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PubMed2005

[Antioxidant status of patients with primary colorectal cancer and liver metastases of colorectal cancer].

In the present work we examined selected parameters of antioxidant status in patients with primary colorectal cancer and liver metastasis of colorectal cancer. Total antioxidant status (TAS), activity of superoxide dismutase (SOD) and catalase (CAT) were examined in colorectal primary cancer, liver metastasis of colorectal cancer and in blood serum of patients before and after surgery. It was found that patients have disordered function of the the antioxidant system. This is demonstrated by decreased TAS and changes in the activity of SOD and CAT, both in tumor tissue and blood serum.

Adenocarcinoma↗
PubMed1993

Perceived religiousness is protective for colorectal cancer: data from the Melbourne Colorectal Cancer Study.

The perceived or self-reported degree of 'religiousness' was obtained by interview from 715 colorectal cancer patients and 727 age/sex matched community controls, as part of a large, comprehensive population-based study of colorectal cancer incidence, aetiology and survival (The Melbourne Colorectal Cancer Study) conducted in Melbourne, Australia. Self-reported or perceived 'religiousness', as defined in the study, was a statistically significant protective factor [relative risk (RR) = 0.70, 95% confidence interval (CI) = 0.6-0.9, P = 0.002]. This statistically significant protection remained after the previously determined major risk factors found in the study, namely a family history of colorectal cancer, dietary risk factors, beer consumption, number of children and age at birth of the first child, were statistically corrected for (P = 0.004). There was no association between Dukes' staging of the cancer and perceived degree of 'religiousness' (P = 0.42). Although self-reported or perceived 'religiousness' was associated with a median survival time of 62 months compared with 52 months in those self-reporting as being 'non-religious', this difference was not statistically significant (P = 0.64).

Adenocarcinoma↗
PubMed2006

Accumulation profile of frameshift mutations during development and progression of colorectal cancer from patients with hereditary nonpolyposis colorectal cancer.

PURPOSE: Role and timing of frameshift mutations during carcinogenesis in hereditary nonpolyposis colorectal cancer have not been examined. This study was designed to clarify the relationship between frameshift mutations and clinicopathologic features in colorectal cancer from patients with hereditary nonpolyposis colorectal cancer. METHODS: Thirty-one colorectal cancers from patients with hereditary nonpolyposis colorectal cancer at different clinicopathologic stages were analyzed for frameshift mutation in 18 genes. RESULTS: The frameshift mutations of the ACVR2 and PTHLH genes were found to have an extremely high frequency (94-100 percent) in all pathologic stages, and mutation of the MARCKS gene also was high (94 percent) in Dukes B and C cancers. These frequencies were higher than the frequency of TGFbetaRII gene inactivation (64-88 percent). Mutations of the hMSH3, TCF4, CASP5, RIZ, RAD50, and MBD4 genes were comparatively frequent (>35 percent) in all stages. Frequencies of inactivation of the MARCKS, BAX, IGFIIR, and PTEN genes were significantly higher in Dukes B and C cancers than in Dukes A cancer (P < 0.05). The number of accumulated frameshift mutations was larger in Dukes B and C cancers (9.4) than in Dukes A cancer (6.8) (P = 0.003). CONCLUSIONS: The present data suggest that the disruption of the transforming growth factor-beta super-family signaling pathway by the alteration of the ACVR2 and/or TGFbetaRII genes and the disruption of antiproliferative function by the PTHLH gene alteration contribute to the development of early colorectal cancer. Moreover, the further accumulation of alterations in the MARCKS, BAX, IGFIIR, and PTEN genes seem to be associated with progression from early to advanced colorectal cancer from patients with hereditary nonpolyposis colorectal cancer.

Adenocarcinoma↗
PubMed1986

Antitumor immune response to colorectal cancer antigen detected by the leukocyte adherence inhibition test (LAI) in groups at high risk for colorectal cancer.

Colorectal cancer is the second leading cause of cancer death in western populations. As treatment outcome is highly correlated with stage at diagnosis, early detection is a very important task. Three high-risk groups for colorectal cancer (first-degree relatives of colorectal cancer patients; individuals with past history of colorectal neoplasms, polyps, or carcinoma; and patients with ulcerative colitis) were screened for colonic neoplasms. The study program included the leukocyte adherence inhibition test (LAI), a specific immune response test for colorectal cancer antigen; fiberoptic sigmoidoscopy or colonoscopy; and guaiac impregnated slide test. The main finding was the detection of 92 positive LAI tests out of 451 high-risk individuals tested (20%), compared to eight positive tests out of 194 (4.1%) in a control group. Fifty-six colonic neoplasms were found out of 344 (16%) colonoscopies performed, most of them adenomatous polyps and a few carcinomas. Our findings, compared with the expected 2-3% neoplasms in low-risk groups, would prove that the screenees were indeed at high risk. However, only 11/56 (19%) of the polyps identified were LAI positive. The number of polyps found among LAI positive individuals were, so far, 11/92 (11%). The guaiac impregnated slide test for occult blood in the stool was performed in 221 screenees. Of these only 10 were positive (4.5%) compared with the average of 1% positive tests in low-risk groups.

Antigens, Neoplasm↗
PubMed1980

What can experimental colorectal cancer tell us about colorectal cancer in man?

From a survey of the etiology of colorectal cancer, consideration of the basic pathologic characteristics of ulcerative colitis and familial polyposis of the colon suggests that they might be sister diseases. Similarities in the primary and secondary target organs and in fecal steroid metabolism might be more than coincidental. Thus, it would seem reasonable to pay particular attention to several groups of patients who are receiving therapy or have had operations that alter bile acid and/or cholesterol metabolism: 1) patients who have had jejunoileal bypass procedures for morbid obesity or hypercholesterolemia, 2) patients taking cholestyramine and/or other anti-hyperlipidemic agents, 3) patients receiving chenodeoxycholic therapy to dissolve gallstones, 4) patients taking the birth control pill, and 5) young patients who have had a cholecystectomy. Proponents of such therapy and physicians treating patients who develop colonic cancer or polypoid disease after having had such therapy are encouraged to provide accurate reports.

Adult↗
PubMed2004

[The significance of urine di-acetyl spermine level as a cancer marker for colorectal cancer].

We analyzed the significance of the measurement of urine di-acetyl spermine (DiAcSpm) as a cancer marker for colorectal cancer treatment. We measured both the urine DiAcSpm(ELISA, normal range: 0-0.25 mumol/creatinine) and serum CEA (normal range: 0-5.0 ng/ml) of preoperative and postoperative colorectal cancer patients every month. We compared the positive rate from the cancer stage and the power of prognostic prediction. We divided the colorectal cancer patients into 4 groups: Group A: both levels were high; Group B: only the CEA level was high; Group C: only the DiAcSpm level was high; Group D: both levels were within a normal range. The positive rates of DiAcSpm and CEA from cancer staging were as follows: Stage 0: 62% and 9.5%, Stage I: 60% and 10%, Stage II: 70% and 42%, Stage III: 82% and 47%, and Stage IV: 88% and 63%, respectively. There was a significant difference (p < 0.0001) between both levels, especially for early-stage cases. The two-year survival rate was 0% in Group A, 100% in Group B, 72.7% in Group C and 100% in Group D. The difference among the 4 groups was significant (p < 0.0001). This showed that urine DiAcSpm predicted the prognosis after colorectal cancer surgery more exactly than serum CEA.

Biomarkers, Tumor↗
PubMed2003

Cholecystectomy and the risk for developing colorectal cancer and distal colorectal adenomas.

Earlier work describes a modest association between cholecystectomy and the risk of colorectal cancer. We conducted a prospective study of 85 184 women, 36-61 years old, who had no history of cancer to evaluate whether known risk factors for colorectal cancer, including dietary history, that have not been controlled for in previous analyses can help explain the observed association. During 16 years of follow-up, 877 cases of colorectal cancer were documented and 1452 women who underwent endoscopy during the follow-up time were diagnosed with distal adenomas. After adjustment for age and other known or suspected risk factors, we found a significant, positive association between cholecystectomy and the risk of colorectal cancer (multivariate relative risk RR 1.21, 95% CI 1.01-1.46). The risk was highest for cancers of the proximal colon (RR 1.34, 95% CI 0.97-1.88) and the rectum (RR 1.58, 95% CI 1.05-2.36). However, we did not observe a significant association between cholecystectomy and distal colorectal adenomas. In this large prospective cohort study, a history of cholecystectomy appears to increase modestly the risk of colorectal cancer, even after adjustment for other colorectal cancer risk factors.

Adenoma↗
PubMed2003

Current capacity for endoscopic colorectal cancer screening in the United States: data from the National Cancer Institute Survey of Colorectal Cancer Screening Practices.

PURPOSE: There is a national goal in the United States to increase the level of colorectal cancer screening, but there is currently little information on resources for the delivery of endoscopic screening and follow-up diagnostic and surveillance procedures. The purpose of this study was to provide nationally representative data on endoscopic resources at the provider level. METHODS: A nationally representative survey of primary care physicians, general surgeons, and gastroenterologists that was conducted during 1999 to 2000 provided data from survey responses by 1235 primary care physicians, 349 gastroenterologists, and 316 general surgeons. RESULTS: We estimated that 65% of all sigmoidoscopy procedures were performed by primary care physicians, 25% by gastroenterologists, and 10% by general surgeons. Only 30% of all primary care physicians performed any procedures, and average volume among those who did was relatively low (seven per month). Gastroenterologists performed two thirds of all colonoscopy procedures, with most of the remainder performed by general surgeons. CONCLUSION: There is potential to increase the capacity to perform screening sigmoidoscopy procedures through primary care delivery. However, without careful consideration of organizational factors, this could result in increased cost and quality control problems. Increasing the capacity for screening colonoscopy is feasible, but will require attention to other problems, such as avoiding overfrequent (e.g., annual or biennial) procedures in low-risk patients.

Academies and Institutes↗
PubMed2000

Does hereditary nonpolyposis colorectal cancer explain the observed excess risk of colorectal cancer associated with family history?

Several studies have found an increased risk of colorectal cancer associated with a family history of colorectal cancer. Some studies, although not all, have also suggested that family history of colorectal cancer may be a risk factor for adenomatous polyps. Hereditary nonpolyposis colorectal cancer is a known genetic syndrome predisposing to colorectal cancer. The hypothesis of this paper is that the preponderance of the genetic or familial risk for colorectal cancer in the United States is mediated by hereditary nonpolyposis colorectal cancer. To test this hypothesis, I have incorporated what is known about hereditary nonpolyposis colorectal cancer into a genetic model that generates probabilities of family clustering of colorectal cancer. Using this model, which assumes that all familial risk for colorectal cancer is due to hereditary nonpolyposis colorectal cancer, the expected relative risks for colorectal cancer (and adenomas) associated with given types of family histories were calculated. The relative risks predicted by the model fairly closely matched the results found in the literature, especially those reported from a large cohort study. As observed in several studies, the model predicts that relative risks decrease sharply with age. In contrast to the elevated risk for colorectal cancer, the model predicts no elevated risk for adenomas associated with family history of colorectal cancer.

Cluster Analysis↗
PubMed2000

Role of virtual computed tomographic colonography in patients with colorectal cancers and obstructing colorectal lesions.

PURPOSE: The aim of this study was to assess the ability of computed tomographic colonography to diagnose colorectal masses, stage colorectal cancers, image the proximal colon in obstructing colorectal lesions, and evaluate the anastomoses in patients with previous colorectal surgery. METHODS: We prospectively performed computed tomographic colonography examinations in 34 patients (20 males; mean age, 64.2; range, 19-91 years): 20 patients had colorectal masses (defined at endoscopy as intraluminal masses 2 cm or larger), 7 patients had benign obstructing colorectal strictures, and 7 patients had a prior colorectal resection. Final tumor staging was available in all 16 patients who had colorectal cancers and 15 patients were referred after incomplete colonoscopy. The ability of computed tomographic colonography to stage colorectal cancers, identify synchronous lesions in patients with colorectal masses, and image the proximal colon in patients with obstructing colorectal lesions was assessed. RESULTS: Computed tomographic colonography identified all colorectal masses, but overcalled two masses in patients who were either poorly distended or poorly prepared. Computed tomographic colonography correctly staged 13 of 16 colorectal cancers (81 percent) and detected 16 of 17 (93 percent) synchronous polyps. Computed tomographic colonography over-staged two Dukes Stage A cancers and understaged one Dukes Stage C cancer. A total of 97 percent (87/90) of all colonic segments were adequately visualized at computed tomographic colonography in patients with obstructing colorectal lesions compared with 60 percent (26/42) of segments at barium enema (P < 0.01). Colonic anastomoses were visualized in all nine patients, but in one patient, computed tomographic colonography could not distinguish between local tumor recurrence and surgical changes. CONCLUSION: Computed tomographic colonography can accurately identify all colorectal masses but may overcall stool as masses in poorly distended or poorly prepared colons. Computed tomographic colonography has an overall staging accuracy of 81 percent for colorectal cancer and is superior to barium enema in visualizing colonic segments proximal to obstructing colorectal lesions.

Adult↗
PubMed2003

Survivin and molecular pathogenesis of colorectal cancer.

BACKGROUND: Colorectal cancer is thought to originate in the expansion of colonic crypt cells as a result of aberrant gene expression caused by transcription factors of the T-cell factor (TCF)/beta-catenin family. Survivin is a bifunctional regulator of cell death and cell proliferation expressed during embryonic development but undetectable in healthy adult tissues and re-expressed in many cancers, including colorectal cancer. METHODS: We investigated gene expression by promoter analysis, mutagenesis, and electrophoretic mobility shift assay in colorectal cancer cells. Survivin expression in human and mouse embryonic intestine was determined by in-situ hybridisation and immunohistochemistry. Changes in apoptosis were monitored in cell lines engineered to express stabilising mutations in beta catenin. FINDINGS: TCF/beta catenin stimulated a six-fold to 12-fold increased expression of the survivin gene in colorectal cancer cells. Three TCF-binding elements (TBE) in the survivin promoter were occupied by nuclear factors in colorectal cancer cells, and mutagenesis of the two proximal TBE sites abolished survivin gene expression by 75-79%. Strongly expressed at the bottom of human and mouse embryonic intestinal crypts, expression of survivin was lost in TCF-4 knockout animals, and a TCF-4 dominant negative mutant blocked survivin gene transcription in colorectal cancer cells. Expression of non-destructible beta catenin mutants increased survivin expression and protected against ultraviolet-B-induced apoptosis. INTERPRETATION: Stimulation of survivin expression by TCF/beta catenin might impose a stem cell-like phenotype to colonic crypt epithelium coupling enhanced cell proliferation with resistance to apoptosis, and contribute to the molecular pathogenesis of colorectal cancer.

Animals↗
PubMed1989

Children, age at first birth, and colorectal cancer risk. Data from the Melbourne Colorectal Cancer Study.

During 1980 and 1981, data were obtained on the number of children and age at birth of the first child in 675 cases of colorectal cancer and in 720 age-sex frequency-matched controls as part of a large epidemiologic study of colorectal cancer conducted in Melbourne, Australia. For colorectal cancer, the relative risk (RR) for those with one or more children compared with those with no children was statistically significantly lower than one (RR = 0.61, 95% confidence interval (CI): 0.45-0.81, p less than 0.001), and with simultaneous adjustment for number of children, there was an increasing risk with increasing age at birth of first child (RR = 1.03, with each increasing year of age at birth of first child, 95% CI: 1.00-1.05, p = 0.02). The relation between both the number of children and the age at birth of the first child and colorectal cancer risk was not statistically significantly different for males and females. The risk of colorectal cancer with respect to number of children and age at birth of the first child was unaffected by the potential confounding factors of age, occupation, previous diet, oral contraceptive use in females, and a family history of colorectal cancer. Since the protection against colorectal cancer associated with having children and with earlier age at birth of the first child was found to be similar for both males and females in the Melbourne study, a life-style factor, as yet unidentified, rather than a female hormonal factor, is postulated as the mediator of these effects.

Aged↗
PubMed1993

Adenoma residua in colorectal cancer. A study of 34 colorectal cancers detected by an immunological occult blood test.

A retrospective histological study was made searching for adenoma remnants in 34 colorectal cancer specimens detected by the quantitative and human Hb-specific immunological FECA-EIA test for occult blood in the faeces. As a control group, 34 colorectal cancer preparations from routine hospital material were studied in a similar manner. A difference was found between these materials, 12 out of 34 study cancers showing adenoma residua compared with only two in the control group. Even if a proportion of colorectal cancers is apparently not associated with adenomas, it is suggested that the existence of adenoma remnants is a sign of biologically early tumour development and consequently, it might correlate with a favourable prognosis.

Aged↗
PubMed2004

Clinical and genetic features of International Collaborative Group-hereditary nonpolyposis colorectal cancer families and suspected hereditary nonpolyposis colorectal cancer families.

BACKGROUND: Hereditary nonpolyposis colorectal cancer (HNPPC) is one of the most common genetic syndrome related with mutation of human mismatch repair genes. This study was to evaluate the clinical significance of suspected hereditary nonpolyposis colorectal cancer (sHNPCC) criteria I and the clinical and genetic features of International Collaborative Group-HNPCC (ICG-HNPCC) and sHNPCC families. METHODS: Twenty-nine ICG-HNPCC families fulfilling the Amsterdam criteria and 34 sHNPCC families fulfilling the sHNPCC criteria I were collected. PCR-SSCP and DNA sequencing analysis were employed to screen the germline mutations of the hMLH1 and hMSH2 genes in these families. RESULTS: The ICG group had more colorectal cancer (CRC) patients per family than did the suspected group (P < 0.05). No statistical difference was observed in Lynch classification and familial tumor spectrum. In both groups of families, colorectal cancer was the most frequent malignancy, and carcinomas of the stomach, pancreas and uterus were the three most common extracolonic malignancies. Mutation screening showed that ICG-HNPCC and sHNPCC families had a similar mutation rate (31.0% vs 29.4%, P > 0.05), mutation type, and mutation distribution. Comparison of the families with and without mutation showed no significant difference in CRC patients per family, Lynch classification, and tumor spectrum. CONCLUSIONS: ICG-HNPCC and sHNPCC families that have similar clinical manifestations and genetic basis indicate a similar nature for cancer development. The application of sHNPCC criteria I will facilitate clinical diagnosis and treatment of small families.

Adaptor Proteins, Signal Transducing↗
PubMed2006

Frequency of hereditary non-polyposis colorectal cancer among unselected patients with colorectal cancer in Germany.

INTRODUCTION: Hereditary non-polyposis colorectal cancer (HNPCC) is a major form of familial colorectal cancer (CRC). It is diagnosed when either the Amsterdam criteria (AC) are fulfilled or mutations in one of the mismatch repair (MMR) genes have been identified. This project aims at estimating the proportion of HNPCC among unselected patients with CRC. PATIENTS AND METHODS: During a period of 2 years, a total of 351 non-selected patients with CRC were registered prospectively. 92 patients met the Bethesda criteria (9 of them fulfilled the AC) and 259 did not. 348 tumours were examined for microsatellite instability (MSI) and expression of MMR proteins. RESULTS: MSI-H and MSI-L were identified in 17 and 6%, respectively. Loss of MSH2 or MLH1 was found in 1.5 and 8.8%, respectively. Based on the results of tumour tissue analyses, 80 patients with MSI and/or loss of MSH2 or MLH1 expression were identified as candidates for germline mutation screening. DNA of 40/80 patients was available. These patients were screened for MSH2 and MLH1 mutations; 19/40 patients with MSI and normal MSH2 or MLH1 expression were screened for mutations in MSH6. Three patients had relevant MMR gene mutations and six variants of unknown functional relevance were detected. CONCLUSIONS: After adjusting for the cases not evaluable for germline mutations, 1.7% of the CRC patients had HNPCC proven by molecular genetics.

Adaptor Proteins, Signal Transducing↗
PubMedDate not supplied

Management of colorectal cancer patients in Australia: the National Colorectal Cancer Care Survey.

BACKGROUND: The National Colorectal Cancer Care Survey was undertaken to determine the management patterns for individuals newly diagnosed with colorectal cancer in Australia. METHODS: Between 1 February and 30 April 2000, all new cases of colorectal cancer registered at each Cancer Registry within Australia were entered into the survey. This generated a questionnaire that was sent to the treating surgeons. Chi-squared and logistic regression analyses were used to determine levels of statistical significance for the various comparisons of interest. RESULTS: Of 2383 surgical questionnaires generated, 2015 (85%) were completed. A total of 1911 patients (95% of those who responded to the questionnaire) had an operation. Of the 86 guidelines for the management of colorectal cancer published by the National Health and Medical Research Council, the survey allowed for comparison between 18 of these, which covered a spectrum of surgical management. Thromboembolic prophylaxis was given to 1843 patients (96.4%) undergoing surgery. Prophylactic antibiotics were commonly used, but there appear to be issues regarding the best regimen to use. Curative resections were carried out in 1563 patients (81.8%), with anterior resections being the most commonly performed procedure. Adjuvant therapy was regularly used, but not all eligible patients were offered such treatment. CONCLUSION: With the considerable resources required to develop clinical practice guidelines, studies like this are essential to monitor the impact of the guidelines. To ensure that the guidelines are in line with current evidence, regular reviews of the guideline recommendations are required.

Adolescent↗
PubMed2005

Preoperative serum levels of the carcinoembryonic antigen in hereditary non-polyposis colorectal cancer compared to levels in sporadic colorectal cancer.

BACKGROUND: Carcinoembryonic antigen (CEA) serves as the most widely used and most cost-effective tumor marker in colorectal cancer for almost 30 years. Recent publications about serum CEA levels are based on patient groups without definite differentiation between hereditary and non-hereditary forms of colorectal cancer. PATIENTS AND METHODS: We compared preoperative CEA serum levels from 105 patients with hereditary non-polyposis colorectal cancer (HNPCC) and 107 patients with sporadic colorectal cancer including influences of age and Dukes stage. CEA values in cases of HNPCC were correlated to the findings of microsatellite analyses, mutation analyses of the MMR genes (MLH1, MSH2) and respective immunohistochemistries. RESULTS: Thirty-three HNPCC patients (31%) and 37 patients with sporadic CRC (34%) revealed elevated CEA levels higher than 5 ng/ml. The mean preoperative CEA level in all Dukes stages of HNPCC patients was lower with 31.7 +/- 180 ng/ml than in sporadic colorectal cancer with 68.3 +/- 424 ng/ml, but without significance (p = 0.72). HNPCC tumors with signs of de-differentiation (G3 and G4) revealed significantly higher CEA values with 62.2 +/- 262 ng/ml in comparison to well-differentiated tumors (G1 and G2) with 5.0 +/- 9.6 ng/ml (p = 0.02). HNPCC patients with "classical characteristics" (high microsatellite instability (MSI), MMR gene mutation, loss of MMR protein expression) had lower preoperative CEA serum levels than those without equivalent genetic alterations, but without reaching statistical significance. CEA levels of HNPCC tumors increased significantly under occurrence of metastases with mean values of 170.3 +/- 343 (p < 0.02). CONCLUSIONS: Normal preoperative serum CEA levels do not have the same validity for all colorectal cancer patients. Low CEA levels in HNPCC patients could occur due to well-differentiated tumors and should be considered more critically than in sporadic CRC patients. Further studies including comparison of postoperative CEA development are necessary to elucidate the importance of these results.

Adaptor Proteins, Signal Transducing↗
PubMed2005

Frequency of hereditary non-polyposis colorectal cancer among Uruguayan patients with colorectal cancer.

Few studies have investigated the frequency of hereditary non-polyposis colorectal cancer (HNPCC) in patients with colorectal cancer (CRC), and these have shown marked geographic variations. The aim of this study was to estimate the frequency of HNPCC in a cohort of Uruguayan CRC patients. We included all patients operated consecutively for CRC in the Hospital Central de las Fuerzas Armadas (Uruguay) between 1987 and 2003. Cases were classified into three groups: (i) those fulfilling Amsterdam criteria; (ii) those not fulfilling Amsterdam criteria but considered as a population at increased risk of cancer; and (iii) sporadic CRC. Genetic analysis to detect point mutations in hMLH/hMSH2/hMSH6 genes was performed in group 1 patients. Cases not showing mutations were tested by multiplex ligation-dependent probe amplification. Among 461 patients, group 1 represented 2.6%, group 2 represented 5.6%, and sporadic cases 91.8%. hMLH1/hMSH2/hMSH6 mutations were found in 25% of cases classified as HNPCC (two in hMLH1 and one in hMSH2). No mutations were detected in hMSH6 gene. The proportion of CRC patients that fulfilled Amsterdam criteria agrees with other reports. However, the percentage of HNPCC cases with identified mutations (25%) may be lower than that reported from other populations. This may reflect, among other possible causes, a different genetic profile in the Uruguayan population.

Adaptor Proteins, Signal Transducing↗