Abstract
Over 60 years ago Huggins and Hodges demonstrated the importance of androgens and prostate cancer. Since then, significant research has revealed that this relationship is multi-faceted and is interwoven with different signaling cascades and protein coactivators. The complex interrelationship between hormone and cancer is best exemplified by the recurrence and progression of prostate cancer after hormonal therapy to a lethally resistant phenotype despite initially encouraging therapeutic responses. If we are to significantly improve survival with novel therapies, further understanding of the emergence of this resistant phenotype is essential. The purpose of this article is to review the mechanisms of androgen action and its relation to hormonal therapy and mechanisms of hormonal resistance.
MeSH terms
-
Androgen Antagonists / therapeutic use
-
Androgens / adverse effects
-
Androgens / physiology*
-
Clusterin
-
Genes, bcl-2 / genetics
-
Glycoproteins / genetics
-
Growth Substances / physiology
-
Humans
-
Hypersensitivity / etiology
-
Intracellular Signaling Peptides and Proteins
-
Male
-
Molecular Chaperones / genetics
-
Mutation
-
Prostatic Neoplasms / drug therapy
-
Prostatic Neoplasms / etiology*
-
Prostatic Neoplasms / genetics
-
Prostatic Neoplasms / pathology
-
Protein Serine-Threonine Kinases / genetics
-
Receptors, Androgen / genetics
-
Receptors, Androgen / physiology
-
Up-Regulation
Substances
-
Androgen Antagonists
-
Androgens
-
CLU protein, human
-
Clusterin
-
Glycoproteins
-
Growth Substances
-
Intracellular Signaling Peptides and Proteins
-
Molecular Chaperones
-
Receptors, Androgen
-
MAP-kinase-activated kinase 2
-
Protein Serine-Threonine Kinases