Samrat Roy Choudhury
Assistant Professor
University of Arkansas for Medical Sciences
faculty
Peds Pediatrics, College of Medicine
Research Areas
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Biography and Research Information
OverviewAI-generated summary
Dr. Samrat Roy Choudhury's research focuses on investigating the epigenetic regulatory mechanisms that drive malignant proliferation and invasion in acute myeloid leukemia (AML). His laboratory utilizes a multi-omics platform to identify alterations in DNA methylation, histone modifications, and transcription factor accessibility in leukemic cells. This work aims to understand how these epigenetic changes contribute to leukemogenesis across different molecular subgroups of AML patients.
His recent publications demonstrate a broad interest in epigenetic modifications and their role in various cancers, including multiple myeloma, colorectal cancer, and melanoma. Dr. Choudhury has also explored the application of nanotechnology in antimicrobial activities. His scholarly contributions are reflected in an h-index of 20, with over 1,400 citations across 68 publications. He leads a research group and collaborates with researchers at the University of Arkansas for Medical Sciences, including Brian Koss, Erin M. Taylor, Akhilesh Kaushal, and Nükhet Aykin‐Burns.
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: 1,486
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
- 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
- Transcriptional rewiring by enhancer methylation in CBFA2T3-GLIS2–driven pediatric acute megakaryoblastic leukemia (2025) DOI
- Epigenetic Dysregulation and Therapeutic Targeting of RET Receptor Tyrosine Kinase in High-Risk KMT2A-Rearranged Pediatric Acute Myeloid Leukemia (2025) DOI
- SET-NUP214-induced hypermethylation landscape promotes abnormal overexpression of HOXC cluster genes in acute megakaryoblastic leukemia (2024) DOI
- Trichloroethylene metabolite modulates DNA methylation-dependent gene expression in Th1-polarized CD4+ T cells from autoimmune-prone mice (2024) DOI
- Abstract 1733: SET-NUP214 rearranges the DNA-methylation landscape to upregulate the HOX-gene cluster in acute myeloid leukemia (2024) DOI
- Abstract P16: CBFA2T3-GLIS2 fusion leads to a distinct DNA methylation enhancer landscape in pediatric acute myeloid leukemia (2024) DOI
- A NOTCH3-CXCL12-driven myeloma-tumor niche signaling axis promotes chemoresistance in multiple myeloma (2024) DOI
- Enhancer‐activated <scp>RET</scp> confers protection against oxidative stress to <scp>KMT2A</scp>‐rearranged acute myeloid leukemia (2024) DOI
- Abstract 4762: Oncogenic over-expression of MED12 is epigenetically fostered in the core-binding factor subgroups of acute myeloid leukemia (2023) DOI
- CRISPR/dCas9-KRAB-Mediated Suppression of S100b Restores p53-Mediated Apoptosis in Melanoma Cells (2023) DOI
- Expression of integrin β-7 is epigenetically enhanced in multiple myeloma subgroups with high-risk cytogenetics (2023) DOI
- Abstract 3737: DNA-methylation is tightly linked with super-enhancer marks to upregulate ERG in ETO2-GLIS2 positive leukemia (2022) DOI
- Epigenetic Deregulation of Telomere-Related Genes in Newly Diagnosed Multiple Myeloma Patients (2021) DOI
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
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