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Investigation of cooperative oncogenes in the emergence of IL7R-mediated leukemia

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Author(s):
Tiago Selau Rodrigues
Total Authors: 1
Document type: Master's Dissertation
Press: Ribeirão Preto.
Institution: Universidade de São Paulo (USP). Faculdade de Medicina de Ribeirão Preto (PCARP/BC)
Defense date:
Examining board members:
Leticia Fröhlich Archangelo; Luis Lamberti Pinto da Silva; Vanessa da Silva Silveira; José Andrés Yunes
Advisor: Leticia Fröhlich Archangelo
Abstract

Acute lymphoblastic leukemia (ALL) is characterized by clonal expansion of lymphoid progenitor cells carrying inherited genetic mutations and/or accumulated epigenetic alterations. Interleukin-7 (IL-7) is a cytokine necessary for normal development of lymphoid cells and promotes survival and proliferative responses through its ligation with IL-7 receptors (IL-7R). Gain-of-function mutations in the IL7R gene causes ALLs, since mutated receptors either become extremely sensible to ligand or activate proliferative signaling path constitutively. Even though this malignant phenotype is related to lymphoid progenitors, a case of a patient with acute myelogenous leukemia (AML) bearing mutated IL7R was reported. This same patient also presented the fusion protein RUNX1-RUNX1T1 generated by chromosome translocation t(8;21). In order to verify a possible oncogenic cooperative role between mutated IL7R and RUNX1-RUNX1T1, we introduced such alterations in a IL-3-dependent murine lymphocyte model (Ba/F3) to evaluate their transforming - make Ba/F3 growth independent of IL-3 - and additive effect as potencial oncogenes. (AU)

FAPESP's process: 16/20071-8 - Investigation of cooperative oncogenes in IL7R-mediated acute lymphoblastic leukemia emergence
Grantee:Tiago Selau Rodrigues
Support type: Scholarships in Brazil - Master