Olaparib Induced Senescence is Bypassed through G2/M Checkpoint Override in Olaparib Resistant Prostate Cancer

Investigators characterized responses to olaparib in sensitive LNCaP and C4-2B cells and developed two olaparib resistant derivative cell line models from each. In LNCaP and C4-2B cells, they found that olaparib induced massive DNA damage, leading to activation of the G2/M checkpoint, activation of p53, and cell cycle arrest.
[Molecular Cancer therapeutics]
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Prostate Cancer Immunotherapy

The authors present completed and ongoing research projects regarding prostate cancer immunotherapy. Ipilimumab and olaparib were proved to prolong overall survival significantly against placebo, but a lot of research is going on to identify which patients and at what stage of disease will benefit the most before incorporating them in clinical practice.
[Expert Opinion On Biological Therapy]
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The Ubiquitin-Dependent ATPase p97 Removes Cytotoxic Trapped PARP1 from Chromatin

Using wild-type and a trapping-deficient poly (ADP-ribose) polymerase (PARP1) mutant combined with rapid immunoprecipitation mass spectrometry of endogenous proteins and Apex2 proximity labeling, investigators delineated mass spectrometry-based interactomes of trapped and non-trapped PARP1.
[Nature Cell Biology]
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Stem-Like Breast Cancer Cells in the Activated State Resist Genetic Stress via TGFBI-ZEB1

The authors characterized a population of stem-like breast cancer cells expressing the integrin αvβ3 as transcriptionally related to activated stem/basal cells in the normal human mammary gland.
[npj Breast Cancer]
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FDI-6 Inhibits the Expression and Function of FOXM1 to Sensitize BRCA-Proficient Triple-Negative Breast Cancer Cells to Olaparib by Regulating Cell Cycle Progression and DNA Damage Repair

Scientists found that repression of the oncogenic transcription factor FOXM1 using FOXM1 shRNA or FOXM1 inhibitor FDI-6 could sensitize BRCA-proficient TNBC to PARP inhibitor Olaparib in vitro and in vivo.
[Cell Death & Disease]
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Prognostic and Therapeutic Significance of COP9 Signalosome Subunit CSN5 in Prostate Cancer

Deregulation of CSN5, a putative androgen receptor (AR), could affect diverse cellular functions that contribute to tumor development. Inhibition of CSN5 repressed metabolic pathways, including oxidative phosphorylation and glycolysis in AR-negative prostate cancer cells.
[Oncogene]
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Treatment Landscape of Triple-Negative Breast Cancer — Expanded Options, Evolving Needs

Scientists describe the current and upcoming therapeutic landscape of TNBC and discuss how an integrated view of the TNBC ecosystem can define different levels of risk and provide improved opportunities for tailoring treatment.
[Nature Reviews Clinical Oncology]
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Rakovina Therapeutics Partners with St. Baldrick’s Foundation to Research and Develop New Treatments for Childhood Bone Cancer

Rakovina Therapeutics, Inc. announced that the company has been selected to join a three year US $975,000 research program funded by the St. Baldrick’s Foundation Martha’s BEST Grant for All, which is aimed at developing new treatments for Ewing sarcoma, an aggressive bone and soft tissue cancer in children and young adults.
[Rakovina Therapeutics, Inc.]
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MET Inhibition Enhances PARP Inhibitor Efficacy in Castration-Resistant Prostate Cancer by Suppressing the ATM/ATR and PI3K/AKT Pathways

Researchers demonstrated that mesenchymal–epithelial transition (MET) inhibition enhanced sensitivity of CRPC to poly adenosine diphosphate–ribose polymerase (PARP) inhibitors by suppressing the ATM/ATR and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathways.
[Journal of Cellular and Molecular Medicine]
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Poly(ADP-Ribose) Polymerase Inhibitors in Prostate Cancer: A Cornerstone in Precision Oncology

Scientists summarize the key poly-(ADP-ribose) polymerase inhibitors, which act in cells with defects in homologous recombination DNA repair caused by genomic aberrations such as BRCA mutations, that are published and ongoing trials in prostate cancer.
[Pharmacogenomics]
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Niraparib Exhibits a Synergistic Anti-Tumor Effect with PD-L1 Blockade by Inducing an Immune Response in Ovarian Cancer

Programmed death ligand 1 (PD-L1) expression in human ovarian cancer cells after PARP inhibitors treatment was examined by western blotting and flow cytometry.
[Journal of Translational Medicine]
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