• Braunschweiger, Paul G (PI)

Project: Research project

Project Details


Previous studies in a variety of experimental solid tumor models in mice
and rats indicated that dexamethasone (dex) can induce a reversible G 1 block in cell cycle progression. Following cessation of treatment, the
time for cell cycle progression (delta t) is directly related to dex dose
and glucocorticoid receptor content (GR) of the tumor and can be described
by delta t = (Tc) (mg/m 2 ) (2.2 x 10 -4 GR + 2.3 x 10 -3 ). Studies
employing 5FU, VCR, 5FU + VCR, and CP indicated that the effectiveness of
these agents could be significantly increased if administered during the
delta t interval. The purpose of this project is to investigate the
predictability of the dex response model as xenograft models of human
melanoma and lung cancer, as well as in selected patients with advanced
metastatic disease. Other studies are designed to evaluate the feasibility
of using corticosteroid hormone treatments to predictably manipulate the
timing of proliferative recovery in solid tumors after cytotoxic
cytoreduction and how such strategies effect recovery and chemosensitivity
of critical normal tissues. (D)
Effective start/end date9/1/8210/31/86


  • National Institutes of Health


  • Medicine(all)


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