Tags

Type your tag names separated by a space and hit enter

Multistep carcinogenesis in colorectal cancers.
Southeast Asian J Trop Med Public Health. 1995; 26 Suppl 1:190-6.SA

Abstract

Recent advances in molecular genetics have revealed that multiple genetic alterations including activation of oncogenes and inactivation of tumor suppressor genes are required for tumor development and progression. Tumorigenesis of colorectal cancer, in which most cancers are considered to arise from preceding benign adenomas, has been well documented at the molecular level. Familial adenomatous polyposis (FAP), which is characterized by the development of hundreds to thousands of adenomatous polyps in the colon and rectum, one or more of which can progress to cancer if left without surgical treatment, is a good model for elucidation of genetic alterations involved in colorectal tumorigenesis. The adenomatous polyposis coli (APC) gene responsible for FAP was isolated in 1991, and germinal and somatic mutations of the APC gene have been identified. Moreover, activation of K-ras oncogene and inactivation of several tumor suppressor genes such as MCC, p53, and DCC are supposed to play important roles at specific stages of colorectal tumorigenesis. More recently, two genes, MSH2 and MLH1, responsible for hereditary non-polyposis colorectal cancer (HNPCC) have been identified. Thus the molecular mechanism of colorectal tumorigenesis now seems to be more complicated than has been supposed.

Authors+Show Affiliations

Department of Medical Genetics, Osaka University Medical School, Japan.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

8629105

Citation

Takami, K, et al. "Multistep Carcinogenesis in Colorectal Cancers." The Southeast Asian Journal of Tropical Medicine and Public Health, vol. 26 Suppl 1, 1995, pp. 190-6.
Takami K, Yana I, Kurahashi H, et al. Multistep carcinogenesis in colorectal cancers. Southeast Asian J Trop Med Public Health. 1995;26 Suppl 1:190-6.
Takami, K., Yana, I., Kurahashi, H., & Nishisho, I. (1995). Multistep carcinogenesis in colorectal cancers. The Southeast Asian Journal of Tropical Medicine and Public Health, 26 Suppl 1, 190-6.
Takami K, et al. Multistep Carcinogenesis in Colorectal Cancers. Southeast Asian J Trop Med Public Health. 1995;26 Suppl 1:190-6. PubMed PMID: 8629105.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Multistep carcinogenesis in colorectal cancers. AU - Takami,K, AU - Yana,I, AU - Kurahashi,H, AU - Nishisho,I, PY - 1995/1/1/pubmed PY - 1995/1/1/medline PY - 1995/1/1/entrez SP - 190 EP - 6 JF - The Southeast Asian journal of tropical medicine and public health JO - Southeast Asian J. Trop. Med. Public Health VL - 26 Suppl 1 N2 - Recent advances in molecular genetics have revealed that multiple genetic alterations including activation of oncogenes and inactivation of tumor suppressor genes are required for tumor development and progression. Tumorigenesis of colorectal cancer, in which most cancers are considered to arise from preceding benign adenomas, has been well documented at the molecular level. Familial adenomatous polyposis (FAP), which is characterized by the development of hundreds to thousands of adenomatous polyps in the colon and rectum, one or more of which can progress to cancer if left without surgical treatment, is a good model for elucidation of genetic alterations involved in colorectal tumorigenesis. The adenomatous polyposis coli (APC) gene responsible for FAP was isolated in 1991, and germinal and somatic mutations of the APC gene have been identified. Moreover, activation of K-ras oncogene and inactivation of several tumor suppressor genes such as MCC, p53, and DCC are supposed to play important roles at specific stages of colorectal tumorigenesis. More recently, two genes, MSH2 and MLH1, responsible for hereditary non-polyposis colorectal cancer (HNPCC) have been identified. Thus the molecular mechanism of colorectal tumorigenesis now seems to be more complicated than has been supposed. SN - 0125-1562 UR - https://www.unboundmedicine.com/medline/citation/8629105/Multistep_carcinogenesis_in_colorectal_cancers_ L2 - https://medlineplus.gov/colorectalcancer.html DB - PRIME DP - Unbound Medicine ER -