Artículo

Advancing glioblastoma treatment through iron metabolism: A focus on TfR1 and Ferroptosis innovations

Caverzan, Matias Daniel Icon; Ibarra, Luis Exequiel Icon

Otros responsables

Fecha

08/2024

Editorial

Elsevier Science

Revista

International Journal of Biological Macromolecules

Título del libro

Nombre del evento

Fecha del evento

Institución organizadora

ISSN

0141-8130

eISSN

ISBN

Idioma

Inglés

Tipo del evento

Clasificación temática

Resumen

Glioblastoma (GBM) represents a formidable challenge in oncology, characterized by aggressive proliferation and poor prognosis. Iron metabolism plays a critical player in GBM progression, with dysregulated iron uptake and utilization contributing to tumor growth and therapeutic resistance. Iron´s pivotal role in DNA synthesis, oxidative stress, and angiogenesis underscores its significance in GBM pathogenesis. Elevated expression of iron transporters, such as transferrin receptor1 (TfR1), highlights the tumor´s reliance on iron for survival. Innovative treatment strategies targeting iron dysregulation hold promise for overcoming therapeutic challenges in GBM management. Approaches such as iron chelation therapies, induction of ferroptosis to nanoparticle based drug delivery systems exploit iron dependent vulnerabilities, offering avenues for enhance treatmentefficacy and improve patient outcomes. As research advances, understanding the complex ities of iron-mediated carcinogenesis provides a foundation for developing precision medicine approaches tailored to combat GBM effectively. This review explores the intricate relationship between iron metabolism and GBM, elucidating its multifaceted implications and therapeutic opportunities. By consolidating the latest insights into iron metabolism in GBM, this review underscores its potential as a therapeutic target for improving patient care in combination with the standard of care approach.

Aprobación

Revisión

Complementado por

Referenciado por

Licencia Creative Commons

Excepto donde se indique lo contrario, la licencia de este ítem se describe como by-nc-sa