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A National Cancer Institute Workshop on Microsatellite Instability for cancer detection and familial predisposition: development of international criteria for the determination of microsatellite…
The spectrum of microsatellite alterations in noncolonic tumors was reviewed, and it was concluded that the above recommendations apply only to colorectal neoplasms.
Revised Bethesda Guidelines for hereditary nonpolyposis colorectal cancer (Lynch syndrome) and microsatellite instability.
- A. Umar, C. Boland, +20 authors S. Srivastava
- MedicineJournal of the National Cancer Institute
- 18 February 2004
This commentary summarizes the Workshop presentations on HNPCC and MSI testing; presents the issues relating to the performance, specificity, and specificity of the Bethesda Guidelines; outlines the revised Bethesda Guidelines for identifying individuals at risk for H NPCC; and recommend criteria for MSI testing.
Clues to the pathogenesis of familial colorectal cancer.
Molecular features of "familial" cancers were compared with those of sporadic colon cancers, and a mechanism for familial tumorigenesis different from that mediated by classic tumor suppressor genes is suggested.
Comprehensive molecular characterization of human colon and rectal cancer
Integrative analyses suggest new markers for aggressive colorectal carcinoma and an important role for MYC-directed transcriptional activation and repression.
Genetic alterations during colorectal-tumor development.
- B. Vogelstein, E. Fearon, +7 authors J. Bos
- Biology, MedicineThe New England journal of medicine
- 1 September 1988
It is found that ras-gene mutations occurred in 58 percent of adenomas larger than 1 cm and in 47 percent of carcinomas, which are consistent with a model of colorectal tumorigenesis in which the steps required for the development of cancer often involve the mutational activation of an oncogene coupled with the loss of several genes that normally suppress tumors.
Pathology and genetics of tumours of the digestive system
Incidence and functional consequences of hMLH1 promoter hypermethylation in colorectal carcinoma.
- J. Herman, A. Umar, +12 authors S. Baylin
- Biology, MedicineProceedings of the National Academy of Sciences…
- 9 June 1998
The results suggest that microsatellite instability in sporadic colorectal cancer often results from epigenetic inactivation of hMLH1 in association with DNA methylation.
APC mutations occur early during colorectal tumorigenesis
Evidence is provided that mutations of the APC gene play a major role in the early development of colorectal neoplasms, and the frequency of such mutations remained constant as tumours progressed from benign to malignant stages.
Inactivation of the DNA repair gene O6-methylguanine-DNA methyltransferase by promoter hypermethylation is a common event in primary human neoplasia.
- M. Esteller, S. Hamilton, P. Burger, S. Baylin, J. Herman
- Biology, MedicineCancer research
- 15 February 1999
The presence of aberrant hypermethylation was associated with loss of MGMT protein, in contrast to retention of protein in the majority of tumors without aberrantHypermethylation, suggesting that epigenetic inactivation of MG MT plays an important role in primary human neoplasia.
Tumor microsatellite-instability status as a predictor of benefit from fluorouracil-based adjuvant chemotherapy for colon cancer.
- C. Ribic, D. Sargent, +10 authors S. Gallinger
- MedicineThe New England journal of medicine
- 17 July 2003
F fluorouracil-based adjuvant chemotherapy benefited patients with stage II or stage III colon cancer with microsatellite-stable tumors or tumors exhibiting low-frequency micros satellite instability but not those with tumors exhibiting high-frequencymicrosatellite instability.