BRD2 upregulation as a pan-cancer adaptive resistance mechanism to BET inhibition
Suyakarn Archasappawat, Juliette Jacques, EunJung Lee, Chang-il Hwang · 2026
Read BRD2 upregulation as a pan-cancer adaptive resistance mechanism to BET inhibition by Suyakarn Archasappawat, Juliette Jacques, EunJung Lee, Chang-il Hwang (2026) in the Tower of Babel, a free online library of public-domain works preserved in clean, searchable text. No sign-up. The full text is served as a plain-text file at a predictable URL, where text is present: https://antarctic-labs.com/tower-of-babel/pmc-13362212.txt.
Description
Suyakarn Archasappawat, Juliette Jacques, EunJung Lee, and Chang-il Hwang identify, in twenty twenty-six, a resistance mechanism that lets many cancers survive BET inhibitor drugs. These drugs target epigenetic reader proteins, above all BRD4, and show promise in cancer therapy. Resistance limits their use. The team found that cells respond by raising a sister protein, BRD2, across multiple cancer types. They reasoned that BRD2 compensates for BRD4 loss and keeps key gene programs running. Knocking BRD2 down made cells sensitive to the drugs again.
Combining BRD2 depletion with the drug JQ1 strongly impaired tumor growth in animals. In pancreatic cells, resistant ones kept more BRD2 on chromatin than sensitive ones. A factor named NFYA drives the BRD2 rise. Co-targeting BRD2 may extend these drugs' benefit.
Catalog record
| CREATOR | Suyakarn Archasappawat, Juliette Jacques, EunJung Lee, Chang-il Hwang |
|---|---|
| YEAR | 2026 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 70 KB |
| VERSION | 1.0 |
| LICENSE | CC BY 4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |