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December 8, 2025Blood

HMGA1 chromatin regulators drive transcriptional networks governing cell cycle progression, immune escape, and menin-inhibitor resistance in KMT2A-r Acute Myeloid Leukemia

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Authors

ZTZanshé ThompsonYDY. W. DuASAudrey-Ann Supreme

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Overview

CRISPR silencing of HMGA1 disrupts immune escape in KMT2A-r AML, suggesting it as a target for therapy.

Key Points

  • The study aims to understand the role of HMGA1 in resisting menin inhibitors and immune evasion in KMT2A-r AML.
  • Silencing HMGA1 using CRISPR or shRNA in AML cell lines
  • Testing leukemogenic properties in vitro and in mice
  • Integrating RNAseq and ATACseq for multiomic analysis
  • Using AI to predict drug targets for HMGA1 networks
  • HMGA1 is overexpressed in KMT2A-r AML compared to healthy controls.
  • Silencing HMGA1 decreased proliferation and induced differentiation in AML cells.
  • HMGA1 deficiency prolonged survival in immunodeficient mouse models.
  • HMGA1 activates immune escape mechanisms in KMT2A-r AML.

Cite This Study

Thompson et al. (2025) studied this question.

synapsesocial.com/papers/693624d74fa91c937236d119https://doi.org/10.1182/blood-2025-5027
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Abstract 5592: HMGA1 modulates chromatin state and transcriptional networks involved in plasticity in refractory myeloid leukemia2024
  2. 2Abstract 2631: HMGA1 chromatin regulators drive immune evasion in myeloproliferative neoplasms by repressing gene networks involved in antigen presentation2024
  3. 3Post allo-HCT menin-inhibition enhances graft-versus-leukemia effects by endogenous retrovirus induction in AML and T-cell activation2025
  4. 4The KMT2A-PTD oncoprotein depends on ENL but not menin to drive AML gene expression2025 · 1 citations
  5. 5Menin Inhibition in Acute Myeloid Leukemia: Rewiring Leukemic Transcriptional Networks2026