Therapy escape mechanisms in the malignant prostate.
Semin Cancer Biol, 2015/12;35:133-44.
Santer FR[1], Erb HH[2], McNeill RV[3]
Affiliations
PMID: 26299608
Impact factor: 17.012
Abstract
Androgen receptor (AR) is the main target for prostate cancer therapy. Clinical approaches for AR inactivation include chemical castration, inhibition of androgen synthesis and AR antagonists (anti-androgens). However, treatment resistance occurs for which an important number of therapy escape mechanisms have been identified. Herein, we summarise the current knowledge of molecular mechanisms underlying therapy resistance in prostate cancer. Moreover, the tumour escape mechanisms are arranged into the concepts of target modification, bypass signalling, histologic transformation, cancer stem cells and miscellaneous mechanisms. This may help researchers to compare and understand same or similar concepts of therapy resistance in prostate cancer and other cancer types.
Keywords: AR-targeting therapies; Bypass signalling; Cancer stem cells; Histologic transformation; Target modification; Therapy resistance mechanisms
MeSH terms
Animals; Cell Transdifferentiation; Cell Transformation, Neoplastic; Combined Modality Therapy; Drug Resistance, Neoplasm; Epithelial-Mesenchymal Transition; Gene Expression Regulation, Neoplastic; Humans; Male; Molecular Targeted Therapy; Mutation; Neoplastic Stem Cells; Prostatic Neoplasms; Prostatic Neoplasms, Castration-Resistant; Radiation Tolerance; Receptors, Androgen; Signal Transduction
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