Abstract

The overall goal of the proposed research is to investigate the roles of cellular homologs of retroviral transforming genes in non-virus induced neoplasms. Transforming genes detected by transfection of tumor DNAs will be compared with retroviral transforming genes by nucleic acid hybridization. Since the transforming genes of human bladder and lung carcinomas are cellular homologs of the ras genes of Harvey and Kirsten sarcoma viruses, we will investigate the range of carcinomas in which activated ras genes can be detected. Molecular clones of ras genes activated in neoplams will be compared with molecular clones of normal cell ras genes to determine the alterations responsible for activation of transforming potential during carcinogenesis. Expression of these genes in carcinomas and normal cells will be studied to investigate the correlation between gene expression and activation of transforming activity during neoplasia.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Project (R01)
Project #
5R01CA018689-11
Application #
3165029
Study Section
Molecular Biology Study Section (MBY)
Project Start
1976-06-30
Project End
1988-04-30
Budget Start
1986-05-01
Budget End
1987-04-30
Support Year
11
Fiscal Year
1986
Total Cost
Indirect Cost

  Institution

Name
Dana-Farber Cancer Institute
Department
Type
DUNS #
149617367
City
Boston
State
MA
Country
United States
Zip Code
02115

  Publications

Adams, Kenneth W; Kletsov, Sergey; Lamm, Ryan J et al. (2017) Role for Egr1 in the Transcriptional Program Associated with Neuronal Differentiation of PC12 Cells. PLoS One 12:e0170076
Nayak, G; Cooper, G M (2012) p53 is a major component of the transcriptional and apoptotic program regulated by PI 3-kinase/Akt/GSK3 signaling. Cell Death Dis 3:e400
Terragni, Jolyon; Nayak, Gauri; Banerjee, Swati et al. (2011) The E-box binding factors Max/Mnt, MITF, and USF1 act coordinately with FoxO to regulate expression of proapoptotic and cell cycle control genes by phosphatidylinositol 3-kinase/Akt/glycogen synthase kinase 3 signaling. J Biol Chem 286:36215-27
Tullai, John W; Graham, Julie R; Cooper, Geoffrey M (2011) A GSK-3-mediated transcriptional network maintains repression of immediate early genes in quiescent cells. Cell Cycle 10:3072-7
Tullai, John W; Tacheva, Silvia; Owens, Laura J et al. (2011) AP-1 is a component of the transcriptional network regulated by GSK-3 in quiescent cells. PLoS One 6:e20150
Mullenbrock, Steven; Shah, Janki; Cooper, Geoffrey M (2011) Global expression analysis identified a preferentially nerve growth factor-induced transcriptional program regulated by sustained mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) and AP-1 protein activation during PC12 cell dif J Biol Chem 286:45131-45
Graham, Julie R; Tullai, John W; Cooper, Geoffrey M (2010) GSK-3 represses growth factor-inducible genes by inhibiting NF-kappaB in quiescent cells. J Biol Chem 285:4472-80
Graham, Julie R; Hendershott, Melissa C; Terragni, Jolyon et al. (2010) mRNA degradation plays a significant role in the program of gene expression regulated by phosphatidylinositol 3-kinase signaling. Mol Cell Biol 30:5295-305
Saxena, Utsav H; Owens, Laura; Graham, Julie R et al. (2010) Prolyl isomerase Pin1 regulates transcription factor LSF (TFCP2) by facilitating dephosphorylation at two serine-proline motifs. J Biol Chem 285:31139-47
Saxena, Utsav H; Powell, Christina M H; Fecko, Jill K et al. (2009) Phosphorylation by cyclin C/cyclin-dependent kinase 2 following mitogenic stimulation of murine fibroblasts inhibits transcriptional activity of LSF during G1 progression. Mol Cell Biol 29:2335-45

Showing the most recent 10 out of 44 publications