Tumor plasticity, epigenetic reprogramming and the dynamic tumor microenvironment shape the biology of CRC, AML and melanoma and influence their therapeutic vulnerability. Modern therapeutic approaches combine molecular profiles, TME signatures and functional biomarkers to break through resistance programs and enable more precise, patient-specific therapies.
Autoren
- Dr. oec. Odile Schwarz-Herion
Publikation
- InFo ONKOLOGIE & HÄMATOLOGIE
Related Topics
- Activation NF-κB-
- Adaptive resistance mechanisms
- AML
- AXL axis (melanoma)
- CRC
- CXCL12/CXCR4 axis (AML niche)
- DNMT3A and TET2 mutations (AML)
- Epigenetic plasticity
- Epigenetic reprogramming
- Functional biomarkers
- Fusobacterium nucleatum
- HAND1 expression
- IFN-γ signatures
- Immune checkpoint resistance (melanoma)
- Immunological dysfunction
- Intratumoral heterogeneity
- Melanoma
- Metabolic-epigenetic coupling
- microbiome
- MITF
- molecular mechanisms
- Multi-Omics profiles
- Myeloid suppression
- OXPHOS-dependent AML subtypes
- Precision Oncology
- Promotion of proliferative and anti-apoptotic signaling pathways
- SMAD4-dependent signaling pathways
- Stabilization of immunosuppressive cell types (MDSCs and tumor-associated macrophages)
- STAT- and MAPK-dependent programs
- T-cell exhaustion; JAK/STAT signaling pathways
- TME dynamics
- Tumor microenvironment (TME)
- Tumor plasticity
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