No thesis selected. While there is a wide spectrum of cancers that people can develop, the main cause of death each year among these patients occurs when the primary tumor metastasizes. The current approaches used to combat cancer, such as radiation or commercial drugs, genereally have a low frequency of success if the tumors have already metastasized. Therefore, understanding the mechanism behind metastasis may provide the knowledge needed to develop more effective therapies. In order for metastasis to occur, malignant cells must be able to break free from the solid tumor mass and survive without signals from surrounding tumor cells. This suggests that disruption of cell-cell adhesions is a key step in promoting metastasis. By studying the mechanisms and components involved in maintaining these important interactions, especially in mouse models where progression of metastasis can be monitored in vivo, will provide a clearer understanding of how cell adhesion is disrupted in metastasis and the steps needed to prevent such an occurrence.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Predoctoral Individual National Research Service Award (F31)
Project #
1F31CA119944-01
Application #
7062681
Study Section
Special Emphasis Panel (ZRG1-ONC-P (29))
Program Officer
Bini, Alessandra M
Project Start
2005-09-30
Project End
2009-09-29
Budget Start
2005-09-30
Budget End
2006-09-29
Support Year
1
Fiscal Year
2005
Total Cost
$50,454
Indirect Cost
Name
Stanford University
Department
Radiation-Diagnostic/Oncology
Type
Schools of Medicine
DUNS #
009214214
City
Stanford
State
CA
Country
United States
Zip Code
94305
Beaudry, Veronica G; Jiang, Dadi; Dusek, Rachel L et al. (2010) Loss of the p53/p63 regulated desmosomal protein Perp promotes tumorigenesis. PLoS Genet 6:e1001168
Beaudry, Veronica G; Pathak, Navneeta; Koster, Maranke I et al. (2009) Differential PERP regulation by TP63 mutants provides insight into AEC pathogenesis. Am J Med Genet A 149A:1952-7