Journal article
Cyclin E1 deregulation occurs early in secretory cell transformation to promote formation of fallopian tube-derived high-grade serous ovarian cancers
AM Karst, PM Jones, N Vena, AH Ligon, JF Liu, MS Hirsch, D Etemadmoghadam, DDL Bowtell, R Drapkin
Cancer Research | Published : 2014
Abstract
The fallopian tube is now generally considered the dominant site of origin for high-grade serous ovarian carcinoma. However, the molecular pathogenesis of fallopian tube-derived serous carcinomas is poorly understood and there are few experimental studies examining the transformation of human fallopian tube cells. Prompted by recent genomic analyses that identified cyclin E1 (CCNE1) gene amplification as a candidate oncogenic driver in high-grade serous ovarian carcinoma, we evaluated the functional role of cyclin E1 in serous carcinogenesis. Cyclin E1 was expressed in early-and late-stage human tumor samples. In primary human fallopian tube secretory epithelial cells, cyclin E1 expression i..
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Awarded by National Cancer Institute
Funding Acknowledgements
This work was supported by grants from the National Cancer Institute at the NIH P50-CA105009 (R. Drapkin), NIH U01 CA-152990 (R. Drapkin), NIH R21 CA-156021 (R. Drapkin); the Honorable Tina Brozman 'Tina's Wish' Foundation (R. Drapkin), the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation (R. Drapkin), the Robert and Debra First Fund (R. Drapkin), the Gamel Family Fund (R. Drapkin), a Canadian Institutes of Health Research Fellowship (A. M. Karst), a Kaleidoscope of Hope Foundation Young Investigator Research Grant (A. M. Karst), and a National Health and Medical Research Council project grant (APP 1042358; D. D. L. Bowtell).