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At least 811 records · Page 45Linked to original sources
PubMed2003

Nuclear beta catenin as a potential prognostic and diagnostic marker in patients with colorectal cancer from Hong Kong.

AIMS: To study the expression of nuclear beta catenin in patients with colorectal cancer, colorectal adenoma, and colorectal polyps to elucidate its role in carcinogenesis, and its potential for prognosis and diagnosis. METHODS: The expression of nuclear beta catenin was studied by immunohistochemistry using paraffin wax embedded specimens. Sixty specimens each of colorectal carcinoma, colorectal adenoma, colorectal polyp, and normal colorectal specimens were analysed. The potential for prognosis was assessed by correlating nuclear beta catenin expression in 60 and 75 patients with colorectal cancer with lymph node metastasis and survival, respectively. The diagnostic capacity was explored by comparing nuclear beta catenin expression in 60 patients with colorectal cancer with other cytokeratin 20 (CK20) positive adenocarcinomas, namely: 30 colonic mucinous adenocarcinomas, 30 gastric adenocarcinomas, 27 pancreatic adenocarcinomas, and 12 ovarian mucinous adenocarcinomas. RESULTS: Nuclear beta catenin expression was highly associated with progression of colorectal tissue from normal epithelial tissue, polyps, adenomas, to carcinomas (r = 0.875; p < 0.0001). Nineteen patients with colorectal adenoma who subsequently developed colorectal carcinoma had higher nuclear beta catenin expression than those with colorectal adenomas alone (p < 0.0001). Moreover, those patients with colorectal cancer and high nuclear beta catenin expression had a higher incidence of lymph node metastasis (chi(2) = 16.99; p < 0.005) and shorter overall survival (p < 0.0001). Finally, nuclear beta catenin expression in colorectal adenocarcinomas was significantly higher than in other CK20 positive adenocarcinomas. CONCLUSIONS: Nuclear beta catenin expression is a potential prognostic factor in patients with colorectal cancer, and together with CK20, it could be used to identify colorectal carcinoma in the Hong Kong population.

Adenoma↗
PubMed2003

HNK-1-Reactive oligosaccharide, sulfate-O-3GlcAbeta1-4Xylbeta1-MU, synthesized by cultured human colorectal cancer cells.

Human colorectal cancer cells were incubated with medium containing 4-methylumbelliferyl-beta-D-xyloside (Xyl-MU). The cells synthesized Xyl-MU-derivatives which were detected in the culture medium by gel-filtration high-performance liquid chromatography. These included a Xyl-MU-induced glycosaminoglycan and its biosynthetic intermediates, Galbeta1-4Xylbeta1-MU and Galbeta1-3Galbeta1-4Xylbeta1-MU, and other Xyl-MU-induced oligosaccharides, not related to Xyl-MU-induced glycosaminoglycan, were also synthesized. One of these oligosaccharides, sulfate-O-3GlcAbeta1-4Xylbeta1-MU, reacted with HNK-1, a mouse monoclonal antibody raised against human natural killer cells. Human neural cells and skin fibroblasts have also been reported to synthesize HNK-1-reactive sugar chains. Since HNK-1-reactive sugar chains are known to be involved in cell adhesion in the nervous system, the present results suggest that epithelium-derived colorectal cancer cells might also be able to utilize them in cell adhesion.

Animals↗
PubMed2005

Association between cyclooxygenase-2-expressing macrophages, ulceration and microvessel density in colorectal cancer.

AIM: In colorectal carcinomas, cyclooxygenase-2 (COX-2) is expressed predominantly by epithelial cells and is implicated in tumour progression. Tumour-associated macrophages may influence tumour growth, proliferative rate and angiogenesis and also express COX-2 when activated. Thus they may play an important stromal-epithelial role in carcinogenesis. Tauhe aim of this study was to define the relationship between microvessel density (MVD), tumour COX-2 and macrophage COX-2 expression. METHODS AND RESULTS: Sixty-five cases of formalin-fixed paraffin-embedded colorectal cancer were included in the study. Tissues were immunostained for COX-2, CD68 (macrophage marker) and CD34 (endothelial marker to assess MVD). Thirty-six cases were grossly ulcerated cancers and 29 cases showed focal/microscopic ulceration. Macrophages were in high concentration at the base of ulcerated areas, and were also diffusely dispersed within tumoral stroma. However, the pattern of macrophage COX-2 expression revealed two populations of macrophages--those deep within the tumour (negative for COX-2) and those at the base of ulcers (positive for COX-2). In all cases, the tumour epithelial cells expressed COX-2. MVD was higher at the base of ulcers, adjacent to COX-2+ macrophages, and was lower deep within the tumour. CONCLUSIONS: In colorectal cancers, macrophages may have a dual role. Those concentrated at the base of the ulcers, where there is an associated high MVD, may induce angiogenesis, but their function may be in a healing/repair process. The lack of COX-2+ macrophages and lower MVD deep within the tumour suggests that it may be the epithelial COX-2 component that is important in tumour progression.

Antigens, CD↗
PubMed2003

Palliative treatment of patients with colorectal cancer.

BACKGROUND: Metastatic colorectal cancer has a poor prognosis, and the majority of patients are left with palliative measures. The development seen using palliative chemotherapy is reviewed. MATERIAL AND METHODS: A systematic approach to the literature-based evidence was aimed at. RESULTS: The continuous improvements during the past 13-15 years have been documented in several large conclusive trials. At the end of the 1980s, the evidence that chemotherapy should be used at all was very limited, whereas presently most patients can be offered two lines of chemotherapy based upon good scientific evidence. Median survival has gradually improved from below 6 months to above 18 months in some recent trials. Several important issues remain to be solved, such as the best sequence of treatments, what regimens to use in various situations, when to start and when to stop if a response is seen, and whether cure may be possible in a small subset of patients. CONCLUSIONS: Progress has been rapid in advanced colorectal cancer. This is likely a result of well-designed trials in collaboration between academy and industry, showing a great interest in the disease. Future collaborations may hopefully introduce new treatment concepts, further improving outcome.

Antimetabolites, Antineoplastic↗
PubMed2002

[Estimate of regional prevalence of colorectal cancer in France].

BACKGROUND: Colorectal cancer prevalence is an important determinant of the health demand that completes information provided by cancer incidence. Current estimations established from data for the years 1985 and 1995 can be used to establish a precise description of changing healthcare needs for colorectal cancer. METHOD: Prevalence estimates method were based on incidence data computed on the regional scale by the FRANCIM network and mortality data provided by INSERM. We used the relationship that exists between the net risk of cancer, the net risk of dying of the given cancer and the age-specific prevalence of cancer. RESULTS: In 1995, the prevalence of patients who had a diagnosis of colorectal cancer amounted to 200 000 persons. The estimated number of prevalent cases was never lower than 3500 in any region and in 7 regions this number was higher than 10 000. From 1985 to 1995, there has been an increase of 35% in the prevalence rates. CONCLUSION: The evaluation of the number of persons who have had a diagnosis of colorectal cancer provides knowledge for health care planning. Such information on the regional scale is very useful for the health organisation (SROS). This geographical level induces difficulties not encountered at the national level.

Colorectal Neoplasms↗
PubMed2006

[Colorectal cancer: a risk-adapted screening and the role of the physician in the prevention of this cancer].

The benefit of colorectal cancer screening in the average-risk population, as well as in the presence of high risk genetic predispositions, has been validated by a significant reduction of the mortality associated with the disease. Several screening options are recognized and compliance with these measures remains a public health problem. The physician plays a key role in the promotion of the colorectal cancer screening. Collecting a precise family history is crucial for the identification of individuals at high risk. Validated clinical criteria are helpful for the identification of individuals with a genetic predisposition to colorectal cancer. Molecular screening for the main colorectal cancer predisposing genes should now be integrated in the clinical management of these patients and their families.

Colorectal Neoplasms↗
PubMed1999

The I1307K polymorphism of the APC gene in colorectal cancer.

BACKGROUND & AIMS: Colorectal cancer is one of the most frequent cancers in humans. Recently, a germline missense mutation, I1307K, was identified in the adenomatous polyposis coli (APC) gene that was suggested to increase cancer predisposition in Ashkenazi Jews. However, a second study indicated that the I1307K mutation did not contribute greatly to the risk of colon cancer in Ashkenazi breast-ovarian cancer families, and a role of mismatch repair deficiency was suggested. This study investigated the frequency of the I1307K mutation in several non-Ashkenazi Jewish populations. We also compared the distribution and frequency of APC mutations from colon tumors that were positive and negative for the I1307K mutation. Finally, the association between the presence of mutations in the I1307K region and mismatch repair deficiency was studied. METHODS: We tested for I1307K in 345 patients who were not Ashkenazi Jews using a heteroduplex screen. We also performed an extensive mutational analysis in this region of the APC gene on DNA extracted from 240 Italian, Finnish, and Hawaiian-Japanese colon tumors and determined replication error status. RESULTS: The I1307K mutation was not found among 345 non-Ashkenazis. Somatic mutations occurred at a lower frequency and were more randomly distributed when the I1307K allele was not present. The most common characteristic somatic mutation occurring around codon 1307 in I1307K-positive patients did not occur in tumors negative for the I1307K mutation. An association between mutations in the region around APC codon 1307 and mismatch repair deficiency was not found. CONCLUSIONS: Our findings support the hypothesis that the I1307K mutation is unique to the Ashkenazi Jews, contributes to tumor predisposition in colorectal cancer, and is unrelated to mismatch repair deficiency.

Adenomatous Polyposis Coli Protein↗
PubMedDate not supplied

Stable disease in advanced colorectal cancer: therapeutic implications.

Colorectal cancer is one of the most common neoplasms in Western Countries and ranks second as a cause of death due to cancer. The overall mortality at 5 years is about 40%. Patients with resectable metastatic disease can be cured, but for those who cannot, treatment is purely palliative, and overall survival (OS) is from approximately 7 to 24 months. Infusional regimen with modulated 5Fluorouracil (5FU) gives an objective response rate (RR) of up to 30-40%. The addition of CPT11 or oxaliplatin to 5FU improves RR, time to progression (TTP) and OS with a stabilization of disease (SD) in 40-70% of cases and 20-40%, respectively. The concurrent utilization of selective biological agents as growth factor receptors acting at a molecular level and influencing the processes of tumor formation and growth, increases tumor cell apoptosis and inhibits tumor growth; as a result, the tumor regresses or is inhibited, with consequently prolonged OS and TTP. This paper examines the problem related to the treatment of metastatic colorectal cancer with SD. Current doubts regarding the continuation of one treatment until disease progression (PD) with a risk of toxicity, whether or not to use a less toxic "maintenance" therapy after a fairly aggressive "induction" therapy in "stabilized" responders, or whether to stop the treatment in the presence of a SD confirmed after at least two consecutive evaluations, are present.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1979

Screening for colorectal cancer.

A voluntary colorectal screening program was carried out in North Carolina to evaluate the public's willingness to perform a do-it-yourself bowel test, to educate the public on the importance of routine colorectal screening, and to assess the efficacy of a small-scale screening program in detecting colorectal cancer. A screening kit was requested by 1,204 individuals after hearing or reading about the program; 770 kits were returned. Of 29 (3.7%) positive test results, six were negative after retesting. Adequate follow-up was available for 18 of the remaining 23 positive results. Thirteen were due to anal bleeding, diverticulosis, or heavy ingestion of aspirin; five were considered false-positive results, since no evidence of disease could be found. No cases of polypoid tumors or carcinoma were detected. The main value of such a program in an area with a small population base is to increase the awareness of the public of the importance of routine screening for colorectal cancer.

Adult↗
PubMed1995

Life-time risk of different cancers in hereditary non-polyposis colorectal cancer (HNPCC) syndrome.

Identification of hereditary non-polyposis colorectal cancer (HNPCC) indicates theoretical life-time risks of 50% for the descendants of an affected family member and of 100% for the true gene carriers. However, besides colorectal cancer (CRC), many other cancer types and sites are also involved, which gives reason to evaluate the magnitude of risk for various other cancer types. A detailed pedigree analysis of 40 families with HNPCC identified 414 patients affected with cancer. A Kaplan-Meier life-table analysis for the cumulative risk of various cancers was performed on the basis of the 293 putative gene carriers who had adequate clinical and histological documentation of their tumors. Cumulative risks were highest for colorectal (78%) and endometrial cancers (43%, women only), followed by gastric, biliary tract, urinary tract and ovarian cancers (19-9%). For the other probably HNPCC-related cancer types, such as small bowel carcinoma and brain tumors, the life-time risk was only 1%. The risk of any metachronous cancer reached 90% after treatment of CRC and 75% after endometrial cancer; the second tumor was most often a new CRC or endometrial cancer. CRC remains the most important cancer type in the HNPCC syndrome but does not develop in all gene carriers. This makes the decision of possible prophylactic colectomy for test-detected gene carriers difficult. Of the many other cancer types involved, at least endometrial cancer is common enough to necessitate a specific surveillance program.

Adenomatous Polyposis Coli↗
PubMed1985

Genetic and familial factors in colorectal cancer.

Of the patients with colorectal cancer, there are some with hereditary disorders such as familial polyposis coli, Gardner's syndrome, Turcot's syndrome, and cancer family syndrome in which colorectal adenocarcinoma develops at a significantly high frequency, and these hereditary diseases are very important and interesting from the viewpoint of carcinogenesis as well as tumorigenesis. On the other hand, Peutz-Jeghers syndrome and juvenile polyposis which likewise are hereditary diseases are often considered to be accompanied with colorectal cancer. On these grounds, 49 cases of familial polyposis coli (including Gardner's syndrome), 12 cases of Peutz-Jeghers syndrome, one case of juvenile polyposis, six pedigrees of cancer family syndrome, experienced at the National Cancer Center Hospital from 1962 to 1984 were reviewed with particular emphasis placed on the recent progress and the natural history of these diseases. Furthermore, a comparative study between single colorectal cancers (1,034 cases) and multiple ones (89 cases) was carried out from the standpoint of familial aggregation and cumulative age incidence. A high association with genetic factors was found in multiple primary colorectal cancer with a family history of colorectal cancer as well as in the well-known hereditary diseases mentioned above. The author presented a conception of the relationship between the human body and tumors from the viewpoint of a comparison among infantile and childhood tumors, hereditary tumors, familial aggregative tumors and the usual tumors observed in old age.

Adenoma↗
PubMed1996

Potential role of DNA polymerase beta in gene therapy against cancer: a case for colorectal cancer.

Genetic instability characterized by the accumulation of mutations of tumor suppressor genes and oncogenes appears to be associated with carcinogenesis in colorectal and other cancers. Mutations of DNA polymerase beta (pol beta) and related chromosomal alterations appear to be consistent with the causal role of a "mutator phenotype' in carcinogenesis. However, homozygous knockout pol beta mutations appear to interfere with embryogenesis. Increased pol beta activity (i.e. relative to pol alpha activity) has been associated with cell cycle arrest. The related aphidicolin-resistant DNA replication has been observed primarily in differentiating cells, including the mammalian blastocyst, adrenal cortex, thyroid, anterior pituitary, and the mechanism of endoreduplication (amitotic over-replication of DNA) can be traced to lower eukaryotes. This increased activity in relation to terminal commitment is inconsistent with a simple "DNA repair' view of pol beta. It is therefore proposed that pol beta may play a more fundamental role in cellular differentiation through involvement in a putative subgenomic DNA replication-based model of terminal gene expression. Thus genetic instability, loss of differentiation, and carcinogenesis may result from aberration(s) or "derailment' of such replication-based mechanism of terminal gene expression. It is suggested to examine the relationship of DNA pol beta to genomic instability and carcinogenesis using genetic analyses and antisense technology with possible applications for gene therapy against colorectal cancer.

Animals↗
PubMed2002

Efficacy and tolerability of irinotecan in patients with advanced colorectal cancer in Singapore.

INTRODUCTION: Colorectal cancer is the commonest malignancy encountered in Singapore. The long-term outcome of patients with advanced diseases is poor. For many decades, 5-fluorouracil was the only effective cytotoxic drug against colorectal cancers. Randomised trials have documented the efficacy of irinotecan in patients with metastatic colorectal cancer. We investigated the efficacy and safety profile of irinotecan (CPT-11), as a second-line treatment for an Asian population who had failed 5-fluorouracil-based chemotherapy. MATERIALS AND METHODS: A total of 33 patients were enrolled in the study between October 1996 and May 1999. This was an open label phase II study. All patients who had received at least one dose of CPT-11 were evaluated for toxicity. Thirty patients were evaluated for response. RESULTS: Six patients (20%) had partial responses and 1 (3%) experienced minor response. Fourteen patients (47%) progressed. Nine patients (30%) had stable disease. The range of time to progression was 5.8 months to 21 months. The median survival was 9.5 months. There was no treatment-related death. Seven patients (23%) who received treatment had diarrhoea. Only 2 of the 7 patients had grade 3-4 diarrhoea. Eleven patients (37%) suffered from haematological toxicity, of whom 2 patients had grade 3-4 neutropenia. CONCLUSION: We demonstrated efficacy and tolerability of CPT-11 in Singaporean patients with advanced colorectal cancer.

Adult↗
PubMed1995

Mutant K-ras in apparently normal mucosa of colorectal cancer patients. Its potential as a biomarker of colorectal tumorigenesis.

BACKGROUND: The best way to reduce the incidence of colorectal cancer mortality would be to prevent this cancer. However, none of the biomarkers proposed can accurately identify persons at increased risk of colorectal cancer or those at low risk. As a possible genetic biomarker, K-ras mutations, which are frequently found in colorectal cancers, were analyzed in apparently normal colorectal mucosa. METHODS: Nonneoplastic mucosa and tumor tissues were collected at surgery from 70 patients with colorectal cancer: one sample each from 50 patients (group A) and multiple samples from the other 20 patients (group B). Mutant K-ras codon 12 was analyzed by the enriched polymerase chain reaction (EPCR), by which one mutant can be detected among 10(3) to 10(4) normal alleles. RESULTS: Only with the aid of EPCR was mutant K-ras detected in nonneoplastic mucosa of nine patients (18%) in Group A and five patients (25%) in Group B. This increased incidence could be attributed to the multiple tissue sampling. The presence of mutant K-ras in nonneoplastic mucosae was not consistently correlated with that in the tumors. These findings suggest that the mutant K-ras identified in nonneoplastic mucosa actually represents de novo mutations, which may be initiated by different etiologic factors and at different times. CONCLUSION: Mutant K-ras detected in apparently normal mucosa should be a useful biomarker for identifying persons at higher risk of colorectal cancer. Our study also emphasizes the need for improving the method for sample collection to achieve true representation of the colorectal mucosa.

Adenocarcinoma↗
PubMed2003

Hereditary nonpolyposis colorectal cancer: preventive management.

Hereditary nonpolyposis colorectal cancer (HNPCC) is the most common form of hereditary colorectal cancer. Inherited mutations in the mismatch repair genes associated with this syndrome have an approximate 80% lifetime risk of colorectal cancer. Since there are no premonitory signs of susceptibility to HNPCC, family history is the initial method for identifying those at increased risk. At risk individuals should undergo genetic counseling and testing. Although an algorithmic indication for genetic testing in at risk HNPCC patients is yet to be determined, many advocate initial screening for microsatellite instability (MSI) of the cancer specimen in individuals suspected of carrying HNPCC mutations. Those who test positive for MSI can then undergo further testing for mutations in the associated germline mismatch repair genes. Techniques for detecting these mutations currently include in vitro synthesized-protein assay, single-strand conformational polymorphism, and DNA sequencing. Given the aggressive nature of HNPCC adenomas, individuals who test positive for HNPCC mutations are recommended to undergo yearly colonoscopic surveillance starting at the age of 25. A reasonable alternative to lifetime colonoscopic surveillance for the prevention of colorectal cancer in these individuals is prophylactic colectomy. The prevention of colorectal cancer through pharmacological means is under investigation as another option in the management of HNPCC patients. Specifically, chemoprevention trials are currently ongoing to evaluate the efficacy of COX-2 inhibitors in the prevention of colorectal cancer in HNPCC and familial adenomatous polyposis patients.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2006

Guidelines for colonoscopy surveillance after cancer resection: a consensus update by the American Cancer Society and the 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 and the 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 Stages 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 performed 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 examination is normal, then the interval before the next subsequent examination should be 5 years. Shorter intervals may be indicated by associated adenoma findings (see "Guidelines for Colonoscopy Surveillance After Polypectomy: A Consensus Update by the US Multi-Society Task Force on Colorectal Cancer and the American Cancer Society"). Shorter intervals also are 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.

Colectomy↗
PubMed2005

Cancer risk in hereditary nonpolyposis colorectal cancer syndrome: later age of onset.

BACKGROUND & AIMS: Mutations in the mismatch repair genes cause hereditary nonpolyposis colorectal cancer (HNPCC) syndrome and convey high lifetime cancer risks for colorectal (CRC) and endometrial cancer. Currently, cancer risks for individuals with HNPCC are based on data from clinically ascertained families. The purpose of this study was to re-examine the penetrance in HNPCC using a comprehensive dataset from a geographically defined region. METHODS: A combined dataset of 70 HNPCC families ascertained by traditional high-risk criteria and by molecular screening comprising 88 probands and 373 mutation-positive family members was used. Statistical methods were modified survival analysis techniques. RESULTS: In mutation-positive relatives (excluding probands), the median age at diagnosis of CRC was 61.2 years (confidence interval [CI], 56.3-68.0 y). The lifetime risk for CRC was 68.7% (CI, 58.6%-78.9%) for men and 52.2% (CI, 37.6%-66.9%) for women. Considering only probands, the median age at diagnosis of CRC was 44.0 years (CI, 41.0-46.3 y). Median age of onset of EC was 62.0 years (CI, 55.9 y to an upper limit too high to calculate) with a lifetime cancer risk of 54% (CI, 41.9%-66.1%). CONCLUSIONS: A markedly later age of onset for CRC at 61 y than previously reported (approximately 44 y) is suggested, resulting mainly from a more rigorous method of analysis in which all gene-positive individuals (both affected and unaffected with cancer) are considered. Lifetime cancer risks may be lower for CRC and endometrial cancer than presently assumed. If confirmed, these data suggest a need to alter counseling practices, and to consider HNPCC in older individuals than before.

Adaptor Proteins, Signal Transducing↗