The objective of this proposal is to investigate the hormonal requirements for the development of ovarian and testicular tumors in inhibin-deficient mice and the cachexia that is associated with the progression of these tumors. Using the inhibin-deficient mouse model developed by the investigator, the following studies are proposed.
Aim 1 will examine the individual roles of FSH and LH in tumor development and progression in inhibin-deficient mice.
Aim 2 will characterize the requirements for gonadal steroids in the development and progression of tumors in the inhibin-deficient mice.
Aim 3 will determine if overexpression of follistatin can prevent the activin-mediated cachexia-like syndrome that occurs in the inhibin-deficient mice.
Aim 4 will define the pattern of expression/extinction of cell cycle regulatory molecules that accompanies tumor development and growth.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Project (R01)
Project #
5R01CA060651-06
Application #
2683541
Study Section
Biochemical Endocrinology Study Section (BCE)
Program Officer
Marks, Cheryl L
Project Start
1993-08-01
Project End
2001-03-31
Budget Start
1998-04-01
Budget End
1999-03-31
Support Year
6
Fiscal Year
1998
Total Cost
Indirect Cost
Name
Baylor College of Medicine
Department
Pathology
Type
Schools of Medicine
DUNS #
074615394
City
Houston
State
TX
Country
United States
Zip Code
77030
Balhara, Jyoti; Shan, Lianyu; Zhang, Jingbo et al. (2017) Pentraxin 3 deletion aggravates allergic inflammation through a TH17-dominant phenotype and enhanced CD4 T-cell survival. J Allergy Clin Immunol 139:950-963.e9
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Yatsenko, A N; Iwamori, N; Iwamori, T et al. (2010) The power of mouse genetics to study spermatogenesis. J Androl 31:34-44

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