sciencedaily - Cancer drugs known as BET inhibitors once looked like a breakthrough, but in real patients they’ve often fallen short. New research reveals a key reason why: two closely related proteins, BRD2 and BRD4, don’t actually do the same job. Instead, BRD2 acts l…
AI Summary: Scientists uncovered a cellular survival mechanism that helps tumors withstand DNA damage, offering a concrete explanation for why numerous promising anti‑cancer agents stumble in clinical trials. The discovery exposes a resistance pathway that blunts drug efficacy and suggests new targets to sensitize tumors and potentially revive stalled therapies — which, yes, might finally save some development budgets.
Agenus halts BATTMAN trial, launches ROBBIN replacement / 5 wks
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Belzutifan plus lenvatinib outperforms cabozantinib in advanced RCC / 11 days
First patient enrolled in AACR-ADOPT-GEA gastroesophageal cancer trial / 22 days
Phase 1 trial shows cevostamab activity in relapsed multiple myeloma / 5 wks
EMERALD‑3 tests tremelimumab/durvalumab combos for embolisation‑eligible HCC / 1 month
Long‑term Botensilimab+Balstilimab data show durable responses in MSS CRC / 2 months
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