التفاصيل البيبلوغرافية
| العنوان: |
Metabolic challengers selecting tumor-persistent cells. |
| المؤلفون: |
Mancini, Caterina1 (AUTHOR), Lori, Giulia1 (AUTHOR), Pranzini, Erica1,2 (AUTHOR) erica.pranzini@unifi.it, Taddei, Maria Letizia1 (AUTHOR) marialetizia.taddei@unifi.it |
| المصدر: |
Trends in Endocrinology & Metabolism. Mar2024, Vol. 35 Issue 3, p263-276. 14p. |
| مصطلحات موضوعية: |
*TUMOR microenvironment, *DRUG resistance, *PHENOTYPIC plasticity, *EPIGENETICS, *CANCER relapse |
| مستخلص: |
Microenvironmental pressures foster intratumor heterogeneity. Metabolic adaptations induced by the tumor microenvironment modify the epigenetic landscape of cancer cells. Epigenetically primed cells represent the reservoir for the selection of tumor-persistent cells which may sustain the emergence of therapy-resistant clones and drive cancer recurrence. Resistance to anticancer therapy still represents one of the main obstacles to cancer treatment. Numerous components of the tumor microenvironment (TME) contribute significantly to the acquisition of drug resistance. Microenvironmental pressures arising during cancer evolution foster tumor heterogeneity (TH) and facilitate the emergence of drug-resistant clones. In particular, metabolic pressures arising in the TME may favor epigenetic adaptations supporting the acquisition of persistence features in tumor cells. Tumor-persistent cells (TPCs) are characterized by high phenotypic and metabolic plasticity, representing a noticeable advantage in chemo- and radio-resistance. Understanding the crosslink between the evolution of metabolic pressures in the TME, epigenetics, and TPC evolution is significant for developing novel therapeutic strategies specifically targeting TPC vulnerabilities to overcome drug resistance. Resistance to anticancer therapy still represents one of the main obstacles to cancer treatment. Numerous components of the tumor microenvironment (TME) contribute significantly to the acquisition of drug resistance. Microenvironmental pressures arising during cancer evolution foster tumor heterogeneity and facilitate the emergence of drug-resistant clones. In particular, metabolic pressures arising in the TME may favor epigenetic adaptations supporting the acquisition of persistence features in tumor cells. Tumor-persistent cells (TPCs) are characterized by high phenotypic and metabolic plasticity, representing a noticeable advantage in chemo- and radio-resistance. Understanding the crosslink between the evolution of metabolic pressures in the TME, epigenetics, and TPC evolution is significant for developing novel therapeutic strategies specifically targeting TPC vulnerabilities to overcome drug resistance. [ABSTRACT FROM AUTHOR] |
| قاعدة البيانات: |
Academic Search Index |
