Angiogenesis-targeted therapies in prostate cancer

Primo N Lara, Przemyslaw Twardowski, David I. Quinn

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Most patients with metastatic prostate cancer will respond initially to ablation of gonadal androgen production. Eventually, all patients will develop progressive disease despite continued androgen suppression, a condition called androgen-independent or hormone-refractory prostate cancer. Hormone-refractory prostate cancer is characterized by virulent biologic and clinical behavior. Recently, docetaxel-based chemotherapy has been shown to improve survival and quality of life in this disease when compared with mitoxantrone-based therapy. However, results remain suboptimal. Recently, there have been remarkable advances in the delineation of the mechanisms of cancer growth, metastasis, and the intricate interactions between tumor cells and the surrounding normal tissues. The accumulated evidence has confirmed the importance of angiogenesis in these processes and validated the theory that inhibition of neovascularization is a promising therapeutic anticancer strategy. Currently, dozens of compounds that interfere with different steps of the angiogenic cascade are in preclinical and clinical development. Some of these agents have exhibited promising antitumor activity in hormone-refractory prostate cancer. This review summarizes the molecular mechanisms implicating angiogenesis in the development and progression of advanced-stage prostate cancer, as well as the drug development efforts that are targeting this process.

Original languageEnglish (US)
Pages (from-to)165-173
Number of pages9
JournalClinical Prostate Cancer
Volume3
Issue number3
StatePublished - Dec 2004

Fingerprint

Prostatic Neoplasms
Androgens
docetaxel
Hormones
Therapeutics
Mitoxantrone
Neoplasms
Quality of Life
Neoplasm Metastasis
Drug Therapy
Survival
Growth
Pharmaceutical Preparations

Keywords

  • Atrasentan
  • Bevacizumab
  • Endothelin
  • Matrix metalloproteinases
  • Vascular endothelial growth factor

ASJC Scopus subject areas

  • Oncology
  • Urology

Cite this

Lara, P. N., Twardowski, P., & Quinn, D. I. (2004). Angiogenesis-targeted therapies in prostate cancer. Clinical Prostate Cancer, 3(3), 165-173.

Angiogenesis-targeted therapies in prostate cancer. / Lara, Primo N; Twardowski, Przemyslaw; Quinn, David I.

In: Clinical Prostate Cancer, Vol. 3, No. 3, 12.2004, p. 165-173.

Research output: Contribution to journalArticle

Lara, PN, Twardowski, P & Quinn, DI 2004, 'Angiogenesis-targeted therapies in prostate cancer', Clinical Prostate Cancer, vol. 3, no. 3, pp. 165-173.
Lara, Primo N ; Twardowski, Przemyslaw ; Quinn, David I. / Angiogenesis-targeted therapies in prostate cancer. In: Clinical Prostate Cancer. 2004 ; Vol. 3, No. 3. pp. 165-173.
@article{a3c9bc613e844ea3879549cd1d1e247c,
title = "Angiogenesis-targeted therapies in prostate cancer",
abstract = "Most patients with metastatic prostate cancer will respond initially to ablation of gonadal androgen production. Eventually, all patients will develop progressive disease despite continued androgen suppression, a condition called androgen-independent or hormone-refractory prostate cancer. Hormone-refractory prostate cancer is characterized by virulent biologic and clinical behavior. Recently, docetaxel-based chemotherapy has been shown to improve survival and quality of life in this disease when compared with mitoxantrone-based therapy. However, results remain suboptimal. Recently, there have been remarkable advances in the delineation of the mechanisms of cancer growth, metastasis, and the intricate interactions between tumor cells and the surrounding normal tissues. The accumulated evidence has confirmed the importance of angiogenesis in these processes and validated the theory that inhibition of neovascularization is a promising therapeutic anticancer strategy. Currently, dozens of compounds that interfere with different steps of the angiogenic cascade are in preclinical and clinical development. Some of these agents have exhibited promising antitumor activity in hormone-refractory prostate cancer. This review summarizes the molecular mechanisms implicating angiogenesis in the development and progression of advanced-stage prostate cancer, as well as the drug development efforts that are targeting this process.",
keywords = "Atrasentan, Bevacizumab, Endothelin, Matrix metalloproteinases, Vascular endothelial growth factor",
author = "Lara, {Primo N} and Przemyslaw Twardowski and Quinn, {David I.}",
year = "2004",
month = "12",
language = "English (US)",
volume = "3",
pages = "165--173",
journal = "Clinical Genitourinary Cancer",
issn = "1558-7673",
publisher = "Elsevier",
number = "3",

}

TY - JOUR

T1 - Angiogenesis-targeted therapies in prostate cancer

AU - Lara, Primo N

AU - Twardowski, Przemyslaw

AU - Quinn, David I.

PY - 2004/12

Y1 - 2004/12

N2 - Most patients with metastatic prostate cancer will respond initially to ablation of gonadal androgen production. Eventually, all patients will develop progressive disease despite continued androgen suppression, a condition called androgen-independent or hormone-refractory prostate cancer. Hormone-refractory prostate cancer is characterized by virulent biologic and clinical behavior. Recently, docetaxel-based chemotherapy has been shown to improve survival and quality of life in this disease when compared with mitoxantrone-based therapy. However, results remain suboptimal. Recently, there have been remarkable advances in the delineation of the mechanisms of cancer growth, metastasis, and the intricate interactions between tumor cells and the surrounding normal tissues. The accumulated evidence has confirmed the importance of angiogenesis in these processes and validated the theory that inhibition of neovascularization is a promising therapeutic anticancer strategy. Currently, dozens of compounds that interfere with different steps of the angiogenic cascade are in preclinical and clinical development. Some of these agents have exhibited promising antitumor activity in hormone-refractory prostate cancer. This review summarizes the molecular mechanisms implicating angiogenesis in the development and progression of advanced-stage prostate cancer, as well as the drug development efforts that are targeting this process.

AB - Most patients with metastatic prostate cancer will respond initially to ablation of gonadal androgen production. Eventually, all patients will develop progressive disease despite continued androgen suppression, a condition called androgen-independent or hormone-refractory prostate cancer. Hormone-refractory prostate cancer is characterized by virulent biologic and clinical behavior. Recently, docetaxel-based chemotherapy has been shown to improve survival and quality of life in this disease when compared with mitoxantrone-based therapy. However, results remain suboptimal. Recently, there have been remarkable advances in the delineation of the mechanisms of cancer growth, metastasis, and the intricate interactions between tumor cells and the surrounding normal tissues. The accumulated evidence has confirmed the importance of angiogenesis in these processes and validated the theory that inhibition of neovascularization is a promising therapeutic anticancer strategy. Currently, dozens of compounds that interfere with different steps of the angiogenic cascade are in preclinical and clinical development. Some of these agents have exhibited promising antitumor activity in hormone-refractory prostate cancer. This review summarizes the molecular mechanisms implicating angiogenesis in the development and progression of advanced-stage prostate cancer, as well as the drug development efforts that are targeting this process.

KW - Atrasentan

KW - Bevacizumab

KW - Endothelin

KW - Matrix metalloproteinases

KW - Vascular endothelial growth factor

UR - http://www.scopus.com/inward/record.url?scp=11144232324&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=11144232324&partnerID=8YFLogxK

M3 - Article

C2 - 15636683

AN - SCOPUS:11144232324

VL - 3

SP - 165

EP - 173

JO - Clinical Genitourinary Cancer

JF - Clinical Genitourinary Cancer

SN - 1558-7673

IS - 3

ER -