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The Tumor's Acidity Rewired Drug Resistance

An ERK–p300–PARP1 pathway helped ovarian-cancer models evade PARP inhibitors and offered a route to resensitization.

Published Updated Story ID: mp-2026-07-30-011
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Summary

An ERK–p300–PARP1 pathway helped ovarian-cancer models evade PARP inhibitors and offered a route to resensitization.

MD Anderson researchers found that acidic conditions activated ERK, p300 and PARP1 signaling that reduced PARP trapping and made ovarian-cancer cells less sensitive to PARP inhibitors. Blocking p300 restored drug sensitivity across preclinical models, including resistant ones; the result supports future combination studies but does not yet establish patient benefit.

Why it matters

An ERK–p300–PARP1 pathway helped ovarian-cancer models evade PARP inhibitors and offered a route to resensitization.

Limits and context

  • Blocking p300 restored drug sensitivity across preclinical models, including resistant ones; the result supports future combination studies but does not yet establish patient benefit.

Key claims

  1. An ERK–p300–PARP1 pathway helped ovarian-cancer models evade PARP inhibitors and offered a route to resensitization.

    Qualification: Blocking p300 restored drug sensitivity across preclinical models, including resistant ones; the result supports future combination studies but does not yet establish patient benefit.

    Evidence: source-2026-07-30-011

Sources

  1. MD Anderson via Newswise: Acidic tumor pathway drives PARP-inhibitor resistanceMD Anderson · secondary reporting

Corrections

No corrections have been recorded for this story.