THYROID HORMONES MODULATE JAK/STAT ONCOGENIC PATHWAYS VIA INTEGRIN ΑVΒ3 ACTIVATION: IMPLICATIONS ON BEXAROTENE TREATMENT FOR T CELL LYMPHOMAS

CAYROL F; DEBERNARDI MM; STERLE HA; ALVARADO L; GONZALEZ G; DÍAZ ALBUJA JA; CAMPOS HAEDO MN; CREMASCHI GA

Mar del Plata

Congreso; Reunión Anual de Sociedades de Biociencias; 2023

Sociedad Argentina de Investigación Clínica

T-cell lymphomas (TCL) are a heterogeneous group of lymphoproliferative disorders with an aggressive clinical course and dismal prognosis since the available therapeutic regimens have poor results. Activation of JAK/STAT pathways is associated with a bad prognosis in TCL patients. We previously showed that thyroid hormones (THs) are physiological factors that induce TCL proliferation and activate these oncogenic pathways through their membrane receptor, integrin αVβ3. Here we study the mechanisms underlying TH´s effects on JAK/STAT activation and on bexarotene therapy. Using TCL cells from different subtypes, we found that THs-induced STATs phosphorylation is followed by an increase of MMP2 and MMP9 activity (p