Relevant bibliographies by topics / Cell cycle phases checkpoints of tumor and non-tumor cells

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  1. Journal articles
  2. Dissertations / Theses
  3. Conference papers

Academic literature on the topic 'Cell cycle phases checkpoints of tumor and non-tumor cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 February 2022

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Journal articles on the topic "Cell cycle phases checkpoints of tumor and non-tumor cells"

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McArthur, G. A., J. Raleigh, A. Blasina, et al. "Imaging with FLT-PET demonstrates that PF-477736, an inhibitor of CHK1 kinase, overcomes a cell cycle checkpoint induced by gemcitabine in PC-3 xenografts." Journal of Clinical Oncology 24, no. 18_suppl (2006): 3045. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.3045.

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3045 Background: The development of strategies to monitor the molecular and cellular response to novel agents that target the cell cycle is vital to provide proof of mechanism and biological activity of these compounds. The protein kinase CHK1 is activated following DNA damage in the S and G2-phases of the cell cycle and mediates cell cycle arrest. In vitro studies demonstrate that inhibition of CHK1 can overcome cell cycle arrest induced by DNA damage and enhance cytotoxic activity of DNA damaging agents. In vivo studies show that combining DNA damaging agents with a CHK1 inhibitor potentiate
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Cuneo, Kyle Clifford, Meredith Morgan, Matthew J. Schipper, et al. "Phase I study of definitive chemoradiation with gemcitabine and the WEE1 inhibitor AZD1775 in unresectable pancreatic cancer." Journal of Clinical Oncology 35, no. 4_suppl (2017): TPS512. http://dx.doi.org/10.1200/jco.2017.35.4_suppl.tps512.

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TPS512 Background: Targeting cell cycle checkpoints has the potential to enhance the efficacy of chemoradiation therapy. Tumor cells commonly have an abnormal G1 checkpoint due to mutations in the p53 pathway making them reliant on the G2 checkpoint to repair DNA damage. In our preclinical studies, WEE1 inhibition with AZD1775 abrogates the G2 checkpoint and sensitizes pancreatic cancer cell lines and xenografts to chemoradiation. Additionally, AZD1775 attenuates homologous recombination repair and promotes replication stress in cancer cells. Given our preclinical findings, we designed a phase
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Mohanty, Suchismita, Atish Mohanty, Natalie Sandoval, et al. "Cyclin D1 Maintains Mantle Cell Lymphoma Through CDK4-Independent Regulation Of DNA Replicative Checkpoints." Blood 122, no. 21 (2013): 2512. http://dx.doi.org/10.1182/blood.v122.21.2512.2512.

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Abstract Mantle cell lymphoma (MCL) is rarely curable and therapy resistance often leaves few viable treatment options for patients. Previous studies have identified the importance of cyclin D1 (CCND1) translocation and overexpression in MCL pathogenesis, which leads to increased cyclin-dependent kinase 4 (CDK4) activity and accelerated cell cycle progression. However, targeting this abnormal cell cycle control, mainly through CDK4 inhibition causes only G1-phase growth arrest without significant cell death (Marzec et al. 2006). In contrast, prolonged inhibition of CCND1 with RNA interference
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Flippot, Ronan, Bradley Alexander McGregor, Abdallah Flaifel, et al. "Atezolizumab plus bevacizumab in non-clear cell renal cell carcinoma (NccRCC) and clear cell renal cell carcinoma with sarcomatoid differentiation (ccRCCsd): Updated results of activity and predictive biomarkers from a phase II study." Journal of Clinical Oncology 37, no. 15_suppl (2019): 4583. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.4583.

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4583 Background: NccRCC and ccRCCsd are aggressive tumors associated with poor prognosis and response to therapy. Combination strategies co-targeting VEGF signaling and inhibitory immune checkpoints are highly active in clear-cell renal cell carcinoma, but data is lacking in NccRCC and ccRCCsd. We conducted a multicenter, open-label, single arm phase II trial of atezolizumab plus bevacizumab in NccRCC and ccRCCsd. Methods: Patients with NccRCC and ccRCCsd ( > 20% sarcomatoid differentiation), and ECOG performance status of 0-2 were eligible. Prior systemic treatment was allowed with the exc
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Callaghan, Cameron, Ibrahim Abukhiran, Richard VanRheeden, et al. "Pharmacologic ascorbate enhances the therapeutic index of ATM-inhibitor based chemoradiation for colorectal cancer." Journal of Clinical Oncology 39, no. 15_suppl (2021): 3609. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.3609.

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3609 Background: Ataxia telangectasia mutated protein (ATM) is one of the key sensors of DNA damage and specific inhibitors of ATM are potent radiosensitizers. However, their clinical utility with radiation (RT) is limited because they lack tissue specificity and increase normal tissue injury. Pharmacologic (high dose) ascorbate (P-AscH-) selectively increases oxidative stress in tumors while functioning as a donor antioxidant and reducing RT damage in normal tissues. We hypothesized that P-AscH- could enhance the therapeutic index of ATM-inhibitor based chemoradiation (CRT) for colorectal can
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Querfeld, Christiane, Xiwei Wu, Tracy Stiller, et al. "Phase 1 Results of Anti-PD-Ligand 1 (Durvalumab) & Lenalidomide in Patients with Cutaneous T Cell Lymphoma and Correlation with Programmed Death Ligand 1 Expression and Gene Expression Profile." Blood 134, Supplement_1 (2019): 4024. http://dx.doi.org/10.1182/blood-2019-126358.

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Background: T cells in CTCL are functionally exhausted and are characterized by the expression of immune inhibitory molecules such as PD1 and PD-L1 (Cancer Immunol Res 6; 2018). These findings justify the evaluation of immune checkpoint inhibition to reverse T cell exhaustion in CTCL. We initiated a phase 1/2 clinical trial of lenalidomide and durvalumab to determine the safety and efficacy of this regimen. Durvalumab is a human monoclonal antibody with high affinity and selectivity for PD-L1, targeting exhausted T cells and distinct cells within their environment. Lenalidomide, an oral immuno
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Devlin, David, Eva Szegezdi, Paavilainen Tanja, et al. "G2/M Arrest Sensitizes Chronic Myelogenous Leukemia Cells to TRAIL-Induced Apoptosis." Blood 116, no. 21 (2010): 4465. http://dx.doi.org/10.1182/blood.v116.21.4465.4465.

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Abstract Abstract 4465 The death ligand, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receives great interest as it targets and kills cancerous cells, but not non-transformed cells. While it is in phase I/II clinical trials for a range of solid tumours, the generally low sensitivity of leukemia cells to TRAIL makes it a less attractive therapeutic for these cancers. We found that doxorubicin and cytarabine, agents that induce DNA damage and impair cell cycle progression, can sensitize CML cells to TRAIL with CI<1 at Fa of ED25 and ED50 (based on median-effect method using
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Cho, Hearn J., Anna Mei, Tricia Nardiello, et al. "MAGE-A3 Inhibits p53 and Promotes Proliferation and Survival in Multiple Myeloma." Blood 114, no. 22 (2009): 1795. http://dx.doi.org/10.1182/blood.v114.22.1795.1795.

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Abstract Abstract 1795 Poster Board I-821 The type I Melanoma Antigen GEne (MAGE) proteins MAGE-A3 and CT7 (MAGE-C1) were commonly detected in primary tumor cells from multiple myeloma patients and their expression was correlated with advanced disease and proliferation. They belong to the Cancer-Testis antigen (CTAg) family of tumor-associated proteins. In gene expression analyses of primary myeloma cells, CTAg were associated with proliferative gene signatures and poor clinical outcome. These findings suggest that type I MAGE may play a pathogenic role in proliferation or survival in multiple
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Ishizawa, Jo, Eiji Sugihara, Norisato Hashimoto, et al. "Loss of Function of The Cell Cycle Regulator Cdh1 Causes Cell Fragility due to Aberrant G2/M Checkpoint and Develops Resistant Disease in a B-ALL/LBL Mouse Model." Blood 122, no. 21 (2013): 344. http://dx.doi.org/10.1182/blood.v122.21.344.344.

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Abstract Cdh1, one of the co-activators for anaphase-promoting complex/cyclosome, plays a crucial role in the mitotic phase, but also has been reported as G2/M checkpoint regulator activated by irradiation-induced DNA damage. Focusing on Cdh1 functions in the hematopoietic system, we have generated Cdh1 conditional gene-trap (Cdh1f/f) mice and crossed them with Mx1-Cre transgenic mice to obtain Mx1-Cre (+) / Cdh1f/f mice. These animals illustrate that the irradiation-induced G2/M checkpoint is defective in Cdh1-deficient bone marrow (BM) cells, which causes the loss of stem/progenitor cells th
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Gorin, Norbert C., Elihu Estey, Richard J. Jones, Hyam I. Levitsky, Ivan Borrello, and Shimon Slavin. "New Developments in the Therapy of Acute Myelocytic Leukemia." Hematology 2000, no. 1 (2000): 69–89. http://dx.doi.org/10.1182/asheducation.v2000.1.69.20000069.

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Current conventional treatment for patients with acute myelogenous leukemia results in a high percentage of clinical responses in most patients. However, a high percentage of patients still remain refractory to primary therapy or relapse later. This review examines the search for new agents and new modes of therapy. In Section I, Dr. Estey discusses new agents directed at various targets, such as CD33, angiogenesis, inappropriately methylated (suppressor) genes, cell cycle checkpoints, proteosomes, multidrug resistance (MDR) gene, mitochondrial apoptotic pathway. He also reviews preliminary re
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Dissertations / Theses on the topic "Cell cycle phases checkpoints of tumor and non-tumor cells"

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Doran, Bellastrid. "Les différents rôles de STAUFEN1 dans les points de contrôle du cycle cellulaire tumoral vs non tumoral." Thesis, 2020. http://hdl.handle.net/1866/24727.

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STAUFEN1 (STAU1) est une protéine de liaison à l’acide ribonucléique (ARN) double brin jouant un rôle important dans le contrôle post-transcriptionnel de nombreux ARN messager (ARNm). Sa déplétion diminue la prolifération des cellules non cancéreuses en altérant les transitions G1/S et G2/M. En revanche, Ceci n’a aucun impact sur la prolifération des cellules tumorales. La déplétion de STAU1 module le niveau d’expression des transcrits et/ou des protéines impliquées dans la régulation des points de contrôle des transitions de phase. Notamment, STAU1 module le niveau d’expression de la protéine
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Thomas, A., T. Perry, S. Berhane, et al. "The dual-acting chemotherapeutic agent Alchemix induces cell death independently of ATM and p53." 2015. http://hdl.handle.net/10454/9412.

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Yes<br>Topoisomerase inhibitors are in common use as chemotherapeutic agents although they can display reduced efficacy in chemotherapy-resistant tumours, which have inactivated DNA damage response (DDR) genes, such as ATM and TP53. Here, we characterise the cellular response to the dual-acting agent, Alchemix (ALX), which is a modified anthraquinone that functions as a topoisomerase inhibitor as well as an alkylating agent. We show that ALX induces a robust DDR at nano-molar concentrations and this is mediated primarily through ATR- and DNA-PK- but not ATM-dependent pathways, despite DNA doub
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Conference papers on the topic "Cell cycle phases checkpoints of tumor and non-tumor cells"

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Oo, Zay Yar, Alexander Stevenson, Catherine Lanagan, Loredana Spoerri, Jill Larsen, and Brian Gabrielli. "Abstract A33: Defect in S phase cell cycle checkpoint renders tumours vulnerable to CHK1 inhibitor single-agent treatment in vitro and in vivo." In Abstracts: AACR Special Conference on DNA Repair: Tumor Development and Therapeutic Response; November 2-5, 2016; Montreal, QC, Canada. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3125.dnarepair16-a33.

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