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Drug Resistance In Cancer: Mechanisms and Overcoming Strategies

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(6,03 MB)

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Tumors develop resistance to therapy through multiple adaptive mechanisms, including drug efflux pumps, enhanced DNA repair, activation of pro-survival pathways, targeted molecule alterations, enzymatic detoxification mechanisms, tumor heterogeneity, and cancer stem cell formation. They also modify the tumor micro-environment to support survival, growth, and metastasis; contributing to the high mortality associated with advanced cancers. To overcome resistance, strategies such as immunotherapy, epigenetic therapies, gene editing, anti-angiogenic drugs, nano-medicine based drug delivery, synthetic lethality approaches (e.g. PARP inhibitors for BRCA-mutated cancers), personalized medicine, dietary interventions, and combination therapies are being developed, showing promising results in reducing the emergence of drug resistant cancer.

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Kulcsszavak

Drug resistance , multidrug resistance (MDR) , intrinsic resistance , acquired resistance , cross-resistance , therapeutic escape , Cancer stem cells (CSCs) , epithelial-to-mesenchymal transition (EMT) , partial EMT (pEMT) , epithelial-mesenchymal plasticity (EMP) , phenotypic stabilizing factors (PSFs) , Muller's Ratchet , tumor heterogeneity , self-renewal , quiescence , ABC transporters , P-glycoprotein (P-gp/ABCB1) , breast cancer resistance protein (BCRP/ABCG2) , multidrug resistance-associated protein 1 (MRP1/ABCC1) , vault proteins , major vault protein (MVP/LRP) , RLIP76 , efflux pump inhibitors , Enzymatic Detoxification , Glutathione S-transferase (GST) , GSTP1 , glutathione (GSH) , UDP-glucuronosyltransferase (UGT) , aldehyde dehydrogenase (ALDH) , NQO1 , cytochrome P450 (CYP450) , Nrf2 , KEAP1 , reactive oxygen species (ROS) , Gatekeeper mutations , T790M , BCR-ABL , EGFR , gene amplification , HER2 , alternative splicing , post-translational modifications , PROTACs , liquid biopsy , ctDNA , Bcl-2 family , BH3 mimetics , inhibitors of apoptosis proteins (IAPs) , SMAC/Diablo , TRAIL , decoy receptors (DcR1/DcR2/DcR3) , c-FLIP , FADD , caspase , cytochrome c , autophagy , Beclin-1 , Tumor microenvironment (TME) , hypoxia , HIF-1α , Warburg effect , angiogenesis , VEGF , cancer-associated fibroblasts (CAFs) , tumor exosomes , myeloid-derived suppressor cells (MDSCs) , T regulatory cells (Tregs) , PD-1 , PD-L1 , immune checkpoint inhibitors , immunosuppression , extracellular matrix (ECM) , Epigenetics , DNA methylation , DNMT inhibitors , histone deacetylase (HDAC) , HDAC inhibitors , BET proteins , BRD4 , SWI/SNF , ncRNA , miRNA , lncRNA , circRNA , epitranscriptomics , drug-tolerant persister cells , CRISPR , prime editing , base editing , multiplex CRISPR , antibody-drug conjugates (ADCs) , synthetic lethality , PARP inhibitors , BRCA1/2 , ATR-CHK1-WEE1 axis , CAR-T cell therapy , nano-medicine , ketogenic diet , artificial intelligence , personalised medicine

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Hivatkozás

https://hdl.handle.net/2437/412630

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Theses (Faculty of Medicine)

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Hozzáférhető a 2022 decemberi felsőoktatási törvénymódosítás értelmében.