Endocrine therapy of advanced carcinoma of the prostate

Daneshgari, Firouz; Crawford, E. David

doi:10.1002/1097-0142(19930201)71:3+<1089::aid-cncr2820711431>3.0.co;2-h

Cited by 45 publications

(12 citation statements)

References 32 publications

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“…1,2 This therapy has significant side effects that include decreased libido, hot flashes, anemia, muscle weakness, and possibly osteoporosis. 3 -6 The use of prostate specific antigen (PSA) in the diagnosis, treatment, and follow-up of prostate cancer patients has significantly changed the definition of disease recurrence.…”

Section: Introductionmentioning

confidence: 99%

Androgen deprivation in men with prostate cancer is associated with an increased rate of bone loss

Preston

Torréns

Harding

et al. 2002

Prostate Cancer Prostatic Dis

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The objective of this work was to determine the effect of androgen deprivation therapy (ADT) on rates of bone mineral density (BMD) loss in men with prostate cancer. It was a prospective study comparing men receiving ADT to age matched controls for 2 y. Subjects received a history, physical exam, bone mineral density measurement, and laboratory evaluation every 6 months. Thirty-nine subjects receiving continuous ADT for prostate cancer (subjects) were compared to 39 agematched controls not receiving ADT (controls). Twenty-three subjects and 30 controls completed the study through 24 months. Men in the ADT group demonstrated greater rates of bone mineral density loss than men in the control group at every site except the lumbar spine. Twenty-four month per cent of bone mineral density loss is presented as mean AE standard error (s.e.). At the distal forearm, the ADT group value was 7 9.4% AE 1.0% and 7 4.4% AE 0.3% for controls (P < 0.0005). The ADT group femoral neck values were 7 1.9% AE 0.7% and 0.6% AE 0.5% in the control group (P ¼ 0.0016). The ADT group total hip value was 7 1.5% AE 1.0% and 0.8% AE 0.5% in the control group (P ¼ 0.0018). The ADT group trochanter value was 7 2.0% AE 1.3% and 7 0.1% AE 0.5% in the control group (P ¼ 0.0019). The ADT group lumbar spine value was 7 0.2% AE 0.8 % and 1.1% AE 0.6% in the control group (P ¼ 0.079). Our data demonstrate greater rates of bone mineral density loss in men receiving androgen deprivation therapy for prostate cancer.

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Section: Introductionmentioning

confidence: 99%

Androgen deprivation in men with prostate cancer is associated with an increased rate of bone loss

Preston

Torréns

Harding

et al. 2002

Prostate Cancer Prostatic Dis

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“…Likewise, prostatic neoplasms are androgen-sensitive tumours that undergo regression after chemical or surgical androgen ablation (Scott et al, 1980;Geller et al, 1988;Deneshagari and Crawford, 1993). However, the vast majority of disseminated prostatic adenocarcinomas recur and progress in the androgen-depleted environment (Lepor et al, 1982).…”

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confidence: 99%

Epidermal growth factor receptor activation in androgen-independent but not androgen-stimulated growth of human prostatic carcinoma cells

Sherwood

Dongen²,

Wood³

et al. 1998

Br J Cancer

111

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Summary These studies were undertaken to assess the relative expression and autocrine activation of the epidermal growth factor receptor (EGFR) in normal and transformed prostatic epithelial cells and to determine whether EGFR activation plays a functional role in androgenstimulated growth of prostate cancer cells in vitro. EGFR expression was determined by Western blot analysis and ELISA immunoassays. Immunoprecipitation of radiophosphorylated EGFR and evaluation of tyrosine phosphorylation was used to assess EGFR activation. The human androgen-independent prostate cancer cell lines PC3 and DU145 exhibited higher levels of EGFR expression and autocrine phosphorylation than normal human prostatic epithelial cells or the human androgen-responsive prostate cancer cell line LNCaP. PC3 and DU145 cells also showed higher levels of autonomous growth under serum-free defined conditions. Normal prostatic epithelial cells expressed EGFR but did not exhibit detectable levels of EGFR phosphorylation when cultured in the absence of exogenous EGF. Addition of EGF stimulated EGFR phosphorylation and induced proliferation of normal cells. LNCaP cells exhibited autocrine phosphorylation of EGFR but did not undergo significant proliferation when cultured in the absence of exogenous growth factors. A biphasic growth curve was observed when LNCaP cells were cultured with dihydrotestosterone (DHT). Maximum proliferation occurred at 1 nM DHT with regression of the growth response at DHT concentrations greater than 1 nm. However, neither EGFR expression nor phosphorylation was altered in LNCaP cells after androgen stimulation. In addition, DHT-stimulated growth of LNCaP cells was not inhibited by anti-EGFR. These studies show that autocrine activation of EGFR is a common feature of prostatic carcinoma cells in contrast to normal epithelial cells. However, EGFR activation does not appear to play a functional role in androgen-stimulated growth of LNCaP cells in vitro.

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“…The initial standard therapy for locally advanced or metastatic disease is androgen deprivation therapy via surgical or medical castration. The initial therapeutic response to the antiandrogen-therapy, is only brief (8 month-3 years), and prostate cancer patients become refractory to additional treatment, as tumors eventually relapse to an androgen independent state [Daneshgari and Crawford, 1993] and development of hormone refractory prostate cancer (HRPC). Docetaxel was shown to prolong survival in patients with HRPC [Petrylak et al, 2004;Pronzato and Rondini, 2005], but chemotherapeutic strategies for effective disease control are still required.…”

Section: Prostate Cancer: the Leading Tumor In Malesmentioning

confidence: 99%

Targeting vasculature in urologic tumors: Mechanistic and therapeutic significance

Sakamoto

Ryan

Kyprianou

2007

J of Cellular Biochemistry

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Recent advances toward understanding the molecular mechanisms regulating cancer initiation and progression provide new insights into the therapeutic value of targeting tumor vascularity by interfering with angiogenic signaling pathways. The functional contribution of key angiogenic factors toward increased vascularity characterizing metastatic tumors and their therapeutic exploitation is considered in three major urologic malignancies, renal, bladder, and prostate cancer. With the realization that the success of the therapeutic efficacy of the various anti-angiogenic approaches for the treatment of urologic tumors has yet to be proven clinically, the challenge remains to select critical angiogenesis pathways that can be targeted for an individual tumor. Here we discuss the major mechanisms that support formation of vasculature in renal, bladder, and prostate tumors and the current results of targeting of specific molecules/regulators for therapeutic intervention against metastastic disease. Keywordsvascularity; tumor growth; apoptosis; VEGF; bladder cancer; renal cancer; prostate cancer In 2007, there will be an estimated 346,440 new cases diagnosed with urologic cancer in the United States and 54,360 Americans will die from a urologic malignancy (SEER Cancer Statistics Review, http://cancernet.nci.nih.gov/statistics). This mortality rate is alarmingly high as it translates to one individual dying every 9 min in the US due to a urologic tumor and thus a significant health issue.Angiogenesis is an essential process in normal physiological functions such as ovarian cycle in female reproductive system [Kaczmarek et al., 2005] and a contributing factor in disease states such as chronic inflammation, arthritis, cancer, and macular degeneration . During the development of the embryo, mesoderm differentiates into angioblasts; these endothelial cells, not yet organized into a lumen, form primitive vessels toward development of blood vessel network, via vasculogenesis. In the adult, new blood vessels form from preexisting vasculature, via angiogenesis [Risau, 1997], while malignant conditions induce a hypercoagulable state in their hosts [Nash et al., 2001]. By early 1960s it was evident that tumors could elaborate diffusible substances that induce angiogenesis from the host vasculature [Algira et al., 1945;Greenblatt and Shubick, 1968]. The increased tumor vascularity was originally believed to be vasodilation of the host endothelium in response to metabolic waste products from within the tumor . A decade later Dr. Folkman's pioneering work identified angiogenesis as a required phenomenon for tumor growth and metastasis, first defining the potential therapeutic value of agents targeting this process , 1971]. Tumor blood vessels exhibit characteristic markers which are not present in normal angiogenic tissues . After enduring the circulation "journey," metastatic cancer cells can escape out of the endothelial vasculature and in the target tissue via extravasation. How do the metastastic cells signal activa...

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Endocrine therapy of advanced carcinoma of the prostate

Cited by 45 publications

References 32 publications

Androgen deprivation in men with prostate cancer is associated with an increased rate of bone loss

Androgen deprivation in men with prostate cancer is associated with an increased rate of bone loss

Epidermal growth factor receptor activation in androgen-independent but not androgen-stimulated growth of human prostatic carcinoma cells

Targeting vasculature in urologic tumors: Mechanistic and therapeutic significance

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