TY  - JOUR
A1  - Cetin, Ronay
A1  - Quandt, Eva
A1  - Kaulich, Manuel
T1  - Functional genomics approaches to elucidate vulnerabilities of intrinsic and acquired chemotherapy resistance
T2  - Cells
N2  - Drug resistance is a commonly unavoidable consequence of cancer treatment that results in therapy failure and disease relapse. Intrinsic (pre-existing) or acquired resistance mechanisms can be drug-specific or be applicable to multiple drugs, resulting in multidrug resistance. The presence of drug resistance is, however, tightly coupled to changes in cellular homeostasis, which can lead to resistance-coupled vulnerabilities. Unbiased gene perturbations through RNAi and CRISPR technologies are invaluable tools to establish genotype-to-phenotype relationships at the genome scale. Moreover, their application to cancer cell lines can uncover new vulnerabilities that are associated with resistance mechanisms. Here, we discuss targeted and unbiased RNAi and CRISPR efforts in the discovery of drug resistance mechanisms by focusing on first-in-line chemotherapy and their enforced vulnerabilities, and we present a view forward on which measures should be taken to accelerate their clinical translation.
KW  - chemotherapy resistance
KW  - cancer and drug vulnerabilities
KW  - functional genomics
KW  - RNAi and CRISPR screens
Y1  - 2021
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/57629
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-576299
SN  - 2073-4409
VL  - 10
IS  - Article 260
PB  - MDPI
CY  - Basel
ER  -