A hall mark of human cancer, particularly solid tumor, is aneuploidy. Through a synthetic lethal screen with the Ras oncogene we have found that Ras mutant cancer cells exhibit increase mitotic stress. PURPOSE To study the effect of Ras mutation in mitosis and in chromosomal segregation. To understand the mechanisms by which mutant Ras affects the mitotic machinery. SIGNIFICANT MATERIALS AND METHODS We will use inducible Ras constructs to study its effect in cells that are synchronized to enter mitosis. FY2010 ACCOMPLISHMENT We have established constructs to expression Ras proteins in an inducible fashion.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Investigator-Initiated Intramural Research Projects (ZIA)
Project #
1ZIABC011259-01
Application #
8175348
Study Section
Project Start
Project End
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Budget End
Support Year
1
Fiscal Year
2010
Total Cost
$94,837
Indirect Cost
Name
National Cancer Institute Division of Basic Sciences
Department
Type
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Maity, Tapan K; Venugopalan, Abhilash; Linnoila, Ilona et al. (2015) Loss of MIG6 Accelerates Initiation and Progression of Mutant Epidermal Growth Factor Receptor-Driven Lung Adenocarcinoma. Cancer Discov 5:534-49
Weng, Meng-Tzu; Lee, Jih-Hsiang; Wei, Shu-Chen et al. (2012) Evolutionarily conserved protein ERH controls CENP-E mRNA splicing and is required for the survival of KRAS mutant cancer cells. Proc Natl Acad Sci U S A 109:E3659-67