Results 81 to 90 of about 111,871 (303)

Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1 [PDF]

, 2014
DNA double-strand breaks (DSBs) are repaired by nonhomologous end joining (NHEJ) or homologous recombination (HR). The C terminal binding protein–interacting protein (CtIP) is phosphorylated in G2 by cyclin-dependent kinases to initiate resection and ...
Anantha, Anger, Bahassi, Beausoleil, Bernard S. Lopez, Beucher, Boboila, Bunting, Chapman, Chapman, Chen, Darroudi, Davis, de Cárcer, Deckbar, Di Virgilio, Donnianni, Elia, Escribano-Díaz, Feng, Golsteyn, Gotoh, Helmink, Huertas, Huertas, Jackman, Jackson, Jiadong Wang, Julia Künzel, Junjie Chen, Kim, Kühne, Lansing, Lee, Lee-Theilen, Li, Lin Feng, Lukas, Lukas, Löbrich, Mansour, Markus Löbrich, Mladenov, Monika Steinlage, Mosesso, Moynahan, Naim, Nakamura, Nodar Makharashvili, Nussenzweig, Nussenzweig, Olivia Barton, Panier, Pearce, Penny A. Jeggo, Peterson, Polo, Quennet, Rass, Reczek, Reinhardt, Rief, Ronja Diemer-Biehs, Rothkamm, Sandro Conrad, Sartori, Shibata, Steffen C. Naumann, Stephan, Tanya T. Paull, van Gent, van Gent, Wang, Wang, Wang, Weichert, Weichert, Weinstock, Ying, Yu, Yu, Yun, Zhang, Zimmerman, Zimmermann   +84 more
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PARP Inhibitors for Chemoprevention—Reply [PDF]

Cancer Prevention Research, 2014
We thank Brody and colleagues ([1][1]) for their thoughtful letter that raised three major issues about PARP inhibitors for chemoprevention: (i) long-term toxicity, (ii) secondary tumors, and (iii) drug resistance.
Ciric, To, Michael B, Sporn, Karen T, Liby   +2 more
openaire   +2 more sources

Cell‐cycle‐specific lesion evolution rather than inhibition of double‐strand‐break repair underpins cisplatin radiosensitization

Molecular Oncology, EarlyView.
We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu, Xixi Lin, Emil Mladenov, Veronika Mladenova, Jürgen Thomale, Ali Sak, Yao Wang, Yunxuan Deng, Eleni Gkika, Martin Stuschke, George Iliakis   +10 more
wiley   +1 more source

Anticancer sensitivities and biological characteristics of HCT116 cells resistant to the selective poly(ADP‐ribose) glycohydrolase inhibitor

FEBS Open Bio, EarlyView.
We analyzed alterations of PAR metabolism‐related proteins in PARG inhibitor‐resistant HCT116RPDD cells. Although PARG levels remained unchanged, HCT116RPDD cells exhibited reduced PARP1 and ARH3 expression and elevated PAR levels. Interestingly, HCT116RPDD cells exhibited slightly elevated intracellular NAD+/NADH and ATP levels. Our findings suggest a
Kaede Tsuda, Yoko Ogino, Akira Sato
wiley   +1 more source

Proteogenomic characterization of cholangiocarcinoma

Hepatology, EarlyView., 2022
Proteogenomic characterization of cholangiocarcinoma with therapeutic strategies Abstract Background and Aims Cholangiocarcinoma (CCA) is a highly heterogeneous cancer with limited understanding and few effective therapeutic approaches. We aimed at providing a proteogenomic CCA characterization to inform biological processes and treatment ...
Mengjie Deng, Peng Ran, Lingli Chen, Yunzhi Wang, Zixiang Yu, Ke Cai, Jinwen Feng, Zhaoyu Qin, Yanan Yin, Subei Tan, Yang Liu, Chen Xu, Guoming Shi, Yuan Ji, Jian‐Yuan Zhao, Jian Zhou, Jia Fan, Yingyong Hou, Chen Ding   +18 more
wiley   +1 more source

Advances in the use of PARP inhibitor therapy for breast cancer

Drugs in Context, 2018
Poly-ADP-ribose polymerase 1 (PARP-1) and PARP-2 are DNA damage sensors that are most active during S-phase of the cell cycle and that have wider-reaching roles in DNA repair than originally described.
Kelly E McCann, Sara A Hurvitz
doaj   +1 more source

PARP Inhibitors as P-glyoprotein Substrates [PDF]

Journal of Pharmaceutical Sciences, 2014
The cytotoxicity of PARP inhibitors olaparib, veliparib, and CEP-8983 were investigated in two P-glycoprotein (P-gp) overexpressing drug-resistant cell models (IGROVCDDP and KB-8-5-11). IGROVCDDP and KB-8-5-11 were both resistant to olaparib and resistance was reversible with the P-gp inhibitors elacridar, zosuquidar, and valspodar.
Lawlor, Denise, Martin, Patricia, Busschots, Steven, Thery, Julien, O'Leary, John J., Hennessy, Bryan T., Stordal, Britta K.   +6 more
openaire   +2 more sources

PARP inhibitors induce a senescence phenotype in non‐small cell lung carcinoma cell lines

FEBS Open Bio, EarlyView.
Talazoparib is the most potent inducer of senescence among different PARP1 inhibitors in human NSCLC cells. In the absence of PARP, no senescence phenotype was observed, demonstrating that PARP1 is necessary for the induction of senescence by this inhibitor.
Camille Huart, Manon Van den Abbeel, Christoph Schifflers, Karim Bouhjar, Andrea Scarmelotto, Alexis Khelfi, Anne‐Catherine Wera, Carine Michiels   +7 more
wiley   +1 more source

Olaparib modulates DNA repair efficiency, sensitizes cervical cancer cells to cisplatin and exhibits anti-metastatic property

Scientific Reports, 2017
PARP1 trapping at DNA lesion by pharmacological inhibitors has been exploited in several cancers exhibiting defects in DNA repair mechanisms. PARP1 hyperactivation is involved in therapeutic resistance in multiple cancers.
Chandra Bhushan Prasad, Shyam Babu Prasad, Suresh Singh Yadav, Laxmi Kant Pandey, Sunita Singh, Satyajit Pradhan, Gopeshwar Narayan   +6 more
doaj   +1 more source

BMN673 sensitizes rhabdomyosarcoma tumors to irradiation in vivo [PDF]

, 2020
Bone and soft tissue sarcomas are mesenchymal tumors that occur rarely in adults, representing only 1% of total malignancies, but comprise up to 13% of malignant tumors in children.1 Rhabdomyosarcoma, a soft tissue sarcoma that commonly affects children,
Jacob, Connor
core