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Michael I. Barbato

Researcher at St. Jude Children's Research Hospital

Publications -  6
Citations -  1684

Michael I. Barbato is an academic researcher from St. Jude Children's Research Hospital. The author has contributed to research in topics: EP300 & Leukemia. The author has an hindex of 3, co-authored 3 publications receiving 1500 citations. Previous affiliations of Michael I. Barbato include Memorial Sloan Kettering Cancer Center.

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Journal ArticleDOI

The genetic basis of early T-cell precursor acute lymphoblastic leukaemia

Jinghui Zhang, +73 more
- 12 Jan 2012 - 
TL;DR: The mutational spectrum is similar to myeloid tumours, and moreover, the global transcriptional profile of ETP ALL was similar to that of normal andMyeloid leukaemia haematopoietic stem cells, suggesting that addition of myeloids-directed therapies might improve the poor outcome of E TP ALL.
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An Inv(16)(p13.3q24.3)-encoded CBFA2T3-GLIS2 fusion protein defines an aggressive subtype of pediatric acute megakaryoblastic leukemia.

TL;DR: In this article, the authors performed transcriptome sequencing on diagnostic blasts from 14 pediatric patients and validated their findings in a recurrency/validation cohort consisting of 34 pediatric and 28 adult AMKL samples.
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Discovery of Novel Recurrent Mutations in Childhood Early T-Cell Precursor Acute Lymphoblastic Leukemia by Whole Genome Sequencing - a Report From the St Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project

TL;DR: Results of whole genome sequencing of tumor and normal DNA from 12 children with ETP ALL show a high frequency of activating mutations in genes regulating cytokine receptor and Ras signalling are identified, including GATA3 regulates early T cell development, and mutations in this gene were observed exclusively in ETP All.
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Donor T cell DNMT3a regulates alloreactivity in mouse models of hematopoietic stem cell transplantation

TL;DR: A critical role for DNMT3a is demonstrated in regulating T cell alloreactivity and pathways that control T cell tolerance are revealed, which provide a platform for deciphering clinical data that associate donor DN MT3a mutations with increased GVHD, decreased relapse, and improved survival.