Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Colorectal Cancer”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed2002

The risk of subsequent primary cancers after colorectal cancer in southeast England.

BACKGROUND: Multiple cancers may occur in an individual because of a genetic predisposition, environmental exposure, cancer therapy, or immunological deficiency. Colorectal cancer is one of the most commonly diagnosed cancers, and inherited factors play an important role in its aetiology. AIMS: To characterise the occurrence of multiple primary cancers in patients diagnosed with colorectal cancer and explore the possibility of a common aetiology for different cancer sites. PATIENTS: The Thames Cancer Registry database was used to identify patients with a first colorectal cancer, resident in the North or South Thames region, diagnosed between 1 January 1961 and 31 December 1995. A total of 127 281 patients were included, 61 433 men and 65 848 women. METHODS: Observed numbers of cancers occurring after the diagnosis of colorectal cancer were compared with expected numbers, calculated using appropriate age, sex, and period specific rates, to obtain standardised incidence ratios. The occurrence of colorectal cancers subsequent to cancers at other sites was also examined. RESULTS: Small intestinal cancer was significantly increased in men diagnosed with colorectal cancer before the age of 60 years and in women diagnosed with colorectal cancer after the age of 65 years. Colorectal cancer was also significantly increased after a first diagnosis of cancer of the small intestine. Other cancer sites with a significant increase after colorectal cancer included the cervix uteri, corpus uteri, and ovary. CONCLUSIONS: Patients with colorectal cancer are at increased risk of developing cancer at a number of other sites. Some of these associations are consistent with the effects of known inherited cancer susceptibility genes.

Adult↗
PubMed1999

Dietary factors in human colorectal cancer.

Colorectal cancer is a significant cause of mortality in Western societies. The progression of the disease from normal colonic epithelium to the acquisition of the malignant phenotype is accompanied by numerous genetic and epigenetic alterations. Compelling experimental and epidemiological evidence indicates that diet and nutrition are key factors in the modulation of colorectal cancer. A salient case in point is the recent observation that a dietary regimen based on a Western-style diet provokes in the rodent colon the appearance of preneoplastic lesions in the absence of any genotoxic insult. This review mainly describes dietary factors that inhibit the development and progression of colorectal cancer. Much is unknown about the precise mechanisms of action of chemically disparate nutrients and how they interfere with the development and progression of this disease. Current knowledge about this important issue is summarized. We believe that continuing scrutiny and precise assessment of the benefits (and potential risks) of nutrients in the treatment and prevention of colorectal cancer will prove significant to controlling this devastating disease.

Animals↗
PubMed2000

The epigenetics of colorectal cancer.

Colorectal cancer has provided an excellent model for studying the genetic basis of cancer and is one of the better-understood malignancies in this regard. The orderly progression of the disease, with distinct genetic alterations at each step, is a useful framework for deciphering the molecular basis of neoplasia. Epigenetics, the study of clonal changes in gene expression without associated genetic lesions, has raised increased interest recently, in part because of the identification of DNA methylation as a potential molecular mediator of the process. Several tumor-suppressor genes are silenced in various neoplasms in association with aberrant promoter methylation, and in the absence of coding region mutations. The study of DNA methylation changes in colorectal cancer has now provided additional clues into the pathogenesis of the disease. This review presents evidence for a model whereby DNA methylation changes play two distinct roles in the molecular evolution of colorectal cancer. Initially, progressive methylation and silencing of a subset of genes takes place in normal tissues as a function of age or time-dependent events and predisposes these normal cells to neoplastic transformation. At a later stage of disease progression, DNA methylation plays an important role in a subset of tumors affected by the CpG island methylator phenotype (CIMP), a recently identified pathway that results in a form of epigenetic instability through the simultaneous silencing of multiple genes. DNA methylation changes have important interactions with genetic lesions in this cancer type. CIMP+ cancers include the majority of tumors with sporadic mismatch repair deficiency through hypermethylation of the hMLH1 promoter, and also account for the majority of tumors with Ki-ras mutations through an unknown mechanism. By contrast, CIMP- cases evolve along a more classic genetic instability pathway, with a high rate of p53 mutations and chromosomal changes. Thus, the integration of epigenetic and genetic information provides a more complete molecular understanding of colorectal cancer and may have implications for the diagnosis, prognosis, and treatment of patients affected by this disease.

Adaptor Proteins, Signal Transducing↗
PubMed2006

Expression and genomic profiling of colorectal cancer.

Colorectal cancer still represents a paradigm for the elucidation of the cellular, genetic and molecular mechanisms that underly solid tumor initiation, progression to malignancy, and metastasis to distal organ sites. The relative ease with which pathological specimens can be obtained by either surgery or endoscopy from different stages of tumor progression has facilitated the application of omics technologies to allow the genome-wide analysis both at the RNA (gene expression) and DNA (aneuploidy) levels. Here, we have reviewed the multiplicity of studies appeared to date in the scientific literature on the expression and genomic analysis of colorectal cancer, and attempted an integration of the profiling data generated and made available in the public domain. This approach is likely to pinpoint specific chromosomal loci and the corresponding genes which (i) play rate-limiting roles in colorectal cancer, (ii) represent putative diagnostic and prognostic markers for the accurate prediction of clinical outcome and response to treatment, and (iii) encompass potential therapeutic targets. Moreover, cross-species data mining and integration of the human colorectal cancer profiles with those obtained from mouse models of intestinal tumorigenesis will even more contribute to the elucidation of highly conserved pathways and cellular functions underlying malignancy in the GI tract. Notwithstanding the above promises, tumor heterogeneity, limited cohort sizes, and methodological differences among experimental and bioinformatic approaches still poses main obstacles towards the optimal utilization and integration of omics profiles.

Adenoma↗
PubMed2000

Catenins and their associated proteins in colorectal cancer.

Colorectal cancer is the second most common cause of cancer mortality in the western world. Colorectal cancer has been well studied, and the genetic steps involved in the adenoma to carcinoma sequence have been well elucidated. The first genetic alteration, found in 85% of adenomas, are mutations in the adenomatous polyposis coli (APC) gene. However, the consequences of this and the exact function of APC in the colon is not fully understood. It has been suggested that APC could function through its regulation of beta-catenin, an ubiquitous cytoskeletal protein with multiple binding specificities resulting in diverse functions including cell growth, adhesion, and migration. Any change in these associations may play a role in colorectal cancer development and progression.

Adenoma↗
PubMed2004

[Early diagnosis of colorectal cancer].

Colorectal cancer is the fourth most common cancer in the world and the second most common and most frequently mentioned cause of cancer death in Poland. Death from colorectal cancer can be reduced through early diagnosis. Currently there are several screening methods: faecal occult blood tests, sigmoidoscopy, colonoscopy, barium enema and emerging methods like virtual colonoscopy and faecal DNA testing. In this article we show the efficacy of these tests with respect to their sensitivity, specificity, costs and safety. Patients at high-risk of colorectal cancer were also considered. There is an urgent need to standardize the methods of diagnosis in patients at high-risk to increasing accessibility and quality of tests.

Biopsy↗
PubMed2002

Screening for colorectal cancer.

Colorectal cancer screening can prevent the development of colorectal cancer and reduce the risk for death. Screening recommendations include fecal occult blood testing, sigmoidoscopy, radiographic imaging of the colon, and colonoscopy. This article focuses on recommendations for average-risk individuals and discusses the potential benefits and limitations of each. High-risk individuals should be screened with colonoscopy. Cost-effectiveness analyses of colorectal cancer screening are summarized.

Colonoscopy↗
PubMed1993

Natural history of the colorectal cancer.

Colorectal cancer appears as a continuous process, starting with the normal cells and progressively growing towards malignancy. The aim of this review is to focus on the stages of that transformation and the means available for reducing the risk of this particular cancer. Although genetic factors have been identified, dietary pattern, the presence of inflammatory bowel disease and adenomas seem to play the most important role in the occurrence of colorectal cancer. The prevention of colorectal cancer should include changes in dietary habits, resection of adenomatous polyps as well as early detection of cancer. Studies testing these approaches are few and so far, none has proven effective in improving survival.

Cell Transformation, Neoplastic↗
PubMed1987

Colorectal cancer.

Colorectal cancer is one of the leading causes of death in older men and women. Therefore, this age-related cancer is of particular importance to geriatricians. The high incidence of this cancer may be decreased by dietary modifications recommended by the American Cancer Society. Early cancer detection is important to improve survival. When colorectal cancer is detected in the asymptomatic patient, there is a high likelihood of cure. Therefore, screening individuals at high risk is a major goal. Because age is the leading risk factor for colorectal cancer, the American Cancer Society has developed guidelines for screening individuals over age 40 years. Treatment decisions are based on stage of disease. For localized disease, surgical resection is the primary therapy. In advanced disease, palliative treatment may include the use of surgery, radiotherapy, chemotherapy, or a combination of these modalities. Because there is no evidence of an age effect, principles of treatment should be applied similarly in geriatric and younger patients.

Aged↗
PubMed1999

Mouse models for colorectal cancer.

Colorectal cancer (CRC) is one of the most common cancers in the Western world. Much has been learned about colorectal cancer from human inherited syndromes, such as familial adenomatous polyposis (FAP) and hereditary non-polyposis colorectal cancer (HNPCC). Mouse models for CRC were generated by introducing mutations into the mouse genes, whose human counterparts were implicated in the onset and progression of CRC. Central among these are mice carrying mutations in the Adenomatous polyposis coli (Apc) gene. Although most of these Apc mutations share some common phenotypes as homozygous embryonic lethality and tumor predisposition, the severity of the tumor predisposition is variable. Mice with mutations in the mismatch repair genes, Msh2 and Mlh1, exhibit a mismatch repair defect and are predisposed to developing gastrointestinal cancer, lymphomas and tumors of other organ systems. Mice carrying a mutation in the Pms2 gene are predisposed to lymphomas and other tumors. Mice with a mutation in the Msh6 gene have a defect in base mismatch repair and show a tumor predisposition phenotype. Mice with mutations in Mlh1, Pms2 and Msh5 have defects in meiosis suggesting unique roles for these genes in gametogenesis.

Adenomatous Polyposis Coli↗
PubMedDate not supplied

Adjuvant treatment for colorectal cancer.

Colorectal cancer is a leading cause of cancer in Western countries. Surgery remains the only way to cure it. Recent trials led to the general acceptance of adjuvant chemotherapy in Dukes C cancer by identifying bolus 5FU and leucovin during 6 months (5 days monthly) as the current standard. The role of adjuvant chemotherapy remains questionable in Dukes B2 (stage II) colon cancer, in rectal cancer and after curative resection of liver metastases. The development of total mesorectum excision (TME) technique has dramatically resulted in improving local recurrence control and will be the standard in rectal cancer surgery; preoperative irradiation is widely used in Europe for stage II and III rectal cancer but its definite place and its optimal regimen await further assessment as well as the role of adjuvant chemotherapy in rectal cancer. New chemotherapeutic combinations based on new effective agents in colorectal cancer such as CPT-11 and oxaliplatine have been currently used for downstaging liver metastases initially unresectable. This new approach, combined with the development of local ablative therapies such as cryotherapy and radiofrequency allows curative strategies in a significant number of patients primarily unfit for surgical resection of liver mets. The present paper aims to review the different aspect of (neo)adjuvant therapies in the multimodal curative management of colorectal cancers.

Aged↗
PubMed2003

Genetic testing for hereditary nonpolyposis colorectal cancer.

Colorectal cancer remains a major cause of morbidity and mortality in United States. While most newly diagnosed cases are sporadic, a small percent of colorectal cancers are due to hereditary cancer syndromes, of which hereditary nonpolyposis colorectal cancer (HNPCC) is the most common. HNPCC is caused by mutations resulting in defective DNA mismatch repair gene function. Advances in molecular technology have enabled us to use genetic testing for HNPCC genes to identify high-risk families. Over the past several years, genetic testing for HNPCC has evolved from a research endeavor to a clinical test that often is an integral part of providing care for high-risk families. This article reviews the available genetic tests, genetic testing recommendations, interpretation of test results, and the clinical impact of genetic testing for HNPCC.

Journal Article↗
PubMed2002

[Current status of nuclear medicine. Clinical application of FDG-PET for cancer diagnosis. Colorectal cancer].

In Japan, colorectal cancer is the third most common cause of death from cancer. The recurrence rate after curative surgical treatment for colorectal cancer has been estimated at 30-40%, most frequently occurring within 3 years. Therefore, more accurate staging of recurrent colorectal cancer is required for more appropriate management decisions. This article focuses on the clinical value of PET with [18F]fluorodeoxyglucose (FDG) in the diagnosis of recurrent and primary colorectal cancers. The technical issues in clinical practice and the cost-effectiveness of FDG-PET in staging recurrent colorectal cancer will be covered.

Colorectal Neoplasms↗
PubMed1998

DNA mismatch repair and colorectal cancer.

Colorectal cancer is the second commonest malignancy in the western world, accounting for 20,000 deaths in the U.K. per year. Over the last 10 years, great strides have been made in our understanding of the molecular controls governing the transition from normal mucosa, through adenoma, and finally to carcinoma. This review focuses on the recently discovered DNA mismatch repair pathway and its role in the development of both sporadic and an inherited form of colorectal cancer, namely hereditary non-polyposis colorectal cancer (HNPCC).

Animals↗
PubMed1996

The role of immunoscintigraphy in the staging and management of colorectal cancer.

Colorectal cancer has continued to increase in incidence over the past 25 years. It now ranks as the second most common noncutaneous malignancy for men and women together. The projected 1995 statistics predict 153,000 new cases in the United States, with 109,000 of colonic origin and 44,000 cancers of the rectum. The shift to more proximal colonic involvement and a decrease in size of the presenting lesion is again noted. Unfortunately, the warning signals (rectal bleeding, change in bowel habits and, later, abdominal pain, distention, and weight loss), often become evident only after the tumor has progressed significantly in the patient. Despite improvements in endoscopic detection, anesthesia, pre- and postoperative care and more extensive en-bloc resections, the cure rate for all patients with colorectal cancer remains unchanged at 53 per cent at five years. Although radical resectional surgery is relied on for locoregional control of the disease, there has been an increased use of cross-sectional radiologic studies for staging of the cancer. This newer management of colorectal cancer is the result of a better understanding of the natural history and biologic behavior of the cancer. The main strategy presently is to diagnose the disease sooner, stage the cancer more accurately, select tumors that will respond to adjuvant therapy, and detect recurrences more efficiently. It is in the area of staging of the primary tumor and accurate localization of recurrences that this new modality, immunoscintigraphy, is felt to have an impact.

Adenocarcinoma↗
PubMed2005

Mathematical models for the early detection and treatment of colorectal cancer.

Colorectal cancer is a major cause of death for men and women in the Western world. When the cancer is detected through an awareness of the symptoms by a patient, typically it is at an advanced stage. It is possible to detect cancer at an early stage through screening and the marked differences in survival for early and late stages provide the incentive for the primary prevention or early detection of colorectal cancer. This paper considers mathematical models for colorectal cancer screening together with models for the treatment of patients. Illustrative results demonstrate that detailed attention to the processes involved in diseases, interventions and treatment enable us to combine data and expert knowledge from various sources. Thus a detailed operational model is a very useful tool in helping to make decisions about screening at national and local levels.

Colorectal Neoplasms↗