By Icon Health Publications
It is a 3-in-1 reference e-book. It offers an entire clinical dictionary overlaying enormous quantities of phrases and expressions with regards to adenoma. It additionally offers huge lists of bibliographic citations. eventually, it offers info to clients on the way to replace their wisdom utilizing numerous net assets. The booklet is designed for physicians, clinical scholars getting ready for Board examinations, clinical researchers, and sufferers who are looking to get to grips with examine devoted to adenoma. in case your time is efficacious, this ebook is for you. First, you won't waste time looking out the web whereas lacking loads of suitable details. moment, the e-book additionally saves you time indexing and defining entries. eventually, you won't waste money and time printing thousands of websites.
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Additional info for Adenoma - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References
Sample text
Results may lead to better understanding of protective mechanisms involving aspirin and nonsteroidal anti-inflammatory drugs. , Room 501 Columbia, Sc 29208 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2004 Summary: (provided by applicant): Colorectal cancer is the second most common cause of cancer mortality in the United States. The maintenance of genomic integrity after DNA damage depends on the coordinated action of cell cycle checkpoint controls and DNA damage repair systems.
Our specific aims are: (i), (ii) To identify important interactions between both known and putative oncogenes and tumor suppressor genes from (a) defined signaling pathways, and (b) candidate genes identified in adenocarcinomas and precursors by cDNA expression array analysis and prioritized in Project 2 and 3. Tumor sample (360 total), including aberrant crypts, adenomas, adenocarcinomas, liver and lung metastasis will be analyzed. We will use molecular changes in key genes from the p53, cell cycle, apoptosis, Wnt signaling, RPTK signaling, and TGFbeta signaling pathways as the foundation for interpreting how such changes provide a cell survival advantage, and contribute to progressive autonomous growth and metastasis of colon cancers.
We hypothesize that germline mutations/polymorphisms of p53R2 result in differential susceptibility to colorectal neoplasia. We propose to 1) determine distributions and frequencies of germline mutations/polymorphisms of p53R2 in participants in a recently concluded community, colonoscopy-based case-control study of incident sporadic colorectal adenoma (n=174 cases and 226 controls); 2) investigate associations of these mutations/polymorphisms with risk for adenoma; 3) identify the precise mutation(s)/polymorphism(s) in the p53R2 gene responsible for altered DNA repair system mechanisms; and 4) conduct preliminary work on the functional significance of genetic variants in the regulatory region of p53R2.