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Oxythiamine and dehydroepiandrosterone inhibit the nonoxidative synthesis of ribose and tumor cell proliferation.
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This study investigates the significance of the glucose-6-phosphate dehydrogenase (G6PD) catalyzed oxidative and the transketolase (TK) catalyzed nonoxidative pentose cycle (PC) reactions in the tumor proliferation process by characterizing tumor growth patterns and synthesis of the RNA ribose
Phase I study of the poly(ADP-ribose) polymerase inhibitor, AG014699, in combination with temozolomide in patients with advanced solid tumors.
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OBJECTIVE
One mechanism of tumor resistance to cytotoxic therapy is repair of damaged DNA. Poly(ADP-ribose) polymerase (PARP)-1 is a nuclear enzyme involved in base excision repair, one of the five major repair pathways. PARP inhibitors are emerging as a new class of agents that can potentiate
Targeting on poly(ADP-ribose) polymerase activity with DNA-damaging hybrid lactam-steroid alkylators in wild-type and BRCA1-mutated ovarian cancer cells.
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Conjugated lactam-steroid alkylators (LSA) have been shown to exhibit superior activity at controlling cancer models and overlap drug resistance to conventional chemjournalapy. Hybrid LSA combine two active compounds in a single molecule and incorporate modified steroids bearing lactam moiety in one
Combining poly(ADP-ribose) polymerase inhibitors and immune checkpoint inhibitors in breast cancer: rationale and preliminary clinical results
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Purpose of review: Recently, both immune checkpoint inhibitors and poly(ADP-ribose) polymerase inhibitors have demonstrated clinical benefit in some subsets of HER2-negative breast cancer patients. A biological rationale exists supporting
Poly (ADP-ribose) polymerase inhibitors in the management of ovarian cancer.
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There is considerable interest and enthusiasm within the clinical gynecologic oncology community regarding the potential for poly (ADP-ribose) polymerase inhibitors to play a critically relevant role in the management of epithelial ovarian cancer and particularly (although not exclusively) in the
Inhibition of poly(ADP-ribose) polymerase in cancer.
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Inhibition of the DNA repair enzyme poly(ADP-ribose) polymerase-1 (PARP-1) has been extensively investigated in the pre-clinical setting as a strategy for chemo- or radio-potentiation. Recent evidence has suggested that PARP inhibitors might be active as single agents in certain rare inherited
Poly(ADP-Ribose) polymerase 1: a therapeutic hope in gynecologic cancers.
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The Poly(ADP-ribose) polymerase-1 (PARP1) is a multifunctional nuclear protein involved in a variety of cellular functions. Recently, its role in the onset, progression and therapy resistance of cancers in general and reproductive cancers in particular has been recognised. The PARP associated
DNA strand breaks and poly(ADP-ribose) synthetase activation in pancreatic islets--a new aspect to development of insulin-dependent diabetes and pancreatic B-cell tumors.
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Alloxan and streptozotocin, which produce diabetes mellitus in experimental animals, have been known to inhibit various functions of pancreatic islets including proinsulin synthesis. However, little is known about the mechanisms underlying the action of these agents in pancreatic islets. Our recent
Poly-ADP-ribose polymerase inhibitor use in ovarian cancer: expanding indications and novel combination strategies.
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The use of poly(ADP-ribose) polymerase (PARP) inhibition is transforming care for the treatment of ovarian cancer, with three different PARP inhibitors (PARPi) gaining US Food and Drug Administration approval since 2014. Given the rapidly expanding use of PARPi, this review aims to summarize the key
Poly (ADP-ribose) polymerase inhibitor: an evolving paradigm in the treatment of prostate cancer.
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Recent phase I studies have reported single-agent activities of poly (ADP-ribose) polymerase (PARP) inhibitor in sporadic and in BRCA-mutant prostate cancers. Two of the most common genetic alterations in prostate cancer, ETS gene rearrangement and loss of PTEN, have been linked to increased
Poly (ADP-ribose) polymerase as a novel therapeutic target in cancer.
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Cancer chemotherapy exploits limitations in repairing DNA damage in order to kill proliferating malignant cells. Recent evidence suggests that cancers within and across tissue types have specific defects in DNA repair pathways, and that these defects may predispose for sensitivity and resistance to
Poly(ADP-ribose) polymerase inhibition in cancer therapy: are we close to maturity?
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BACKGROUND
During the last few years an increasing number of poly(ADP-ribose) polymerase (PARP) inhibitors have been appearing in the context of cancer therapy. This is mainly due to a better knowledge of the best-characterized member of the PARP family of enzymes, PARP-1, further reinforced by the
Poly(ADP-Ribose) polymerase inhibition: "targeted" therapy for triple-negative breast cancer.
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In contrast to endocrine-sensitive and human epidermal growth factor receptor 2 (HER2)-positive breast cancer, novel agents capable of treating advanced triple-negative breast cancer (TNBC) are lacking. Poly(ADP-ribose) polymerase (PARP) inhibitors are emerging as one of the most promising
Inhibition of poly(ADP)-ribose polymerase as a therapeutic strategy for breast cancer.
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As knowledge increases about the processes underlying cancer, it is becoming feasible to design "targeted therapies" directed toward specific pathways that are critical to the genesis or maintenance of the malignant phenotype. Poly(ADP-ribose) polymerase (PARP) inhibitors are an example of this new
Poly(ADP-ribose) polymerase-1 promotes recruitment of meiotic recombination-11 to chromatin and DNA double-strand break repair in Ku70-deficient breast cancer cells.
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Poly(ADP-ribose) polymerase (PARP)-1 may act in an error-prone pathway called alternative end joining (Alt-EJ) for DNA double-strand break (DSB) repair when nonhomologous end joining is defective. We examined the recruitment of PARP-1 to chromatin in response to radiomimetic agents and the effects
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