{
  "id": 7877812,
  "title": "(E,E)-bisantrene suppresses MYC expression and displays anti-leukemic activity in acute myeloid leukemia",
  "url": "https://urgent.news/2026/09/16/e-e-bisantrene-suppresses-myc-expression-and-displays-anti-leukemic",
  "topic": "science",
  "section": "Science",
  "published": "2026-09-16T00:00:00.000Z",
  "source": {
    "name": "bioRxiv",
    "slug": "biorxiv",
    "url": "https://www.biorxiv.org/content/10.64898/2026.09.10.750805v1?rss=1"
  },
  "original_language": "en",
  "account": "Acute myeloid leukemia (AML) presents a significant challenge due to its genetic variability and therapeutic resistance. The transcription factor MYC is a key contributor to AML progression. (E,E)-bisantrene has recently shown the ability to inhibit MYC transcription and its downstream effects through stabilizing G-quadruplex DNA. This study aimed to investigate the mechanism of action and preclinical efficacy of (E,E)-bisantrene in various AML models, including cell lines, xenograft mouse models, and ex vivo human AML mononuclear cells. The effects of (E,E)-bisantrene were assessed by examining transcriptomic, proteomic, and phosphoproteomic changes after treatment. The research revealed potent anti-proliferative activity of (E,E)-bisantrene across multiple AML cell lines, causing apoptosis and reducing the S phase proportion. The prolonged survival in cell and patient-derived xenograft models further supports its potential. Mechanistically, RNA-seq and proteomic analyses demonstrated significant reductions in MYC and E2F activity, as well as cell cycle regulators CDK1/2/4/5 following (E,E)-bisantrene treatment. There was also a dose- and time-dependent decrease in MYC levels, alongside alterations in TP53 and inflammation-associated transcript signatures. These findings suggest that the anti-proliferative effect of (E,E)-bisantrene in preclinical AML models is linked to the downregulation of MYC, CDK1/2/4/5, and E2F. The results support the ongoing clinical evaluation of (E,E)-bisantrene for AML, particularly in cases where MYC is a clinically relevant driver of disease aggressiveness and therapy resistance.",
  "summary": "Background: Acute myeloid leukemia (AML) is genetically diverse with a high unmet clinical need for improved treatment options. Dysregulation of the transcription factor MYC plays a central role in AML progression and therapeutic resistance. (E,E)-bisantrene was recently found to inhibit MYC transcription and downstream activity via G-quadruplex DNA stabilization. This study aimed to evaluate the…",
  "key_points": [],
  "editors_take": null,
  "illustration": null,
  "coverage": {
    "outlets": 1,
    "also_reported_by": []
  },
  "ai_generated": true,
  "disclaimer": "Summaries, key points and the editor’s take are written by software from other outlets’ reporting and may contain errors — always check the linked original."
}