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PubMed1993

Cholecystectomy and colorectal cancer in China.

Colorectal cancer is a major public health problem in China: 79,800 new cases are estimated to occur each year, which ranks it among the five most common tumours in China. Although the association between cholecystectomy and colorectal cancer has been studied elsewhere, few studies have been conducted in the Chinese population, characterized by a lower fat intake, and low colorectal cancer incidence. We conducted this hospital-based case-control study to explore this association. The study included a total of 503 incident cases with pathologically diagnosed colorectal cancer in Drum Tower Hospital at Nanjing in China from 1965 to 1986, and 2188 healthy controls who had annual routine physical examinations at the same hospital. Diagnosis of cholelithiasis was confirmed by ultrasonography or X-ray cholecystography, and the information on cholecystectomy was obtained by checking medical charts for both cases and controls. The prevalence of cholelithiases was 5.8% for cases and 6.1% for controls (P > 0.05). Eight cases (1.6%) and 18 controls (0.8%) had a history of previous cholecystectomy. The period between cases' cholecystectomy and diagnosis of colorectal cancer ranged from 2.5 to 23 years, and the mean interval was 8.9 years. The crude odds ratio for patients having previous cholecystectomy is 1.95 (95% CI: 0.84-4.51) compared with controls. The odds ratio for female patients with previous cholecystectomy was 2.79 (95% CI: 1.03-7.59). When subsites were analysed, a significant association between right colon cancer and cholecystectomy was noted: the odds ratio was 6.2 (95% CI: 2.24-16.9), and that for females was even higher 8.61 (95% CI: 2.44-3.04) with statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)

Case-Control Studies↗
PubMed2002

Changing area socioeconomic patterns in U.S. cancer mortality, 1950-1998: Part II--Lung and colorectal cancers.

BACKGROUND: Lung cancer and colorectal cancer are leading causes of U.S. cancer mortality. Because mortality rates for many cancers vary by socioeconomic characteristics, we used area socioeconomic indices to examine patterns in U.S. lung and colorectal cancer mortality between 1950 and 1998. METHODS: A factor-based area socioeconomic index was linked to 1950-1998 county mortality data to generate annual lung and colorectal cancer mortality rates for each area socioeconomic group. Joinpoint regression analysis was used to model and identify statistically significant changes in the mortality trends. RESULTS: Area socioeconomic patterns in U.S. lung cancer mortality changed dramatically between 1950 and 1998. Men aged 25-64 years and those aged 65 years or older in higher socioeconomic areas generally had higher lung cancer mortality than did those in lower socioeconomic areas during 1950-1964 and 1950-1980, respectively. Area socioeconomic differences in lung cancer mortality began to reverse and widen by the early 1970s for younger men and by the mid-1980s for older men. In 1998, lung cancer mortality was 56% (95% confidence interval [CI] = 49% to 64%) higher for younger men and 38% higher (95% CI = 34% to 43%) for older men in the lowest area socioeconomic group than for the same age groups in the highest area socioeconomic group. Lung cancer mortality among older women in all socioeconomic groups increased sevenfold to eightfold between 1950 and 1998, with higher mortality in higher area socioeconomic groups. The positive socioeconomic gradient in colorectal cancer mortality diminished substantially over time. Although colorectal cancer mortality among women in all area socioeconomic groups showed a consistent downward trend, colorectal cancer mortality among men in low area socioeconomic groups, but not in high area socioeconomic groups, showed an upward trend. CONCLUSIONS: Socioeconomic gradients in male lung cancer mortality reversed between 1950 and 1998, and those in colorectal cancer mortality narrowed over that time. Area measures may be useful for monitoring socioeconomic disparities in cancer mortality and for identifying areas for potential cancer control interventions.

Adult↗
PubMed2001

Prospective study of Ki-67 labeling index in the mucosa adjacent to cancer as a marker for colorectal cancer metastasis.

Multivariate regression analysis has shown that Ki-67 labeling index in the mucosa adjacent to cancer was the most significant marker for colorectal cancer metastasis among several metastasis-related parameters according to our previous retrospective data base (7). We have performed a prospective study to ascertain whether Ki-67 labeling index in the mucosa adjacent to cancer is a useful preoperative diagnostic marker for colorectal cancer metastasis. In 182 registered cases colonoscopically biopsied, we performed surgical resection of the cancer in 37 adenocarcinoma cases, which were registered in the study. In 31 out of the 37 cases except for 6 cases with an insufficient amount of non-neoplastic mucosa, preoperative diagnosis for metastasis was performed using the Ki-67 cutoff line. The cutoff line was set at 15% according to our previous retrospective database. The preoperative diagnosis for metastasis was compared to the pathological findings of the resected specimen. The incidences of correct diagnosis for metastasis was 81% (25/31). There were 3 false positive cases and 3 false negative cases in Dukes' A-B and Dukes' C, respectively. The mean Ki-67 labeling index in the mucosa adjacent to cancer of Dukes' A-B and Dukes' C-D cases, except for the 6 misdiagnosed cases, was 7.4+/-5.0% and 29.9+9.8%, being significant at p<0.0001 by unpaired Mann-Whitney U test. These results suggest that Ki-67 labeling index in the mucosa adjacent to cancer might be a good marker for metastasis in colorectal cancer.

Adenocarcinoma↗
PubMedDate not supplied

Correlation of plasma level and immunohistochemical expression of vascular endothelial growth factor in patients with advanced colorectal cancer.

BACKGROUND: Vascular endothelial growth factor (VEGF) is thought to be the most potent angiogenic factor and may contribute to the progression of various cancers. In colorectal cancer, the immunohistochemical expression of VEGF is reported to be an independent prognostic factor, and elevated plasma levels of VEGF are reported to be a prognostic marker. The purpose of this study is to evaluate whether plasma levels of VEGF correlate with its immunohistochemical expression and with microvessel density (MVD) in patients with colorectal cancer. MATERIALS AND METHODS: Thirty-one patients with advanced colorectal cancer, who underwent surgery between February 1998 and April 2000, were included in this study. We measured the preoperative plasma levels of VEGF using the ELISA kit and immunostained the resected specimens for VEGF and CD34, as a marker of MVD. We then investigated the correlation among plasma levels of VEGF, expression of VEGF and MVD, and between these three factors and several clinical features. RESULTS: The plasma levels of VEGF were significantly associated with liver metastasis, the immunohistochemical expression of VEGF was significantly associated with lymph node metastasis and TNM stage, while MVD was significantly associated with lymph node metastasis, depth of invasion and TNM stage. Among the 3 parameters for angiogenesis studied, the plasma levels of VEGF significantly correlated with its immunohistochemical expression, and immunohistochemical expression of VEGF significantly correlated with MVD. There was no significant correlation between plasma levels of VEGF and MVD. CONCLUSION: Measuring plasma levels of VEGF is a good predictor of the immunohistochemical expression of VEGF in patients with advanced colorectal cancer, and may be a better indicator for tumor VEGF levels, since plasma levels can be measured much more quickly than expression levels.

Colorectal Neoplasms↗
PubMedDate not supplied

A case-control study of colorectal cancer in relation to lifestyle factors and genetic polymorphisms: design and conduct of the Fukuoka colorectal cancer study.

A case-control study was designed to elucidate roles of dietary and other behavioral influences, in combination with genetic susceptibility factors (genetic polymorphisms), in colorectal carcinogenesis. Both cases and controls were residents in Fukuoka City and three adjacent areas. Cases were patients undergoing surgery for a first diagnosis of colorectal cancer at 8 hospitals in the study area, and controls were randomly selected in the community by frequency-matching with respect to the expected distribution by sex, age (10-year class), and residence. Dietary and other lifestyle factors were ascertained by in-person interview, and venous blood was obtained for genotyping and possible biochemical measurements. The cases were interviewed at each hospital during the period from 2000 to 2003, and controls were surveyed during the period from 2001 to 2002. A total of 840 cases of colorectal cancer and 833 controls were interviewed with participation rates of 80% for the cases and 60% for the controls. Informed consent to genotyping was obtained from 685 cases and 778 controls. Further details of the design and conduct are described with respect to methodological aspects.

Adult↗
PubMed2001

Magnetic resonance colonography for colorectal cancer screening.

Colorectal cancer screening has vast potential. Beyond considerations of cost and diagnostic accuracy, the effectiveness of any colorectal screening strategy will be dependent on the degree of patient acceptance. Magnetic resonance (MR) colonography has been shown to be accurate regarding the detection of clinically relevant colonic polyps exceeding 10 mm in size, with reported sensitivity and specificity values exceeding 95%. To further enhance patient acceptance, strategies for fecal tagging have recently been developed. By modulating the signal of fecal material to be identical to the signal characteristics of the enema applied to distend the colon, fecal tagging in conjunction with MR colonography obviates the need for bowel cleansing. This article will describe the techniques underlying MR colonography and early clinical experience with fecal tagging techniques.

Colonography, Computed Tomographic↗
PubMed2005

MGMT promoter methylation and field defect in sporadic colorectal cancer.

BACKGROUND: Sporadic colorectal cancers often arise from a region of cells characterized by a "field defect" that has not been well defined molecularly. DNA methylation has been proposed as a candidate mediator of this field defect. The DNA repair gene O6-methylguanine-DNA methyltransferase (MGMT) is frequently methylated in colorectal cancer. We hypothesized that MGMT methylation could be one of the mediators of field cancerization in the colon mucosa. METHODS: We studied MGMT promoter methylation by three different bisulfite-based techniques in tumor, adjacent mucosa, and non-adjacent mucosa from 95 colorectal cancer patients and in colon mucosa from 33 subjects with no evidence of cancer. Statistical tests were two-sided. RESULTS: MGMT promoter methylation was present in 46% of the tumors. Patients whose cancer had MGMT promoter methylation also had substantial MGMT promoter methylation in apparently normal adjacent mucosa. This methylation was seen with a quantitative assay in 50% (22/44; 95% confidence interval [CI] = 34% to 65%) of normal samples with MGMT promoter methylation in the adjacent tumors, 6% (3/51; 95% CI = 1% to 16%) of samples without MGMT methylation in adjacent tumors, and 12% (4/33; 95% CI = 3% to 28%) of control samples (P < .001 for comparison between each of the latter two groups and the first group). MGMT methylation was detected with a more sensitive assay in 94%, 34%, and 27% of these samples, respectively (P < .001). In grossly normal colonic mucosa of colon cancer patients, methylation was detected 10 cm away from the tumor in 10 of 13 cases. Tumors with MGMT promoter methylation had a higher rate of G-to-A mutation in the KRAS oncogene than tumors without MGMT promoter methylation (10/42 versus 3/46, P = .03). Using a sensitive mutant allele-specific amplification assay for KRAS mutations, we also found KRAS mutations in 12% (3/25; 95% CI = 2.5% to 31%) of colorectal mucosas with detectable MGMT methylation and 3% (2/64; 95% CI = 0.4% to 11%) of colorectal mucosas without MGMT methylation (P = .13). CONCLUSION: Some colorectal cancers arise from a field defect defined by epigenetic inactivation of MGMT. Detection of this abnormality may ultimately be useful in risk assessment for colorectal cancer.

Biomarkers, Tumor↗
PubMed2004

The management of peritoneal surface malignancy of colorectal cancer origin.

Colorectal carcinomas are predominantly spread malignancies. Peritoneal carcinomatosis frequently associates colorectal carcinomas. The tumour grade, the completeness of cytoreduction, the tumour volume, the presence of distant metastases, prior surgery score and the extent of peritoneal implantations are prognostic clinical features of survival. The management of colorectal cancer with peritoneal carcinomatosis is possible by resection of tumour, cytoreduction and intraperitoneal chemotherapy. T3 and T4 colorectal tumours are at risk of developing locoregional recurrence and may be treated by intraperitoneal chemotherapy. Early postoperative intraperitoneal chemotherapy has been used in 40 patients with T3 and T4 tumours, with 15% hospital mortality, and 32.5% morbidity. The overall 3-year survival rate was over 80% and only 15% distant metastases were recorded.

Adenocarcinoma↗
PubMed1990

Polyamines in colorectal cancer. Evaluation of polyamine concentrations in the colon tissue, serum, and urine of 50 patients with colorectal cancer.

Total, free, and acetylated polyamine concentrations were measured simultaneously in colon tissue, serum, and urine of 50 patients with histologically proven colorectal cancer, 40 patients with nonmalignant gastrointestinal diseases, and 30 healthy volunteers. Compared with histologically unaffected colon tissue, concentrations were significantly (P less than 0.001) higher for putrescine, elevated for cadaverine, and nearly identical for spermidine and spermine in colon carcinoma, whereas N1-acetylated and N8-acetylated spermidine were detectable in cancer tissue only. Serum and urine concentrations of all polyamines except total cadaverine and spermine in serum and free spermine in urine were significantly elevated compared with healthy controls and highest sensitivity for colon cancer was found for total spermidine (89.15%) in serum and acetylputrescine (84.5%), total putrescine (84.0%), N1-acetylspermidine (79.3%), and total spermidine (92.1%) in urine. However, nonmalignant gastrointestinal diseases partly showed similar elevations which resulted in a low specificity for polyamines in colorectal cancer. Therefore, polyamines are of little value only as diagnostic markers in colorectal carcinoma. Since polyamine concentrations in serum and urine normalized in patients after curative operation while they were further elevated in patients with proven tumor relapse or metastases, these substances might play a clinical role in predicting therapeutic success or indicating relapse of the tumor. Although a significant dependency of polyamine concentrations in serum or urine to Dukes' classification, tumor localization, CEA, CA 19-9, or CA 125 did not exist, a significant linear correlation was found for tumor size.

Antigens, Tumor-Associated, Carbohydrate↗
PubMedDate not supplied

The role of nonsteroidal anti-inflammatory drugs in colorectal cancer prevention.

Colorectal cancer is the second leading cause of cancer death in the U.S.A. Recent research suggests that nonsteroidal anti-inflammatory drugs (NSAIDs) are effective in the prevention of colorectal neoplasia. This review summarises the results of research in animals and humans of these compounds in preventing tumours of the colorectum.

Animals↗
PubMed2005

Current status of laparoscopic therapy of colorectal cancer.

Laparoscopic colorectal resections offer several benefits postoperatively, including minimal impairment of gastrointestinal and pulmonary function, less immunosuppression, shorter hospital stay and improved reconvalescence. Since the introduction of laparoscopic surgery for the therapy of curable colorectal cancer, some concern was voiced in terms of oncologic radicality, the issue of port-site metastases and tumor cell distribution. However, the clinical reality has demonstrated that oncologic radicality is equivalent to open surgery, and the incidence of port-site metastases is not increased when compared to wound recurrence at the laparotomy site. Focusing on colon and rectum, various indications of laparoscopic-endoscopic 'rendezvous' procedures exist including laparoscopic-assisted endoscopic transluminal resection, endoscopic-assisted wedge or anatomical resections, and, finally, intraoperative tumor location by colonoscopy to achieve oncologic resection margins in laparoscopic curative resections. In terms of colorectal curative resections, long-term results provide level I evidence that laparoscopic surgery for colon cancer is oncologically adequate and can be performed with equivalent morbidity and mortality rates when compared to conventional surgery. In terms of rectal cancer, no level I evidence is available. However, short-term data from experienced centers do not report inferior oncologic outcome particularly related to laparoscopic total mesorectal excision.

Colectomy↗
PubMed2002

Fecal occult blood testing for colorectal cancer: a perspective.

Colorectal cancer is an important health problem in western countries. Early detection of colorectal cancer reduces mortality. The best evidence for the effectiveness of screening for colorectal cancer is with annual or biennial fecal occult blood testing. While the benefit of fecal occult blood testing is small in absolute terms, the incremental cost-effectiveness of this screening strategy appears acceptable. Combining fecal occult blood testing with periodic flexible sigmoidoscopy or replacing it altogether with infrequent colonoscopy are theoretically attractive screening strategies, but the incremental costs and effectiveness of these more intensive screening strategies have not been well defined. Whether and how to implement population-based screening for colorectal cancer depends largely on available resources.

Colorectal Neoplasms↗
PubMed2004

Immunoassay for wild-type protein in lymphocytes predicts germline mutations in patients at risk for hereditary colorectal cancer.

Using colorectal cancer (CRC) as an example, we present the hypothesis that quantitative immunoassays for wild-type (full-length) proteins can be used to identify carriers of traits for hereditary diseases. In the case of hereditary CRC, this involves identifying individuals with germline mutations in a mismatch-repair (MMR) gene (mainly hMSH2 or hMLH1) or in the adenomatous polyposis coli (APC) gene. Because expression of wild-type protein should reflect wild-type gene dosage, we predicted that individuals harboring a germline mutation will have a reduction of approximately 50% in expression in lymphocytes of the corresponding full-length protein. In this pilot study, we tested lymphoblastoid cell lines that had been established from controls and individuals with, or at high risk for, hereditary CRC: 9 lines from healthy, unaffected individuals; 4 from affected members in familial adenomatous polyposis families (with known germ-line APC mutation); 42 from CRC patients in our Familial CRC Registry (increased risk of hereditary nonpolyposis colon cancer as assessed by family history, age at adenoma or carcinoma diagnosis, and other clinical criteria). For MSH2 and MLH1 we used western blots; for APC we used immunoprecipitation. All familial adenomatous polyposis lines had about 50% less immunoprecipitable full-length APC protein. Some cell lines (7 of 42) from Familial CRC Registry patients showed on western blots a reduction (mean 46%) in either MSH2 or MLH1 (relative to the other protein). All 7 subsequently were proved to contain a germline MMR mutation. We conclude that (1) because most of the expected CRC-causing germ line mutations are truncation-causing, immunoassays for wild-type protein should be able to identify most individuals with hereditary CRC-causing traits; (2) these assays, which are more practical and inexpensive than current mutation-detecting tests for hereditary CRC traits, have the potential for commercial development into broad-based population screens of high-risk patients and their families and the potential to save both lives and health-care dollars; (3) this strategy may be useful for other hereditary cancers and even other hereditary diseases; (4) our approach has the potential to greatly benefit public-health programs for cancer control.

Adaptor Proteins, Signal Transducing↗
PubMed2005

Non-steroidal anti-inflammatory drugs and colorectal cancer prevention.

Colorectal cancer is the second leading cause of cancer deaths in the United States. Currently, the most effective strategy available for colon cancer prevention is endoscopic screening, with polypectomy or surgical resection for advanced lesions. This intervention carries with it many concerns regarding cost, patient acceptance, and the growing burden of surveillance colonoscopies for patients with polyps. Further improvements in the understanding of the multistep model of colorectal carcinogenesis will probably lead to the development of other primary and secondary prevention strategies. Data obtained from animal and epidemiological studies and most recently from randomised, placebo controlled trials, suggest that non-steroidal anti-inflammatory drugs may prove effective chemopreventive agents in different groups of people, from patients with familial adenomatous polyposis to those with sporadic adenomas.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2005

Angiogenesis, immune system and growth factors: new targets in colorectal cancer therapy.

Colorectal cancer is the second most common malignant human neoplasia. Over recent years, many efforts have been performed in order to develop and improve therapeutic protocols, and many advances have been accomplished in both the field of adjuvant and palliative therapy. Most of the chemotherapic agents currently used in the clinical setting are the products of decades of research aimed at inhibiting the uncontrolled growth of dysplastic cells. However, new frontiers in this field have recently been opened, with the identification of key molecules involved in physiologic mechanisms that are of fundamental importance for cancer development and progression. Tumor-induced angiogenesis, the cancer-immune system crosstalk and the effect of growth factors on dysplastic cells represent new fields of investigation for anticancer therapy.

Angiogenesis Inhibitors↗
PubMed1999

Family history of cancer in children and young adults with colorectal cancer.

BACKGROUND: Family history of colorectal cancer among adult patients has been reported in the literature. Although extremely rare in children, colorectal cancer in this population may represent a unique group in whom genetic factors play a significant etiologic role. The aim of the present study was to assess genetic contribution, as measured by family history, to the development of colorectal cancer in probands under 21 years of age at diagnosis. PROCEDURE: Detailed family histories were obtained from surviving patients or their parents. The risk [standardized incidence ratio (SIR)] of cancer in the relatives was calculated by comparing the observed and the expected incidence based on rates in the general population and person-years at risk. RESULTS: Twenty-five patients (median age at diagnosis 15 years) diagnosed with colorectal cancer at St. Jude Children's Research Center since 1964 or their surviving next of kin were available for interview. The 461 relatives contributed 18,908 person-years of follow-up. Statistically significant increased risk of colorectal cancer was present among all relatives (SIR = 6.0, 95% CI, 2.7-10.6), and the increased risk of colorectal cancer was confined to relatives of probands who were under 15 years of age at diagnosis (SIR = 10.0, 95% CI, 4.5-17.6). In addition, there was an excess of uterine/cervical cancer among all female relatives (SIR = 6.5, 95% CI, 3.2-10.9). CONCLUSIONS: The observed excess of colorectal cancer, in relatives of younger probands, suggests the need to examine these kindreds for genetic instability resulting from defects in mismatch repair genes to characterize further the patterns of risk observed.

Adolescent↗