Biography and Research Information
OverviewAI-generated summary
Arundhati Chavan's research focuses on the molecular mechanisms underlying acute megakaryoblastic leukemia (AMKL) and acute myeloid leukemia (AML). Her work investigates how genetic fusions, such as CBFA2T3-GLIS2, drive transcriptional rewiring through epigenetic modifications, specifically enhancer methylation. Chavan's publications explore the role of enzymes like DNMT3B in controlling chromatin states and cell cycle networks in AML, identifying potential vulnerabilities for therapeutic intervention. She has co-authored publications with researchers at the University of Arkansas for Medical Sciences, including Samrat Roy Choudhury and Giselle Almeida Gonzalez. Chavan's research is characterized by an h-index of 1 and 5 total publications.
Metrics
- h-index: 1
- Publications: 5
- Citations: 2
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
- DNMT3B Controls Enhancer-Linked Chromatin and Cell Cycle Networks in Acute Myeloid Leukemia
- Transcriptional rewiring by enhancer methylation in CBFA2T3-GLIS2–driven pediatric acute megakaryoblastic leukemia
- DNMT3B Controls Enhancer-Linked Chromatin and Cell Cycle Networks in Acute Myeloid 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
- 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
- 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
- DNMT3B Controls Enhancer-Linked Chromatin and Cell Cycle Networks in Acute Myeloid Leukemia
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