Publications by authors named "Hans J Hertzler"
Article Synopsis
- NUT carcinoma is an aggressive cancer driven by the BRD4-NUT fusion oncoprotein, but treatments using BET bromodomain inhibitors (BETi) alone have limited effectiveness.
- The study shows that inhibiting EZH2, a protein that silences tumor suppressor genes, with a drug called tazemetostat, effectively blocks the growth of NUT carcinoma cells.
- Combining EZH2 and BET inhibitors leads to stronger anti-cancer effects, blocking tumor growth and prolonging survival in models, highlighting a new strategy for treating NUT carcinoma based on targeting epigenetic regulation.
Article Synopsis
- - NUT carcinoma (NC) is a fast-growing cancer driven by the BRD4-NUT fusion protein, which promotes growth by activating genes; while BET bromodomain inhibitors are a potential treatment, they work better when combined with other therapies.
- - EZH2, a gene silencing enzyme, is essential for NC growth, and its inhibition using tazemetostat significantly reduces NC cell proliferation and restores tumor suppressor gene expression without affecting certain oncogenes.
- - Combining EZH2 inhibitors with BET inhibitors enhances the effectiveness of treatment, leading to greater tumor suppression and longer survival in animal models, with some mice even showing complete remission.
NUT carcinoma (NC) is a rare subtype of squamous cell carcinoma defined by NUTM1 rearrangements encoding NUT fusion oncoproteins (the most frequent fusion partner being BRD4 ) that carries a very poor prognosis, with most patients dying in under 1 year. Only rare primary thyroid NCs have been reported. Here, we evaluated a series of 14 cases.
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