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Título : Non-genomic actions of thyroid hormones regulate the growth and angiogenesis of T cell lymphomas
Autor : Cayrol, María Florencia 
Sterle, Helena Andrea 
Díaz Flaqué, María Celeste 
Barreiro Arcos, María Laura 
Cremaschi, Graciela A. 
Fecha de publicación : 2019
Editorial : Frontiers
Cita : Cayrol F, Sterle HA, Díaz Flaqué MC, Barreiro Arcos ML, Cremaschi GA. Non-genomic Actions of Thyroid Hormones Regulate the Growth and Angiogenesis of T Cell Lymphomas [en línea]. Frontiers in Endocrinology. 2019;10. doi:10.3389/fendo.2019.00063 Disponible en:
Resumen : Abstract: T-cell lymphomas (TCL) are a heterogeneous group of aggressive clinical lymphoproliferative disorders with considerable clinical, morphological, immunophenotypic, and genetic variation, including ~10-15% of all lymphoid neoplasms. Several evidences indicate an important role of the non-neoplastic microenvironment in promoting both tumor growth and dissemination in T cell malignancies. Thus, dysregulation of integrin expression and activity is associated with TCL survival and proliferation. We found that thyroid hormones acting via the integrin αvβ3 receptor are crucial factors in tumor microenvironment (TME) affecting the pathophysiology of TCL cells. Specifically, TH-activated αvβ3 integrin signaling promoted TCL proliferation and induced and an angiogenic program via the up-regulation of the vascular endothelial growth factor (VEGF). This was observed both on different TCL cell lines representing the different subtypes of human hematological malignancy, and in preclinical models of TCL tumors xenotransplanted in immunodeficient mice as well. Moreover, development of solid tumors by inoculation of murine TCLs in syngeneic hyperthyroid mice, showed increased tumor growth along with increased expression of cell cycle regulators. The genomic or pharmacological inhibition of integrin αvβ3 decreased VEGF production, induced TCL cell death and decreased in vivo tumor growth and angiogenesis. Here, we review the non-genomic actions of THs on TCL regulation and their contribution to TCL development and evolution. These actions not only provide novel new insights on the endocrine modulation of TCL, but also provide a potential molecular target for its treatment.
ISSN : 1664-2392
Disciplina: MEDICINA
DOI: 10.3389/fendo.2019.00063
Derechos: Acceso Abierto
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