I have found that the c-myb proto-oncogene increases the expression of the IGF-1 growth factor and its receptor. The purpose of the present application is to study the relationship between the growth promoting activity of c-myb and the production of IGF-1 and IGF-1 receptor. Our studies could throw light on the mechanism(s) by which myb exerts its oncogenic potential.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Project (R01)
Project #
1R01CA055541-01A1
Application #
3200029
Study Section
Metabolic Pathology Study Section (MEP)
Project Start
1992-08-01
Project End
1995-07-31
Budget Start
1992-08-01
Budget End
1993-07-31
Support Year
1
Fiscal Year
1992
Total Cost
Indirect Cost
Name
Thomas Jefferson University
Department
Type
Schools of Medicine
DUNS #
061197161
City
Philadelphia
State
PA
Country
United States
Zip Code
19107
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Michieli, P; Chedid, M; Lin, D et al. (1994) Induction of WAF1/CIP1 by a p53-independent pathway. Cancer Res 54:3391-5
Fiscella, M; Zambrano, N; Ullrich, S J et al. (1994) The carboxy-terminal serine 392 phosphorylation site of human p53 is not required for wild-type activities. Oncogene 9:3249-57
Lin, D; Fiscella, M; O'Connor, P M et al. (1994) Constitutive expression of B-myb can bypass p53-induced Waf1/Cip1-mediated G1 arrest. Proc Natl Acad Sci U S A 91:10079-83