talazoparib
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Adding the PARP inhibitor talazoparib to enzalutamide improved prostate-specific antigen response in patients with high-volume metastatic hormone-sensitive prostate cancer in the randomized phase 2 ZZ-FIRST trial. Spatial transcriptomic analysis of paired biopsies showed that androgen receptor inhibition suppresses homologous recombination repair-related programs, and this suppression correlated with proliferation arrest rather than functional HRR deficiency.
Excerpted from nature.com
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- nature.comPickTalazoparib plus enzalutamide in high-volume metastatic hormone-naive prostate cancer: a randomized phase 2 trial
Adding the PARP inhibitor talazoparib to enzalutamide improved prostate-specific antigen response in patients with high-volume metastatic hormone-sensitive prostate cancer in the randomized phase 2 ZZ-FIRST trial. Spatial transcriptomic analysis of paired biopsies showed that androgen receptor inhibition suppresses homologous recombination repair-related programs, and this suppression correlated with proliferation arrest rather than functional HRR deficiency.
- biorxiv.orgEfficacy of Tumor Treating Fields (TTFields) in triple negative breast cancer cells and synergy with PARP inhibitor talazoparib
In TNBC cells, TTFields upregulate p21(WAF1)/CDKN1A independently of TP53 status. Combination with the PARP inhibitor talazoparib further enhances p21 expression, induces γH2AX-mediated DNA damage, and downregulates PDL-1. Both treatments trigger cell death via PARP cleavage while reducing anti-apoptotic proteins including p-STAT3, STAT3, and MCL-1.
- biorxiv.orgTargeting ribosome biogenesis sensitizes PARPi-resistant triple-negative breast cancer
Inhibiting ribosome biogenesis with BMH-21 resensitizes PARPi-resistant triple-negative breast cancer to olaparib. The drug combination was synergistic in 4 PARPi-resistant cell lines and in 3 BRCA wild-type TNBC cell lines with intrinsic PARPi resistance, but not in parental cells. In MDAMB231 cells, the combination increased γH2AX-positive cells up to 7.3-fold, SA-β-gal staining 5.6-fold and p21 3.6-fold, findings mirrored with CX-5461. Patient cohort data linked ribosomal pathway activity to MYC, proliferation, DNA damage and senescence.
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