Genetic deletion or methylation of DNA-sensing/IFN genes or CCL5 chemokine was identified as a potential mechanism to attenuate T cell inflammation.
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Bruand, M., Barras, D., Mina, M., Ghisoni, E., Morotti, M., Lanitis, E., Fahr, N., Desbuisson, M., Grimm, A., Zhang, H., Chong, C., Dagher, J., Chee, S., Tsianou, T., Dorier, J., Stevenson, B. J., Iseli, C., Ronet, C., Bobisse, S., … Coukos, G. (2021). Cell-autonomous inflammation of BRCA1-deficient ovarian cancers drives both tumor-intrinsic immunoreactivity and immune resistance via STING. Cell Reports, 36(3). https://doi.org/10.1016/j.celrep.2021.109412 Cite
Scientists summarize the diverse processes underlying resistance to poly(ADP-ribose) polymerase (PARP) inhibitors and discuss the potential strategies that might overcome these mechanisms such as combinations with chemotherapies, targeting the acquired vulnerabilities associated with resistance to PARP inhibitors or suppressing genomic instability.
[Nature Reviews Clinical Oncology]
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Using a combination of in vivo and in vitro analyses in a novel PyMT-E2A conditional knockout mouse model and derived primary tumor cell lines, researchers reported an essential role of E2A in stemness, metastasis, and therapeutic resistance in breast cancer.
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Investigators provided evidence that the CSC-related transcription factor Oct4 contributes to head and neck squamous cell carcinoma radioresistance by regulating DNA damage response and the CSC phenotype.
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Scientists review the current understanding of the molecular mechanisms underlying DNA damage-triggered immune responses, including cytosolic DNA sensing via the cGAS/STING pathway.
[Genes & Development]
Ongoing research to establish predictive biomarkers for the treatment of tumors with resistance to second-generation androgen receptor antagonists led to the approval of the PARP inhibitors olaparib and rucaparib in pre-treated metastatic castration-resistant prostate cancer.
[Nature Reviews Urology]
The combination of MS023, a type I protein arginine methyltransferases (PRMT) inhibitor, and the PARP inhibitor BMN-673 demonstrated strong synergistic interaction at low nanomolar concentrations in methylthioadenosine phosphorylase-negative NSCLC cell lines A549, SK-LU-1 and HCC4006.
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Synergistic effects of type I PRMT and PARP inhibitors against non-small cell lung cancer cells | Clinical Epigenetics | Full Text. (n.d.). Retrieved March 11, 2021, from https://clinicalepigeneticsjournal.biomedcentral.com/articles/10.1186/s13148-021-01037-1 Cite
The authors investigated the possibility to predict BRCA1 promoter methylation status based on the morphological and immunohistochemical features of TNBCs.
[Journal of Human Genetics]
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Scientists found that dual phosphoinositide 3-kinase (PI3K) and poly (ADP-ribose) polymerase inhibition with BKM120 and olaparib significantly reduced the proliferation of BRCA-proficient TNBC cell lines.
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Scientists provide an overview of the potential response prediction biomarkers and synergistic combinations studied in the preclinical and clinical stages, which may expand the population of patients with prostate cancer who may benefit from PARP inhibitors.
[Acta Pharmacologica Sinica]
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The authors found that Glycogen synthase kinase 3 inhibitors (GSK3i) exhibited a strong synergistic effect with PARPi in a panel of colorectal cancer cell lines with diverse genetic backgrounds.
[Cell Death & Disease]
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Zhang, N., Tian, Y.-N., Zhou, L.-N., Li, M.-Z., Chen, H.-D., Song, S.-S., Huan, X.-J., Bao, X.-B., Zhang, A., Miao, Z.-H., & He, J.-X. (2021). Glycogen synthase kinase 3β inhibition synergizes with PARP inhibitors through the induction of homologous recombination deficiency in colorectal cancer. Cell Death & Disease, 12(2), 1–18. https://doi.org/10.1038/s41419-021-03475-4 Cite