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

Negative feedback regulation of nfkb, MAPK, and JAK-STAT drives adaptive resistance to gilteritinib in AML

View Full Paper
Ask AI
Bookmark
Share

Authors

MAMohammad AzharJSJoshua SchwietermanMAMohammad Azam

Discussion

Loading...

Member takes

Overview

Observational analysis shows drug resistance in AML persists despite tyrosine kinase inhibitors, indicating that targeting BCL2 may improve treatment outcomes.

Key Points

  • Triple combination therapy of momelotinib, gilteritinib, and venetoclax significantly reduces drug resistance in AML.
  • Notably, drug resistance was observed with a cytokine signaling pathway and BCL2 involvement in leukemic cells.
  • Assessment using transcriptomic analysis revealed negative feedback regulation pathways contributing to resistance mechanisms.
  • These findings highlight the potential for enhanced tumor suppression through strategic combination therapies against AML.

Cite This Study

Azhar et al. (2025) studied this question.

synapsesocial.com/papers/69362f604fa91c937236dccahttps://doi.org/10.1182/blood-2025-1514
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. 1Enhanced antileukemic activity of momelotinib in combination with venetoclax and azacitidine compared to gilteritinib-based combination2025
  2. 2Momelotinib-mediated transcriptional reprogramming induces synthetic lethal interaction with calcineurin-NFAT signaling2025
  3. 3Recent advances in the treatment of FLT3-mutated acute myeloid leukemia2026
  4. 4Combined FLT3 and EZH1/2 inhibition reduces LSCs and promotes myeloid differentiation in PDX models of AML2025
  5. 5Gilteritinib response in acute myeloid leukemia harboring a rare FLT3 juxtamembrane domain mutation with subsequent clonal evolution2026