Drug Resistance In Cancer: Mechanisms and Overcoming Strategies
| dc.contributor.advisor | Pórszász, Róbert | |
| dc.contributor.advisordept | Általános Orvostudományi Kar::Farmakológiai és Farmakoterápiai Intézet | |
| dc.contributor.author | Aslam, Muhammad Jawad | |
| dc.contributor.department | DE--Általános Orvostudományi Kar | |
| dc.contributor.opponent | Halasi, Barbara Dóra | |
| dc.contributor.opponent | Megyeri, Attila | |
| dc.contributor.opponentdept | Általános Orvostudományi Kar::Igazságügyi Orvostani Intézet | |
| dc.contributor.opponentdept | Általános Orvostudományi Kar::Farmakológiai és Farmakoterápiai Intézet | |
| dc.date.accessioned | 2026-07-02T10:54:23Z | |
| dc.date.available | 2026-07-02T10:54:23Z | |
| dc.date.created | 2026-05-28 | |
| dc.description.abstract | 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. | |
| dc.description.course | általános orvos | |
| dc.description.courselang | angol | |
| dc.description.degree | egységes, osztatlan | |
| dc.format.extent | 92 | |
| dc.identifier.uri | https://hdl.handle.net/2437/412630 | |
| dc.language.iso | en | |
| dc.rights.info | Hozzáférhető a 2022 decemberi felsőoktatási törvénymódosítás értelmében. | |
| dc.subject | Drug resistance | |
| dc.subject | multidrug resistance (MDR) | |
| dc.subject | intrinsic resistance | |
| dc.subject | acquired resistance | |
| dc.subject | cross-resistance | |
| dc.subject | therapeutic escape | |
| dc.subject | Cancer stem cells (CSCs) | |
| dc.subject | epithelial-to-mesenchymal transition (EMT) | |
| dc.subject | partial EMT (pEMT) | |
| dc.subject | epithelial-mesenchymal plasticity (EMP) | |
| dc.subject | phenotypic stabilizing factors (PSFs) | |
| dc.subject | Muller's Ratchet | |
| dc.subject | tumor heterogeneity | |
| dc.subject | self-renewal | |
| dc.subject | quiescence | |
| dc.subject | ABC transporters | |
| dc.subject | P-glycoprotein (P-gp/ABCB1) | |
| dc.subject | breast cancer resistance protein (BCRP/ABCG2) | |
| dc.subject | multidrug resistance-associated protein 1 (MRP1/ABCC1) | |
| dc.subject | vault proteins | |
| dc.subject | major vault protein (MVP/LRP) | |
| dc.subject | RLIP76 | |
| dc.subject | efflux pump inhibitors | |
| dc.subject | Enzymatic Detoxification | |
| dc.subject | Glutathione S-transferase (GST) | |
| dc.subject | GSTP1 | |
| dc.subject | glutathione (GSH) | |
| dc.subject | UDP-glucuronosyltransferase (UGT) | |
| dc.subject | aldehyde dehydrogenase (ALDH) | |
| dc.subject | NQO1 | |
| dc.subject | cytochrome P450 (CYP450) | |
| dc.subject | Nrf2 | |
| dc.subject | KEAP1 | |
| dc.subject | reactive oxygen species (ROS) | |
| dc.subject | Gatekeeper mutations | |
| dc.subject | T790M | |
| dc.subject | BCR-ABL | |
| dc.subject | EGFR | |
| dc.subject | gene amplification | |
| dc.subject | HER2 | |
| dc.subject | alternative splicing | |
| dc.subject | post-translational modifications | |
| dc.subject | PROTACs | |
| dc.subject | liquid biopsy | |
| dc.subject | ctDNA | |
| dc.subject | Bcl-2 family | |
| dc.subject | BH3 mimetics | |
| dc.subject | inhibitors of apoptosis proteins (IAPs) | |
| dc.subject | SMAC/Diablo | |
| dc.subject | TRAIL | |
| dc.subject | decoy receptors (DcR1/DcR2/DcR3) | |
| dc.subject | c-FLIP | |
| dc.subject | FADD | |
| dc.subject | caspase | |
| dc.subject | cytochrome c | |
| dc.subject | autophagy | |
| dc.subject | Beclin-1 | |
| dc.subject | Tumor microenvironment (TME) | |
| dc.subject | hypoxia | |
| dc.subject | HIF-1α | |
| dc.subject | Warburg effect | |
| dc.subject | angiogenesis | |
| dc.subject | VEGF | |
| dc.subject | cancer-associated fibroblasts (CAFs) | |
| dc.subject | tumor exosomes | |
| dc.subject | myeloid-derived suppressor cells (MDSCs) | |
| dc.subject | T regulatory cells (Tregs) | |
| dc.subject | PD-1 | |
| dc.subject | PD-L1 | |
| dc.subject | immune checkpoint inhibitors | |
| dc.subject | immunosuppression | |
| dc.subject | extracellular matrix (ECM) | |
| dc.subject | Epigenetics | |
| dc.subject | DNA methylation | |
| dc.subject | DNMT inhibitors | |
| dc.subject | histone deacetylase (HDAC) | |
| dc.subject | HDAC inhibitors | |
| dc.subject | BET proteins | |
| dc.subject | BRD4 | |
| dc.subject | SWI/SNF | |
| dc.subject | ncRNA | |
| dc.subject | miRNA | |
| dc.subject | lncRNA | |
| dc.subject | circRNA | |
| dc.subject | epitranscriptomics | |
| dc.subject | drug-tolerant persister cells | |
| dc.subject | CRISPR | |
| dc.subject | prime editing | |
| dc.subject | base editing | |
| dc.subject | multiplex CRISPR | |
| dc.subject | antibody-drug conjugates (ADCs) | |
| dc.subject | synthetic lethality | |
| dc.subject | PARP inhibitors | |
| dc.subject | BRCA1/2 | |
| dc.subject | ATR-CHK1-WEE1 axis | |
| dc.subject | CAR-T cell therapy | |
| dc.subject | nano-medicine | |
| dc.subject | ketogenic diet | |
| dc.subject | artificial intelligence | |
| dc.subject | personalised medicine | |
| dc.subject.dspace | Medicine::Oncology | |
| dc.title | Drug Resistance In Cancer: Mechanisms and Overcoming Strategies |