Samrat Roy Choudhury

High Impact

Assistant Professor

UAMS

Also affiliated: Purdue University West Lafayette (2014–2017); University of Arkansas Medical Center (2024–2025); Purdue University Institute for Cancer Research (2015); Arkansas Children's Research Institute (2021–2026); Indian Agricultural Research Institute (2010); Indian Statistical Institute (2010–2015)

Peds Pediatrics, College of Medicine

20 h-index 68 pubs 1,565 cited

Research Areas

Biomedical Subjects

Links

ORCID Research Group UAMS TRI Profile

OverviewAI-generated summary

Dr. Samrat Roy Choudhury's research focuses on investigating the epigenetic regulatory mechanisms that drive malignant proliferation and invasion during leukemogenesis. His laboratory studies alterations in DNA methylation, histone covalent modifications, and transcription factor accessibility in leukemic blasts across various molecular subgroups of Acute Myeloid Leukemia (AML). This work utilizes a multi-omics platform to identify these changes in genes that are aberrantly expressed both inside and outside topologically associated domains.

Utilizing a combination of molecular biology techniques, Dr. Choudhury's group aims to understand how epigenetic modifications contribute to the development and progression of AML. His scholarly work includes publications on CRISPR-dCas9 mediated TET1 targeting for selective DNA demethylation and the role of nanoparticles in various biological contexts, including antifungal and antimicrobial applications. He has authored or co-authored over 70 publications, with an h-index of 20 and more than 1,500 citations, and is recognized as a highly cited researcher.

Dr. Choudhury leads a research group at the University of Arkansas for Medical Sciences and 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. His recent activity indicates ongoing engagement in research.

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: 68
Citations: 1,565

Positions

Assistant Professor 2020–present

University of Arkansas for Medical Sciences Peds Pediatrics, College of Medicine Institutional directory
Arkansas Children's Research Institute (ACRI) 2020–present

ORCID
Research Associate 2016–2020

University of Arkansas for Medical Sciences Myeloma Center, Winthrop P Rockefeller Cancer Institute. ORCID
Postdoctoral Research Assistant 2013–2016

Purdue University Department of Agricultural & Biological Engineering ORCID

Selected Publications

Abstract 3496: Epigenetic repurposing by CBFA2T3-GLIS2 reveals a druggable DNA methylation axis in high-risk pediatric AML vulnerability in pediatric AML (2026)

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

Cancer Research DOI OpenAlex
Epigenetic dysregulation and therapeutic targeting of RET receptor tyrosine kinase in high‐risk KMT2A ‐rearranged acute myeloid leukaemia (2025)

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

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

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

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

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

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

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

Haematologica 12 citations DOI OpenAlex
Enhancer‐activated RET confers protection against oxidative stress to KMT2A ‐rearranged acute myeloid leukemia (2024)

Cancer Science 9 citations DOI OpenAlex
Abstract 4762: Oncogenic over-expression of MED12 is epigenetically fostered in the core-binding factor subgroups of acute myeloid leukemia (2023)

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

Cells 9 citations DOI OpenAlex
Expression of integrin β-7 is epigenetically enhanced in multiple myeloma subgroups with high-risk cytogenetics (2023)

Clinical Epigenetics 15 citations DOI OpenAlex
Abstract 3737: DNA-methylation is tightly linked with super-enhancer marks to upregulate ERG in ETO2-GLIS2 positive leukemia (2022)

Cancer Research 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