Biography and Research Information
OverviewAI-generated summary
Arundhati Chavan's research focuses on understanding disease mechanisms at the cellular and molecular levels, with a stated goal of accelerating disease diagnosis and treatment. Her work investigates how epigenetic modifications, such as DNA methylation, influence cellular processes and contribute to disease development. Chavan has published on the role of DNMT3B and the CBFA2T3-GLIS2 fusion in acute myeloid leukemia (AML), specifically examining their impact on chromatin structure, cell cycle regulation, and apoptotic resistance.
Her publications explore potential therapeutic vulnerabilities within these epigenetic pathways in high-risk pediatric AML. Chavan collaborates with researchers at the University of Arkansas for Medical Sciences, including Samrat Roy Choudhury, Giselle Almeida Gonzalez, and Pritam Biswas. Her research interests also extend to improving diagnostic methods and developing scalable approaches for disease assessment and drug screening.
Metrics
- h-index: 1
- Publications: 4
- Citations: 2
Positions
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Research Assistant I 2023–presentUniversity of Arkansas for Medical Sciences Pediatric Hematology-Oncology ORCID
Selected Publications
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Abstract 3496: Epigenetic repurposing by CBFA2T3-GLIS2 reveals a druggable DNA methylation axis in high-risk pediatric AML vulnerability in pediatric AML (2026)
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Abstract PR006: CBFA2T3–GLIS2 fusion reprograms enhancer-linked DNA methylation to enforce apoptotic resistance and defines an epigenetic vulnerability in pediatric AML (2026)
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Transcriptional rewiring by enhancer methylation in CBFA2T3-GLIS2–driven pediatric acute megakaryoblastic leukemia (2025)
Collaboration Network
Top Collaborators
- Transcriptional rewiring by enhancer methylation in CBFA2T3-GLIS2–driven pediatric acute megakaryoblastic leukemia
- Abstract PR006: CBFA2T3–GLIS2 fusion reprograms enhancer-linked DNA methylation to enforce apoptotic resistance and defines an epigenetic vulnerability in pediatric AML
- Abstract 3496: Epigenetic repurposing by CBFA2T3-GLIS2 reveals a druggable DNA methylation axis in high-risk pediatric AML vulnerability in pediatric AML
- Transcriptional rewiring by enhancer methylation in CBFA2T3-GLIS2–driven pediatric acute megakaryoblastic leukemia
- Abstract PR006: CBFA2T3–GLIS2 fusion reprograms enhancer-linked DNA methylation to enforce apoptotic resistance and defines an epigenetic vulnerability in pediatric AML
- Abstract 3496: Epigenetic repurposing by CBFA2T3-GLIS2 reveals a druggable DNA methylation axis in high-risk pediatric AML vulnerability in pediatric AML
- Transcriptional rewiring by enhancer methylation in CBFA2T3-GLIS2–driven pediatric acute megakaryoblastic leukemia
- Abstract PR006: CBFA2T3–GLIS2 fusion reprograms enhancer-linked DNA methylation to enforce apoptotic resistance and defines an epigenetic vulnerability in pediatric AML
- Abstract 3496: Epigenetic repurposing by CBFA2T3-GLIS2 reveals a druggable DNA methylation axis in high-risk pediatric AML vulnerability in pediatric AML
- Transcriptional rewiring by enhancer methylation in CBFA2T3-GLIS2–driven pediatric acute megakaryoblastic leukemia
- Transcriptional rewiring by enhancer methylation in CBFA2T3-GLIS2–driven pediatric acute megakaryoblastic leukemia
- Transcriptional rewiring by enhancer methylation in CBFA2T3-GLIS2–driven pediatric acute megakaryoblastic leukemia
- Transcriptional rewiring by enhancer methylation in CBFA2T3-GLIS2–driven pediatric acute megakaryoblastic leukemia
- Transcriptional rewiring by enhancer methylation in CBFA2T3-GLIS2–driven pediatric acute megakaryoblastic leukemia
- Abstract PR006: CBFA2T3–GLIS2 fusion reprograms enhancer-linked DNA methylation to enforce apoptotic resistance and defines an epigenetic vulnerability in pediatric AML
- Abstract PR006: CBFA2T3–GLIS2 fusion reprograms enhancer-linked DNA methylation to enforce apoptotic resistance and defines an epigenetic vulnerability in pediatric AML
- Abstract 3496: Epigenetic repurposing by CBFA2T3-GLIS2 reveals a druggable DNA methylation axis in high-risk pediatric AML vulnerability in pediatric AML
- Abstract 3496: Epigenetic repurposing by CBFA2T3-GLIS2 reveals a druggable DNA methylation axis in high-risk pediatric AML vulnerability in pediatric AML
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