Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
December 8, 2025BloodOpen Access

HMGA1 chromatin regulators drive transcriptional networks involved in megakaryocyte expansion, fibrosis, and sensitivity to interferon signaling in JAK2-V617F MPN

View Full Paper
Ask AI
Bookmark
Share

Authors

BWBailey WestLLLih‐Ling Lin

Discussion

Loading...

Member takes

Overview

Observational analysis revealed HMGA1 impacts thrombocytosis and sensitivity to IFNα in myeloproliferative neoplasms, highlighting its role in disease progression.

Key Points

  • HMGA1 promotes megakaryocyte expansion and fibrosis in myeloproliferative neoplasms, influencing disease progression.
  • Notably, thrombocytosis is linked to HMGA1 activity, suggesting a critical regulatory role in HSC dynamics.
  • Single-cell RNA sequencing identified gene networks activated by HMGA1, including pathways associated with inflammation and cell signaling.
  • These findings indicate that targeting HMGA1 could enhance therapeutic responses to IFNα in myeloproliferative neoplasms.

Cite This Study

West et al. (2025) studied this question.

synapsesocial.com/papers/69362f4e4fa91c937236d8fahttps://doi.org/10.1182/blood-2025-7285
View Full Paper
Ask AI
Bookmark
Share

Also Consider

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

  1. 1HMGA1 chromatin regulator induces inflammatory signals and promotes atherogenesis in Tet2 mutant clonal hematopoiesis2025
  2. 2HMGA1 chromatin regulators drive transcriptional networks governing cell cycle progression, immune escape, and menin-inhibitor resistance in KMT2A-r Acute Myeloid Leukemia2025
  3. 3Advanced myelofibrosis is marked by loss of NKG2D and DNAM-1 NK activating signaling and increased TIM-3 T CD8 exhaustion2025
  4. 4Immunomodulatory role of megakaryocytes in the hematopoietic niche of myeloproliferative neoplasms2026 · 1 citations
  5. 5Association of the composition of the bone marrow tumor microenvironment in BCR::ABL1-negative myeloproliferative neoplasms with IFN-γ signaling and driver mutations2025 · 4 citations