TY - CHAP
T1 - Cancer drug resistance
T2 - A brief overview from a genetic viewpoint
AU - Rueff, J
AU - Rodrigues, AS
PY - 2016
Y1 - 2016
N2 - Cancer drug resistance leading to therapeutic failure in the treatment of many cancers encompasses various mechanisms and may be intrinsic relying on the patient’s genetic makeup or be acquired by tumors that are initially sensitive to cancer drugs. All in all, it may be responsible for treatment failure in over 90 % of patients with metastatic cancer. Cancer drug resistance, in particular acquired resistance, may stem from the microclonality/micro-genetic heterogeneity of the tumors whereby, among others, the following mechanisms may entail resistance: altered expression of drug influx/efflux transporters in the tumor cells mediating lower drug uptake and/or greater efflux of the drug; altered role of DNA repair and impairment of apoptosis; role of epigenomics/epistasis by methylation, acetylation, and altered levels of microRNAs leading to alterations in upstream or downstream effectors; mutation of drug targets in targeted therapy and alterations in the cell cycle and checkpoints; and tumor microenvironment that are briefly reviewed.
AB - Cancer drug resistance leading to therapeutic failure in the treatment of many cancers encompasses various mechanisms and may be intrinsic relying on the patient’s genetic makeup or be acquired by tumors that are initially sensitive to cancer drugs. All in all, it may be responsible for treatment failure in over 90 % of patients with metastatic cancer. Cancer drug resistance, in particular acquired resistance, may stem from the microclonality/micro-genetic heterogeneity of the tumors whereby, among others, the following mechanisms may entail resistance: altered expression of drug influx/efflux transporters in the tumor cells mediating lower drug uptake and/or greater efflux of the drug; altered role of DNA repair and impairment of apoptosis; role of epigenomics/epistasis by methylation, acetylation, and altered levels of microRNAs leading to alterations in upstream or downstream effectors; mutation of drug targets in targeted therapy and alterations in the cell cycle and checkpoints; and tumor microenvironment that are briefly reviewed.
KW - Acquired resistance and adaptive compensatory pathways
KW - Acquired resistance and tumor micro-heterogeneity
KW - DNA repair and resistance
KW - Epigenomics and resistance
KW - Intrinsic resistance and pharmacogenetics
KW - Tumor microenvironment and resistance
KW - Uptake and efflux transporters in resistance
UR - http://www.scopus.com/inward/record.url?scp=84964490688&partnerID=8YFLogxK
U2 - 10.1007/978-1-4939-3347-1_1
DO - 10.1007/978-1-4939-3347-1_1
M3 - Chapter
C2 - 26910065
AN - SCOPUS:84964490688
VL - 1395
T3 - Methods in Molecular Biology
SP - 1
EP - 18
BT - Methods in Molecular Biology
PB - Humana Press
ER -
