associated with the risk of developing colorectal cancer. METHODS: We conducted a nested case-control study in the Physicians' Health Study. Plasma samples were collected from 14 916 cancer-free men from August 1982 through December 1984. Plasma C-peptide concentration, measured with an enzyme-linked immunosorbent assay, was available for 176 case patients who developed incident colorectal cancer through December 31, 1995, and 294 age- and smoking status-matched control subjects. Information on four other insulin resistance-related factors at baseline was obtained. We used conditional logistic regression models to investigate associations. All statistical tests were two-sided. RESULTS: Plasma C-peptide concentration was positively associated with age, body mass index (BMI), and number of insulin resistance-related factors, and it was inversely associated with fasting time before the blood draw, alcohol consumption, and vigorous exercise. An increased concentration of plasma C-peptide was statistically significantly associated with an increased risk of colorectal cancer (relative risk [RR] for the highest versus lowest quintile of plasma C-peptide = 2.7, 95% confidence interval [CI] = 1.2 to 6.2; P(trend) =.047), after adjusting for age, smoking status, fasting, BMI, alcohol consumption, vigorous exercise, and aspirin assignment in the Physicians' Health Study. The association became even stronger when the analysis was further adjusted for factors related to insulin resistance other than insulin levels (RR for the highest versus lowest quintile = 3.4, 95% CI = 1.4 to 8.3; P(trend) =.02) or when data from case patients who were diagnosed during the first 5 years of follow-up were excluded (RR for the highest versus the lowest quintile = 3.4, 95% CI = 1.3 to 8.8; P(trend) =.03). Adjusting for plasma levels of insulin-like growth factor I (IGF-I) and its binding protein 3 (IGFBP-3) did not materially change the results. There was no apparent modification of risk by BMI, insulin resistance-related factors, or vigorous exercise. CONCLUSION: Elevated insulin production, as reflected by elevated concentrations of plasma C-peptide, may predict the risk of developing colorectal cancer, independently of BMI, factors related to insulin resistance, or levels of IGF-I and IGFBP-3.

Adult↗

PubMed1997

Evidence against genetic anticipation in familial colorectal cancer.

Anecdotal reports of hereditary colorectal cancer suggest that genetic anticipation (earlier appearance in successive generations) occurs, but ascertainment bias and cohort effects confound this interpretation. Using approaches that correct for such biases, we examined the age at diagnosis of colorectal cancer from family history questionnaires completed by subjects in the Johns Hopkins Hereditary Colorectal Cancer Registry; 475 parent-offspring pairs in 308 pedigrees were studied. We observed the expected cohort effect among offspring, in that the mean ages at diagnosis of those born before 1921, between 1921 and 1930, and after 1930 were 63 +/- 13 (SD), 57 +/- 10, and 42 +/- 10 years, respectively, while their parents' mean ages were 65 +/- 14, 66 +/- 14, and 58 +/- 15 years, respectively. In the cohort born before 1921, in which observation periods for both parents and offspring were comparable, there was no difference in age at diagnosis by pairwise comparison or life table analysis (P = 0.15 and 0.23, respectively; r = 0.32). Subgroup analysis of 67 pairs from 38 families that met the International Collaborative Group (ICG) criteria for hereditary nonpolyposis colorectal cancer (HNPCC) and of 14 pairs from 7 families with known germline mutations of DNA mismatch repair genes also showed no significant differences (mean age at diagnosis: 56 +/- 14 years for parents and 57 +/- 16 years for offspring from ICG families, and 45 +/- 10 years for parents and 44 +/- 12 years for offspring in families with known mutations). We also found no evidence for effect of parental gender on age at diagnosis in offspring of either gender, nor a secular trend toward younger onset colorectal cancer in this sample. In conclusion, there is no evidence for genetic anticipation or genomic imprinting of age at diagnosis in this sample of colorectal cancer families. Apparent anticipation appears to reflect a birth cohort bias of ascertainment.

Adult↗

PubMed1999

Estrogen replacement therapy and colorectal cancer risk in elderly women.

PURPOSE: Colorectal cancer is the fourth most common incident cancer in the United States and causes more cancer deaths than any site except lung. Twenty-two epidemiologic studies have examined the relationship of estrogen replacement therapy and colon and rectal cancers with inconsistent results. However, recent studies suggest a reduced risk among current users. The purpose of the present study was to analyze the Leisure World Cohort for possible association of estrogen replacement therapy with colorectal cancer risk. METHODS: A cohort of 7,701 female members who were initially free of cancer and self-reported their use of estrogen replacement therapy were followed up from June 1981 through December 1995 for development of colorectal cancer. RESULTS: We observed 249 incident colorectal cancer cases and 89 colorectal cancer deaths. Women who had used estrogen replacement therapy had an age-adjusted colorectal cancer incidence rate of 2.67 per 1,000 person-years compared with 3.30 per 1,000 person-years among lifetime nonusers (relative risk = 0.81; 95 percent confidence interval, 0.63 to 1.04). Among recent users the incidence was one-third lower than among lifetime nonusers (relative risk = 0.66; 95 percent confidence interval, 0.44 to 0.98). Risk did not differ by duration of estrogen replacement therapy, usual dose of conjugated estrogen, or route of estrogen administration. The effects of current estrogen replacement therapy on colon cancer incidence (relative risk = 0.70; 95 percent confidence interval, 0.45 to 1.09), right-sided colon cancer incidence (relative risk = 0.75, 95 percent confidence interval, 0.38 to 1.48), left-sided colon cancer incidence (relative risk = 0.76; 95 percent confidence interval, 0.41 to 1.41), rectal cancer incidence (relative risk = 0.52; 95 percent confidence interval, 0.21 to 1.31), and colorectal cancer mortality (relative risk = 0.82; 95 percent confidence interval, 0.44 to 1.54) were similar. CONCLUSION: A reduced risk of colorectal cancer may be an additional benefit of recent estrogen replacement therapy use, which should be considered by postmenopausal women when deciding whether to use hormones.

Aged↗

PubMed1997

Genomic DNA-based hMSH2 and hMLH1 mutation screening in 32 Eastern United States hereditary nonpolyposis colorectal cancer pedigrees.

Hereditary nonpolyposis colorectal cancer (HNPCC) is an autosomal dominant cancer syndrome characterized by early age of onset colorectal cancer (mean 45 years) as well as endometrial, urinary tract, and upper gastrointestinal adenocarcinomas. The HNPCC phenotype has been shown to segregate with germline mutations in the human homologues of the DNA mismatch repair genes MSH2, MLH1, PMS1, and PMS2. However, the majority of published DNA mismatch repair gene mutation surveys associated with HNPCC kindreds report multiple levels of preselection, including 2p and 3p chromosomal linkage analysis and the evaluation of microsatellite instability of proband colorectal cancers prior to mutation analysis. For this reason, the concise contribution of each of the known DNA mismatch repair genes to the HNPCC phenotype remains unknown. We report the results of a genomic DNA-based analysis of hMSH2 and hMLH1 germline mutations in 32 unrelated Eastern United States HNPCC kindreds. These families were selected for study on the basis of phenotype only. We identified three hMSH2 and six hMLH1 mutations in eight families, for a positive mutation rate of 25%. Two mutations were identified in one of the families. Four of the mutations detected have not been reported in the literature previously. One of the mutation-positive families is African American; the others were of European-American ancestry. These results provide a clarification of the contribution of hMSH2 and hMLH1 to the HNPCC phenotype and suggest that in the majority of Eastern United States HNPCC kindreds selected by phenotype alone, the molecular genetic basis for the disease remains unknown.

Adult↗

PubMedDate not supplied

Effect of Medicare coverage on use of invasive colorectal cancer screening tests.

BACKGROUND: Colorectal cancer is the second leading cause of cancer death in the United States. Screening for colorectal cancer is now widely recommended but underused. Lack of insurance coverage for screening tests may be one reason patients do not undergo these procedures. OBJECTIVE: To determine the effect of Medicare reimbursement on utilization rates of invasive screening tests. Use of fecal occult blood testing was not studied before 1998. METHODS: We performed a retrospective analysis of ambulatory claims data for Washington State Medicare beneficiaries in 1994, 1995, and 1998. We determined the proportion of patients undergoing diagnostic and screening flexible sigmoidoscopy, colonoscopy, or double-contrast barium enema in 1994, 1995, and 1998 and the proportion receiving fecal occult blood testing in 1998. RESULTS: Use of diagnostic and screening colon tests was low in all years. Fewer than 6% of beneficiaries received any colon test, and fewer than 4% received a screening test. Although more patients underwent diagnostic testing after Medicare coverage began, use of screening tests did not significantly change (odds ratio, 0.99; 95% confidence interval, 0.97-1.01 comparing 1994 and 1998 [P =.33]). Women, individuals older than 80 years, and nonwhite patients were statistically significantly less likely to be screened in all 3 years (P<.001). In 1998, fewer than 7% of patients underwent fecal occult blood testing, with men and nonwhites statistically significantly less likely to have this test (P<.001). CONCLUSIONS: Colorectal cancer screening tests are underused in the Washington State Medicare population, and insurance coverage for these tests did not substantially affect utilization rates in the period studied.

Aged↗

PubMed1998

[Recent advance of prognostic factor in human colorectal cancer].

It has become clear that cancers develop and progress through the accumulation of various genetic alterations. Among various human malignancies, none is better understood at the molecular genetic level than colorectal cancer. Colorectal cancer is one of the commonest malignant tumors and has a relatively poor prognosis. Recent advances in the molecular genetics of colorectal cancer have stimulated attempts to evaluate the prognostic significance of specific genetic alterations in this tumor. Although conventional pathological staging has served as the standard measure of prognosis in colorectal cancer, certain molecular genetic markers are now considered to be useful for predicting the behavior of cancer and the clinical outcome of patients. We have described the recent advances in prognostic factors of colorectal cancer, such as oncogenes, tumor suppressor genes, chromosomal deletions, adhesion molecules, proteinases, DNA replication error, and others. The latest improvements in detecting these molecular markers have made it possible to apply them to the clinical setting with relative ease. Some of these markers are considered to be susceptible to, or modifiable by, direct therapeutic intervention. For instance, matrix metalloproteinases could be targets for therapeutic intervention using their inhibitors. We hope that these molecular genetic markers with prognostic significance play an important role in disease management of patients with colorectal cancer in future.

Cell Adhesion Molecules↗

PubMed1997

The cytogenetic identification of high risk members in colorectal cancer families.

Family history of colorectal cancer is recognized as a risk factor for the disease and the development of colorectal cancer represents a suitable model for illustrating multistep tumor development. Bleomycin induced chromosome sensitivity studies were done in 7 colorectal cancer families consisting of 12 colorectal cancer patients and their 34 first degree relatives and 12 sporadic colorectal patients for comparison and identification of high risk family members with genetic instability. All patients and 4 unaffected relatives showed increased bleomycin sensitivity, which might be due to defective DNA repair system. These four relatives may be classified as high risk (without cancer at present) individuals. The study is being continued in more number of familial colorectal cancer patients and their relatives to arrive at definite conclusions.

Adult↗

PubMed1996

Epidemiology and risk factors for colorectal cancer.

The striking geographic differences in colorectal cancer incidence and the changes in disease risk among immigrants suggest an important environmental component to colorectal cancer risk. Table 1 lists risk factors for colorectal cancer. The categories in the table are somewhat arbitrary but are designed to provide an overall semiquantitative summary of the current epidemiologic literature. Certain of the most important risk factors (e.g., age, family history) cannot be modified. Individuals at high risk might benefit from surveillance. Dietary factors appear to be among the most important determinants of colorectal cancer risk. Diet helps to explain geographic variation in disease. A diet that is high in red meat and saturated fat appears to increase risk. Vegetables, fruits, fiber, folate, and calcium may be protective. Obesity, particularly abdominal obesity, and tall stature may be risk factors. Physical activity has been repeatedly shown to reduce the risk of colorectal cancer. Postmenopausal hormone replacement therapy may also be protective. Exciting new data suggest a significantly lower risk of colorectal cancer in regular users of aspirin and NSAIDs. It is important to recognize that the use of these drugs can have adverse as well as beneficial effects, and the appropriate dose and timing are not known. Enough information is available to make recommendations to lower the risk of colorectal cancer. Reducing red meat and fat consumption; increasing fruits, vegetables, and grains; avoiding obesity; and adopting a regular program of physical activity reduce the risk of colorectal cancer. Fortunately, these modifications also decrease the risk of cardiovascular disease, an even more important cause of mortality in Western societies.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMedDate not supplied

Colorectal cancer in younger patients.

Colorectal cancer is uncommon in India and particularly so in the younger age group below 40 years. The present study reports 18 patients with colorectal cancer between the age of 21 to 30 years. Rectum (n = 15, 83%) was the commonest site of the lesion and rectal bleed was the presenting feature in most (n = 16, 89%). Histopathologically, 9 (50%) had poorly differentiated adenocarcinoma. The tumor was unresectable in 5 patients (28%). Fourteen patients (78%) had advanced cancer indicated by TNM stage III or IV disease. Among the 13 patients subjected to surgical treatment followed by adjuvant chemotherapy, only 3 had long term disease free survival beyond 2 years. None of these patients had family history of colonic cancer or polyposis coli. In conclusion, colorectal cancer in younger age is not infrequent and had advanced stage at the time of clinical presentation with poor outcome.

Adenocarcinoma↗