Τίτλος:
Targeted therapeutic approaches for hormone-refractory prostate cancer
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Prostate cancer is one of the leading causes of cancer related death in
men, and remains incurable in the metastatic setting. Despite the
initial response to androgen deprivation, the disease gradually
progresses to a hormone-refractory state due to cumulative genetic
alterations in tumour cells or the microenvironment. Docetaxel
represents the first chemotherapeutic agent with a small survival
benefit for metastatic hormone-refractory prostate cancer (HRPC). In an
attempt to improve survival benefit, several novel drugs targeting
specific pathways involved in cell signaling, proliferation,
angiogenesis, apoptosis and immune modulation are currently under
investigation either as single agents or in combination with cytotoxic
drugs. Clinical trials evaluate the inhibition of prostate cancer cells
growth by targeting the nuclear receptor of vitamin D alongside
cytotoxic therapy. Angiogenesis inhibitors as well as epidermal growth
factor receptor blockage are also under clinical investigation in
several combinations. Immunomodulatory agents and autologous dendritic
cells or allogenic whole cell vaccines have progressed up to phase III
trials. New drugs targeting bone microenvironment or apoptotic and
proliferation pathways may enhance antitumour activity of chemotherapy
in HRCP. Given the complexity of mechanisms underlying prostate cancer
progression, future therapeutic strategies should rely on
multidisciplinary approaches, thus exploiting newer molecular targets in
concert with immunotherapy and cytotoxic chemotherapy. Here, we review
the latest clinical evidence regarding the use of novel agents in HRPC.
(C) 2009 Elsevier Ltd. All rights reserved.
Συγγραφείς:
Stavridi, Flora
Karapanagiotou, Eleni M.
Syrigos, Kostas N.
Περιοδικό:
Cancer Treatment Reviews
Εκδότης:
Elsevier Sci Ltd, Exeter, United Kingdom
Λέξεις-κλειδιά:
Hormone-refractory prostate cancer; Targeted therapy; Vitamin D
analogues; Angiogenesis inhibitors; Endothelin receptor antagonists;
Apoptotic pathways; Molecular chaperone; Tyrosine kinase inhibitors;
Immunotherapy
DOI:
10.1016/j.ctrv.2009.06.001
