Abstract
The major problem in prostate cancer treatment is the development of drug resistance and especially important, cross-resistance. The mechanisms of drug resistance, which are divided into ligand-dependent (requiring the presence of androgens in the cell) and independent (not requiring the presence of androgens) are reviewed. The mechanisms are mainly represented with mutations of the androgen receptor and expression of aberrant constitutively active splice variants, as well as up-regulation of genes involved in androgens synthesis.
Keywords:
abiraterone; androgen receptor; androgens; drug resistance; enzalutamide; mutations; prostate cancer; splice variants.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Androgens / metabolism
-
Antineoplastic Agents / therapeutic use*
-
Drug Resistance, Multiple / genetics*
-
Drug Resistance, Neoplasm / genetics*
-
Gene Expression Regulation, Neoplastic*
-
Humans
-
Male
-
Phosphatidylinositol 3-Kinases / genetics
-
Phosphatidylinositol 3-Kinases / metabolism
-
Phosphoinositide-3 Kinase Inhibitors
-
Prostate / drug effects
-
Prostate / metabolism
-
Prostate / pathology
-
Prostatic Neoplasms / drug therapy
-
Prostatic Neoplasms / genetics*
-
Prostatic Neoplasms / metabolism
-
Prostatic Neoplasms / pathology
-
Proto-Oncogene Proteins c-akt / antagonists & inhibitors
-
Proto-Oncogene Proteins c-akt / genetics
-
Proto-Oncogene Proteins c-akt / metabolism
-
RNA Splicing / drug effects
-
Receptors, Androgen / genetics
-
Receptors, Androgen / metabolism
Substances
-
AR protein, human
-
Androgens
-
Antineoplastic Agents
-
Phosphoinositide-3 Kinase Inhibitors
-
Receptors, Androgen
-
Proto-Oncogene Proteins c-akt