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Carol Bernstein

Professor
Department of Cardiology
Union University
Azerbaijan

Biography

Dr. Bernstein is an associate professor of  Department of Cell biology & Anatomy in University of Arizona,USA. Dr. Bernstein\s proposed research has five major goals  One is to confirm preliminary data indicating dramatic deficiency in expression of DNA repair proteins ERCC1 and Pms2 as frequent early events forming large field defects in progression to colon cancer in humans  A second goal is to characterize the mechanisms by which the ERCC1 and/or Pms2 deficiencies arise  A third goal is to determine the mechanistic consequences of ERCC1 and/or Pms2 deficienciesA fourth goal is to characterize our new unique dietaryrelated wildtype mouse model of colon cancer to relate it to progression to colon cancer in humans  A fifth goal is to use this mouse model to determine the protective effects of dietary caffeic acid resveratrol phenethyl isothiocyanate PEITC found in cruciferous vegetables and curcumin in prevention of colon cancerI have long term demonstrated expertise and motivation to carry out the proposed work  As early as 1991 using deoxycholate and Chinese hamster ovary cells deficient in ERCC1 mutant cells UV4 I proposed that bile acids have an etiologic role in colon cancer by causing DNA damage  Since then I have been first author or coauthor on 41 additional articles on the roles of bile acids field defects and DNA repair enzymes in colon carcinogenesis as well as use of bile acids in mouse models of inflammation Barrett\s esophagus and promotion of colonic adenomas. The current application builds logically on my prior work and my physician coPI is a research oriented physician scientist who is actively involved in elucidating factors involved in progression to colon cancer. Dr. Bernstein is an associate professor of  Department of Cell biology & Anatomy in University of Arizona,USA. Dr. Bernstein\s proposed research has five major goals  One is to confirm preliminary data indicating dramatic deficiency in expression of DNA repair proteins ERCC1 and Pms2 as frequent early events forming large field defects in progression to colon cancer in humans  A second goal is to characterize the mechanisms by which the ERCC1 and/or Pms2 deficiencies arise  A third goal is to determine the mechanistic consequences of ERCC1 and/or Pms2 deficienciesA fourth goal is to characterize our new unique dietaryrelated wildtype mouse model of colon cancer to relate it to progression to colon cancer in humans  A fifth goal is to use this mouse model to determine the protective effects of dietary caffeic acid resveratrol phenethyl isothiocyanate PEITC found in cruciferous vegetables and curcumin in prevention of colon cancerI have long term demonstrated expertise and motivation to carry out the proposed work  As early as 1991 using deoxycholate and Chinese hamster ovary cells deficient in ERCC1 mutant cells UV4 I proposed that bile acids have an etiologic role in colon cancer by causing DNA damage  Since then I have been first author or coauthor on 41 additional articles on the roles of bile acids field defects and DNA repair enzymes in colon carcinogenesis as well as use of bile acids in mouse models of inflammation Barrett\s esophagus and promotion of colonic adenomas. The current application builds logically on my prior work and my physician coPI is a research oriented physician scientist who is actively involved in elucidating factors involved in progression to colon cancer.

Research Interest

DNA damage in initiation and progression to cancer,DNA repair in initiation and progression to cancer, Bile acids as an endogenous carcinogen,Diet in relation to cancer

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