Acute lymphoblastic leukemias (ALL) are the most common childhood cancers throughout the world, with B-cell ALL having the highest frequency in children. Our group previously showed that the actin-binding protein cortactin is overexpressed in leukemic B cells and triggers transendothelial migration, extramedullary infiltration, bone marrow colonization and relapse. Cortactin is prone to different post-translational modifications, such as acetylation, which regulate its functions. HDAC6 is known to regulate important cellular processes and to deacetylate cortactin, thus triggering cell survival and migration in solid tumors. However, it remains elusive whether these modifications modulate the aggressiveness of B-ALL cells. Thus, I am currently investigating the relevance of HDAC6-mediated cortactin deacetylation and the use of a pharmacological inhibitor to reduce migration of leukemic cells in vitro andin vivo, which may unveil cortactin and HDAC6 as potential new therapeutic targets for high risk B-ALL patients to prevent disease relapse.
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