Overcoming cetuximab resistance in HNSCC by Hsp90 inhibition to enhance EGFR degradation
Ranjit K Mehta, Mingjia Tan, Krithika Suresh, Theodore S Lawrence, Mukesh K Nyati · 2026
Read Overcoming cetuximab resistance in HNSCC by Hsp90 inhibition to enhance EGFR degradation by Ranjit K Mehta, Mingjia Tan, Krithika Suresh, Theodore S Lawrence, Mukesh K Nyati (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/PMC13400219.txt.
Description
Ranjit K Mehta and colleagues uncover a trick by which head and neck cancers keep their growth receptor alive under antibody attack, and a way to spring it, in a 2026 study. In resistant cells, cetuximab still switched the receptor off, but the receptor was never destroyed.
The mechanism they name is a monomer trap. The chaperone Hsp90 cradles the switched-off, antibody-bound single receptors, shielding them from degradation and letting them recycle back to the cell surface to signal another day. A minimal, sub-cytotoxic dose of an Hsp90 inhibitor broke the embrace, redirecting the trapped receptors to proteasomal and lysosomal destruction. EGFR levels fell by 70 to 90 percent and the combination killed cells synergistically, including KRAS-mutant ones, without cell-cycle side effects. The authors propose low-dose Hsp90 inhibition as a translational partner for cetuximab in patients who currently have no targeted options.
Catalog record
| CREATOR | Ranjit K Mehta, Mingjia Tan, Krithika Suresh, Theodore S Lawrence, Mukesh K Nyati |
|---|---|
| YEAR | 2026 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 55191 |
| LICENSE | https://creativecommons.org/licenses/by/4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |