LUIS ALBERTO DE PADUA COVAS LAGE
Projetos de Pesquisa
Unidades Organizacionais
Instituto do Câncer do Estado de São Paulo, Hospital das Clínicas, Faculdade de Medicina - Médico
LIM/31 - Laboratório de Genética e Hematologia Molecular, Hospital das Clínicas, Faculdade de Medicina
LIM/31 - Laboratório de Genética e Hematologia Molecular, Hospital das Clínicas, Faculdade de Medicina
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- GATA-3 is a proto-oncogene in T-cell lymphoproliferative neoplasms(2022) GENG, Xiangrong; WANG, Chenguang; GAO, Xin; CHOWDHURY, Pinki; WEISS, Jonathan; VILLEGAS, Jose A.; SAED, Badeia; PERERA, Thilini; HU, Ying; RENEAU, John; SVERDLOV, Maria; WOLFE, Ashley; BROWN, Noah; HARMS, Paul; BAILEY, Nathanael G.; INAMDAR, Kedar; HRISTOV, Alexandra C.; TEJASVI, Trilokraj; MONTES, Jaime; BARRIONUEVO, Carlos; TAXA, Luis; CASAVILCA, Sandro; LAGE, J. Luis Alberto de Padua Covas; CULLER, Hebert Fabricio; PEREIRA, Juliana; RUNGE, John S.; QIN, Tingting; TSOI, Lam C.; HONG, Hanna S.; ZHANG, Li; LYSSIOTIS, Costas A.; OHE, Rintaro; TOUBAI, Tomomi; ZEVALLOS-MORALES, Alejandro; MURGA-ZAMALLOA, Carlos; WILCOX, Ryan A.Neoplasms originating from thymic T-cell progenitors and post-thymic mature T-cell subsets account for a minority of lymphoproliferative neoplasms. These T-cell derived neoplasms, while molecularly and genetically heterogeneous, exploit transcription factors and signaling pathways that are critically important in normal T-cell biology, including those implicated in antigen-, costimulatory-, and cytokine-receptor signaling. The transcription factor GATA-3 regulates the growth and proliferation of both immature and mature T cells and has recently been implicated in T-cell neoplasms, including the most common mature T-cell lymphoma observed in much of the Western world. Here we show that GATA-3 is a proto-oncogene across the spectrum of T-cell neoplasms, including those derived from T-cell progenitors and their mature progeny, and further define the transcriptional programs that are GATA-3 dependent, which include therapeutically targetable gene products. The discovery that p300-dependent acetylation regulates GATA-3 mediated transcription by attenuating DNA binding has novel therapeutic implications. As most patients afflicted with GATA-3 driven T-cell neoplasms will succumb to their disease within a few years of diagnosis, these findings suggest opportunities to improve outcomes for these patients.