Stead Family Department of Pediatrics

Yatin M. Vyas, MD, MBBS

Portrait

Mary Joy and Jerre Stead Professor of Pediatric Hematology/Oncology
Professor of Pediatrics  - Hematology/Oncology

Contact Information

Lab: 3080B ML
Iowa City, IA 52242

Email: yatin-vyas@uiowa.edu

Education

MBBS, Gujarat University, Medicine
MBBS, Gujarat University, Surgery
MD, Gujarat University, Pediatrics
Executive-MBA Certification in Physician Leadership, Katz School of Business, University of Pittsburgh, Pittsburgh, PA

Residency, Gujarat University Civil Hospital, Pediatrics
Chief Resident, Gujarat University Civil Hospital, Pediatrics
Residency, New York University Medical Center, Pediatrics
Fellowship, Memorial Sloan-Kettering Cancer Center, Pediatric Hematology/Oncology
Fellowship, Memorial Sloan-Kettering Cancer Center, Special Clinical Fellow
Research Fellow, Sloan-Kettering Institute for Cancer Research, Immunology Program, SKI

Licensure and Certifications

Iowa Medical License, Iowa Board of Medicine

Research Summary

My laboratory research program focuses on explicating the molecular underpinnings of immune dysregulation and cancer development in children. The laboratory is consistently funded by the National Institutes of Health (NIH) through both R01 and R21 mechanisms. Two broad components of our research program are: 1. Wiskott-Aldrich Syndrome and immune dysregulation: I have a longstanding interest in understanding the molecular underpinnings of the development of human immune responses in health and disease. We have chosen to use the genetic disease model of Wiskott-Aldrich syndrome (WAS) to determine the partners and pathways of WAS protein (WASp) participation in the regulation of CD4 T helper cell differentiation and the development of T cell adaptive immunity. Human WAS is an X-linked genetic disease manifesting in severe immune deficiency, autoimmunity, thrombocytopenia, and lymphoid cancers in young boys. In order to clarify WASp’s role in immune regulation in health, and immune dysregulation in WAS, our laboratory has taken the complementary approach of investigating the functions of WASp from both vantage points, i.e. cytoplasm and nucleus. Research from my laboratory was essential in revealing for the first time a novel nuclear function for WASp in the transcriptional regulation of Th1-differentiation through its effect on epigenetic modifications at the T-BET gene-promoter locus. Since that time, we have been actively involved in further understanding how WASp associates with and regulates protein pathways and gene networks that control development of protective type-1 immunity. We seek to explicate the molecular mechanism of WASp’s nuclear transport and its role on impacting Th1/Th2/Th17/Treg differentiation. We are particularly interested in understanding the molecular basis for the disease severity in WAS patients that carry single missense mutations that still allow the expression of mutant WASp. We are testing the hypothesis that the primary function of WASp is in coordinating the nuclear events of gene transcription that occur independently of its well-described cytoplasmic effect on the actin cytoskeleton. We believe our studies will have direct implications to the better design of therapeutics in WAS, a life-threatening childhood disease. 2. Investigating the Genome and Epigenome of Pediatric Acute Lymphoblastic Leukemia (ALL): We have recently embarked on the studies of childhood ALL. Despite an improved understanding of the pathogenesis of childhood ALL from a cellular and molecular perspectives, the current knowledge of how the multiple genetic alterations (mutations, translocations, etc.) associated with ALL modify the disease severity and response to conventional chemotherapy is ill understood. It is also clear whether these genetic mutations are a cause (i.e., a driver event) or a consequence (i.e., a passenger event) for the development of ALL. Do these genetic/epigenetic events contribute directly to the primary treatment failures in childhood ALL is also unclear. Our research is aimed at understanding if and how the genomic and epigenomic landscapes of the leukemic blasts pattern the different severity grades of ALL. Whether such novel metric could be identified and ultimately used clinically to predict children who will respond to chemotherapy versus ones who will not.

Date Last Modified: 06/07/2014 - 21:56:23