Samrat Roy Choudhury

High Impact

Assistant Professor

UAMS

Last publication 2026 Last refreshed 2026-05-16

faculty

Peds Pediatrics, College of Medicine

sroychoudhury@uams.edu

20 h-index 71 pubs 1,517 cited

Research Areas

Links

ORCID Research Group UAMS TRI Profile

OverviewAI-generated summary

Samrat Roy Choudhury's laboratory investigates the epigenetic regulatory mechanisms that drive malignant proliferation and invasion in acute myeloid leukemia (AML). Focusing on enhancers and promoters of critical oncogenes and tumor suppressors, the research aims to understand how these epigenetic alterations contribute to leukemogenesis across different molecular subgroups of AML patients. Employing a multi-omics platform, the group examines changes in DNA methylation, histone modifications, and transcription factor accessibility in leukemic cells.

Dr. Choudhury's work has contributed to understanding epigenetic deregulation in various cancers. Recent publications include studies on the epigenetic enhancement of integrin β-7 in multiple myeloma, the upregulation of SPRY2 in colorectal cancers via epigenetic DNA modifications, and enhancer-activated RET conferring protection against oxidative stress in KMT2A-rearranged AML. His research also explores the potential of CRISPR/dCas9-KRAB for gene suppression in melanoma and investigates epigenetic deregulation of telomere-related genes in multiple myeloma.

With an h-index of 20, 71 total publications, and 1,510 total citations, Dr. Choudhury leads a research group at the University of Arkansas for Medical Sciences. He collaborates with several colleagues within the institution, including Brian Koss, Erin M. Taylor, Jason E. Farrar, and Akhilesh Kaushal, with whom he has co-authored multiple publications.

Research Overview

Epigenetic alterations, including DNA methylation, histone covalent modifications and super-enhancer regulation of exceptional transcriptional states, have attracted a significant amount of attention for the prevention and treatment of different genetic disorders with cancer at the forefront, mainly due to the inherent reversibility of epigenetic states. Acute myeloid leukemia (AML) is the third most prevalent cancer among the hematological malignancies in the United States, presenting with a diverse array of epigenetic abnormalities including chromosomal alterations or recurrent mutations in the epigenetic modifiers. Dr. Choudhury’s laboratory investigates the epigenetic regulatory mechanisms at the enhancers and promoters of the critical oncogenes and tumor suppressors that drive malignant proliferation and invasion during leukemogenesis across the molecular subgroups of AML patients. Using the multi-omics platform, we intend to identify the alterations in DNA-methylation, histone covalent modifications, and accessibility of the transcription factors to the aberrantly expressed genes in and outside the topologically assorted domains of the leukemic blasts. We employ a combination of in vitro and in vivo mouse models to design and target CRISPR or small molecule based perturbation strategies to reverse the dysfunctional epigenetic states and malignant growth.

Metrics

h-index: 20
Publications: 71
Citations: 1,517

Selected Publications

Abstract PR006: CBFA2T3–GLIS2 fusion reprograms enhancer-linked DNA methylation to enforce apoptotic resistance and defines an epigenetic vulnerability in pediatric AML (2026)

DOI OpenAlex
Epigenetic dysregulation and therapeutic targeting of <scp>RET</scp> receptor tyrosine kinase in high‐risk <scp> <i>KMT2A</i> </scp> ‐rearranged acute myeloid leukaemia (2025)

DOI OpenAlex
Transcriptional rewiring by enhancer methylation in CBFA2T3-GLIS2–driven pediatric acute megakaryoblastic leukemia (2025)

1 citation DOI OpenAlex
Epigenetic Dysregulation and Therapeutic Targeting of RET Receptor Tyrosine Kinase in High-Risk KMT2A-Rearranged Pediatric Acute Myeloid Leukemia (2025)

DOI OpenAlex
SET-NUP214-induced hypermethylation landscape promotes abnormal overexpression of HOXC cluster genes in acute megakaryoblastic leukemia (2024)

1 citation DOI OpenAlex
Trichloroethylene metabolite modulates DNA methylation-dependent gene expression in Th1-polarized CD4+ T cells from autoimmune-prone mice (2024)

1 citation DOI OpenAlex
Abstract 1733: SET-NUP214 rearranges the DNA-methylation landscape to upregulate the HOX-gene cluster in acute myeloid leukemia (2024)

DOI OpenAlex
Abstract P16: CBFA2T3-GLIS2 fusion leads to a distinct DNA methylation enhancer landscape in pediatric acute myeloid leukemia (2024)

1 citation DOI OpenAlex
A NOTCH3-CXCL12-driven myeloma-tumor niche signaling axis promotes chemoresistance in multiple myeloma (2024)

10 citations DOI OpenAlex
Enhancer‐activated <scp>RET</scp> confers protection against oxidative stress to <scp>KMT2A</scp>‐rearranged acute myeloid leukemia (2024)

8 citations DOI OpenAlex
Abstract 4762: Oncogenic over-expression of MED12 is epigenetically fostered in the core-binding factor subgroups of acute myeloid leukemia (2023)

1 citation DOI OpenAlex
CRISPR/dCas9-KRAB-Mediated Suppression of S100b Restores p53-Mediated Apoptosis in Melanoma Cells (2023)

8 citations DOI OpenAlex
Expression of integrin β-7 is epigenetically enhanced in multiple myeloma subgroups with high-risk cytogenetics (2023)

14 citations DOI OpenAlex
Abstract 3737: DNA-methylation is tightly linked with super-enhancer marks to upregulate ERG in ETO2-GLIS2 positive leukemia (2022)

DOI OpenAlex
Epigenetic Deregulation of Telomere-Related Genes in Newly Diagnosed Multiple Myeloma Patients (2021)

4 citations DOI OpenAlex

View all publications on OpenAlex →

Research Interests

Acute Myeloid Leukemia is the third most prevalent cancer among the hematological malignancies in the United States, presented with a diverse array of epigenetic abnormalities including chromosomal alterations or recurrent mutations in the epigenetic modifiers. The Roy Choudhury laboratory investigates the epigenetic regulatory mechanisms at the enhancers and promoters of the critical oncogenes and tumor suppressors that drive malignant proliferation and invasion during leukemogenesis across the molecular subgroups of AML patients. Using the multi-omics platform, we intend to identify the alterations in DNA-methylation, histone covalent modifications and accessibility of the transcription factors to the aberrantly expressed genes in and outside the topologically assorted domains (TAD) of the leukemic blasts. We employ a combination of in vitro and in vivo mouse models to design and target CRISPR or small molecule based perturbation strategies to reverse the dysfunctional epigenetic states and malignant growth.; Cancer Epigenetics; Epigenetic Mechanisms; Acute Myeloid Leukemia; Multiple Myeloma; Environmental Epigenetics