Samrat Roy Choudhury, PhD, MSc

Full Member

Research Program:

Cancer Biology

Faculty Rank:

Assistant Professor

Campus:

Arkansas Children's Hospital

College:

College of Medicine

Department:

Pediatrics

Cancer Research Interest

Disease Site Focus: Leukemia/ Lymphoma, Multiple Myeloma
Research Focus Area: Detection, Informatics, Treatment
Type of Research: Basic
Research Keywords: Acute Myeloid Leukemia, Epigenetics, DNA Methylation, Chromatin Biology, CRISPR , Epigenome Editing
Research Interest Statement: Acute Myeloid Leukemia is the third most prevalent cancer among the hematological malignancies in the United States and in the state of Arkansas. AML is presented with diverse epigenetic alterations, including recurrent mutations in the epigenetic modifiers (DNMT3a, TET2, and IDH1/2) or cytolological abnormalities resulting in the epigenetic gene fusions (KMT2A fusions or AML1-ETO9). Another fascinating feature of the AML is the shift in epigenetic driver mutations across the age groups. However, exceptional transcriptional competence was observed due to the over-expression of Retionoic Acid Receptor alpha (RARα)-PML fusion in a cohort of AML patients, irrespective of the age difference. Despite distinct epigenetic modifiers have been identified in the pediatric and adult course of the disease, similar phenotypic changes favoring the aggressive leukemogenesis have been manifested in many cases. Therefore, there remains a gap in our understanding of the epigenetic switching mechanisms of leukemic development and differentiation between different age groups. To understand the functional epigenetic landscape in AML, we will have the following aims. Aim-1: Our research focus is aimed at investigating the epigenetic regulatory mechanisms at the enhancers and promoters of the critical oncogenes and tumor suppressors that drive malignant proliferation and invasion during leukemogenesis in the AML patients, characterized with BET (BRD4), SET (KMT2A, EZH2, and NSD1) or runt (CBFA2T3) over-expressed domains. Using the multi-omics platform, we intend to identify the alterations in DNA methylation, histone modifications and transcription factor assemblies in and outside the topologically assorted domains (TAD) in AML. Aim-2: We aim to study the recurrent epigenetic mutations in AML patients in relation to their effect on the cancer cell metabolism. Suitable cells or animals will be induced with the mutant proteins to study the deleterious effects on the chromatin spread, transcriptional dysfunctions and metabolic turnover in the course hematopoiesis. CRISPR-multiplex or small molecule based drugs would be screened for their efficacy against the vulnerable targets of the mutant phenotypes.

Contact Information

Email Address: SROYCHOUDHURY@UAMS.EDU
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