Prostate cancer. Chemotherapy

Abstract

Several chemotherapeutic drugs have been shown to be potentially effective in the patient with metastatic hormone refractory prostate cancer. Individual patients who respond to these chemotherapy agents survive longer than nonresponders, but overall objective response rates for the entire group have been disappointingly small, the length of response short, and there has been no overall survival advantage. Combination chemotherapy has not yet been shown to be superior to single-agent chemotherapy in controlled phase III clinical trials. If chemotherapy drugs are administered to such patients, it is desirable to give them as part of protocols designed to gather reliable data on their risks and benefits.

Epidermal growth factor receptor-dependent stimulation of amphiregulin expression in androgen-stimulated human prostate cancer cells.

“…Prostate cancer, the most commonly diagnosed cancer and the second leading cause of cancer death among males in the United States (Boring et al, 1993), is stimulated by androgens, and hormone deprivation is the primary treatment for advanced prostate cancer. Often, the clinical response to androgen withdrawal is temporary and these cancers ultimately recur after which survival is usually less than one year (Gibbons, 1987). It has been suggested that growth factor-mediated autocrine loops, induced by androgens, may contribute to hormone responsive growth and that these autocrine mechanisms may provide the means for cells to survive and continue growth after steroid deprivation (Knabbe et al, 1991).…”

Characterization of Autocrine Growth Factors, Their Receptors and Extracellular Matrix Present in Three-Dimensional Cultures of DU 145 Human Prostate Carcinoma Cells Grown in Simulated Microgravity

“…When tumor growth resumes, survival is usually less than 1 year. 4 Failure of androgen ablation is presumably due to the progression of prostatic carcinoma from androgen-dependent to androgen-independent growth. 5 Knowledge of growth-regulatory pathways affected by this transition is limited.…”

Neurotensin is an autocrine trophic factor stimulated by androgen withdrawal in human prostate cancer.

“…While androgen withdrawal initially reduces the growth of metastatic prostatic tumors, this clinical response is temporary and these cancers ultimately recur. At this point, hormonal deprivation therapy fails and survival is usually <1 year (2,3). To further the understanding ofprostate tumor growth and progression, the growth-regulatory pathways associated with the development of androgen-independent tumor cell -growth must be defined.…”