Regulation of Wnt: Clues for breast cancer pathognesis
|Institution:||University of California, Irvine|
Heidi Theisen , Ph.D. -
|Award Cycle:||1997 (Cycle III)||Grant #: 3FB-0090||Award: $13,849|
|Award Type:||Postdoctoral Fellowship|
|Pathogenesis>Too much cell growth: defective messages and internal signaling|
Initial Award Abstract (1997)
Genes that direct normal development are also involved in controlling cell division. Abnormalities in the regulation of these genes have been linked to breast cancer development. For example, the Wnt gene is required for normal development, but alterations in the amount of Wnt protein it makes are associated with abnormal proliferation in human breast tissue. In order to perform its function, Wnt turns on a series of other proteins in the cell. The interruption of any stage of this process could have an effect on the growth of cells. Another protein that is associated with breast cancer development, TGFb, can both regulate and be regulated by Wnt. An understanding of how these genes function to regulate cell division may elucidate how tumor cells proliferate and invade host tissues. In this project, I will analyze what occurs within cells in response to Wnt and TGFb. I will look at the effect on cellular proliferation when each protein of the series is blocked from being turned on. I will also examine how proteins turned on by Wnt block TGFb function, and how proteins turned on by TGFb block Wnt function. Understanding the interaction of Wnt and TGFb could conceivably permit the development of strategies for designing improved methods for breast cancer intervention and treatment.
Final Report (1997)
PI resigned after 3 months
Regeneration in Insects
Periodical:Seminars in Cell and Developmental Biology
Index Medicus: Semin Cell Dev Biol
Authors: Marsh, J.L. and Theisen, H.
|Yr: 1999||Vol: 10||Nbr: 4||Abs:||Pg:365-75|