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Journal articles 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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1

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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2

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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4

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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6

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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7

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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8

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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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.v2000.1.69.69.

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Abstract 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 preli

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12

Alexander, Brian Michael, Manmeet Singh Ahluwalia, Arati Suvas Desai, et al. "Phase I study of AZD1775 with radiation therapy (RT) and temozolomide (TMZ) in patients with newly diagnosed glioblastoma (GBM) and evaluation of intratumoral drug distribution (IDD) in patients with recurrent GBM." Journal of Clinical Oncology 35, no. 15_suppl (2017): 2005. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.2005.

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2005 Background: The standard of care treatment for newly diagnosed GBM is maximal safe surgical resection followed by two DNA damaging agents, RT and TMZ. Cellular response to DNA damage involves checkpoints that halt the cell cycle to allow DNA repair. AZD1775 is an oral small molecular inhibitor of a nuclear tyrosine kinase Wee1, a key regulator of the G2/M checkpoint. Abrogation of the G2/M checkpoint prevents repair and pushes cells into mitosis with unrepaired DNA damage. AZD1775 was shown to enhance TMZ and RT effects in preclinical models. Methods: The Adult Brain Tumor Consortium 1202

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13

Qiu, Ling, Andrew Burgess, David P. Fairlie, Helen Leonard, Peter G. Parsons, and Brian G. Gabrielli. "Histone Deacetylase Inhibitors Trigger a G2 Checkpoint in Normal Cells That Is Defective in Tumor Cells." Molecular Biology of the Cell 11, no. 6 (2000): 2069–83. http://dx.doi.org/10.1091/mbc.11.6.2069.

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Important aspects of cell cycle regulation are the checkpoints, which respond to a variety of cellular stresses to inhibit cell cycle progression and act as protective mechanisms to ensure genomic integrity. An increasing number of tumor suppressors are being demonstrated to have roles in checkpoint mechanisms, implying that checkpoint dysfunction is likely to be a common feature of cancers. Here we report that histone deacetylase inhibitors, in particular azelaic bishydroxamic acid, triggers a G2 phase cell cycle checkpoint response in normal human cells, and this checkpoint is defective in a

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Alagpulinsa, David, Srinivas Ayyadevara, Shmuel Yaccoby, and Robert shmookler Reis. "Dinaciclib, a CDK Inhibitor, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition." Blood 124, no. 21 (2014): 479. http://dx.doi.org/10.1182/blood.v124.21.479.479.

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Abstract Multiple myeloma (MM) cells are characterized by genomic instability, implicating aberrant DNA damage repair. They exhibit pervasive double strand breaks (DSBs), the most lethal DNA lesions, as indicated by the constitutive abundance of γH2AX foci. DSBs can be repaired through homologous recombination (HR) or nonhomologous end joining (NHEJ). We previously showed elevated HR in MM cells, which were reported to have impaired NHEJ function; they may thus depend on elevated HR for survival. Poly (ADP-ribose) polymerase 1 (PARP1), hyperactivated in MM cells and required for single-strand

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15

De Filippi, Rosaria, Stefania Crisci, Ferdinando Frigeri, et al. "Molecular Determinants of Bendamustine (BDM) Toxicity towards Hodgkin (H) and Reed-Sternberg (RS) Cell Lines From Hodgkin Lymphoma (HL)." Blood 120, no. 21 (2012): 2763. http://dx.doi.org/10.1182/blood.v120.21.2763.2763.

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Abstract Abstract 2763 Patients with HL recurring after stem cell transplantation (SCT) are mostly incurable. Therefore development of new agents and strategies is an impellent medical need in this setting. BDM is a hybrid purine analogue/bi-functional alkylator active in B-cell tumors. Despite preliminary evidences of efficacy in refractory HL, the molecular mechanisms underlying the potential activity of BDM towards malignant H-RS cells were never explored. We investigated patterns of BDM cytotoxicity (12.5 to 100 mmol/L) in a panel of HL-derived cell lines (L1236, L428, KMH2, HDLM2, L540) a

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Morgan, S. E., C. Lovly, T. K. Pandita, Y. Shiloh, and M. B. Kastan. "Fragments of ATM which have dominant-negative or complementing activity." Molecular and Cellular Biology 17, no. 4 (1997): 2020–29. http://dx.doi.org/10.1128/mcb.17.4.2020.

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The ATM protein has been implicated in pathways controlling cell cycle checkpoints, radiosensitivity, genetic instability, and aging. Expression of ATM fragments containing a leucine zipper motif in a human tumor cell line abrogated the S-phase checkpoint after ionizing irradiation and enhanced radiosensitivity and chromosomal breakage. These fragments did not abrogate irradiation-induced G1 or G2 checkpoints, suggesting that cell cycle checkpoint defects alone cannot account for chromosomal instability in ataxia telangiectasia (AT) cells. Expression of the carboxy-terminal portion of ATM, whi

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Simonetti, Giorgia, Antonella Padella, Ítalo Faria do Valle, et al. "A Specific Pattern of Somatic Mutations Associates with Poor Prognosis Aneuploid Acute Myeloid Leukemia: Results from the European NGS-PTL Consortium." Blood 126, no. 23 (2015): 3840. http://dx.doi.org/10.1182/blood.v126.23.3840.3840.

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Abstract Aneuploidy causes a proliferative disadvantage, mitotic and proteotoxic stress in non-malignant cells ( Torres et al. Science 2007). Chromosome gain or loss, which is the hallmark of aneuploidy, is a relatively common event in Acute Myeloid Leukemia (AML). About 10% of adult AML display isolated trisomy 8, 11, 13, 21 (Farag et al. IJO 2002), or either an isolated autosomal monosomy or monosomal karyotype (Breems et al. JCO 2008). This evidence suggests that tumor-specific mechanisms cooperate to overcome the unfitness barrier and maintain aneuploidy. However, the molecular bases of an

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Mantel, Charlie, Stephen E. Braun, Suzanna Reid, et al. "p21cip-1/waf-1 Deficiency Causes Deformed Nuclear Architecture, Centriole Overduplication, Polyploidy, and Relaxed Microtubule Damage Checkpoints in Human Hematopoietic Cells." Blood 93, no. 4 (1999): 1390–98. http://dx.doi.org/10.1182/blood.v93.4.1390.

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Abstract A recent hypothesis suggests that tumor-specific killing by radiation and chemotherapy agents is due to defects or loss of cell cycle checkpoints. An important component of some checkpoints is p53-dependent induction of p21cip-1/waf-1. Both p53 and p21 have been shown to be required for microtubule damage checkpoints in mitosis and in G1 phase of the cell cycle and they thus help to maintain genetic stability. We present here evidence that p21cip-1/waf-1 deficiency relaxes the G1 phase microtubule checkpoint that is activated by microtubule damage induced with nocodazole. Reduced p21c

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Mantel, Charlie, Stephen E. Braun, Suzanna Reid, et al. "p21cip-1/waf-1 Deficiency Causes Deformed Nuclear Architecture, Centriole Overduplication, Polyploidy, and Relaxed Microtubule Damage Checkpoints in Human Hematopoietic Cells." Blood 93, no. 4 (1999): 1390–98. http://dx.doi.org/10.1182/blood.v93.4.1390.404k25_1390_1398.

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A recent hypothesis suggests that tumor-specific killing by radiation and chemotherapy agents is due to defects or loss of cell cycle checkpoints. An important component of some checkpoints is p53-dependent induction of p21cip-1/waf-1. Both p53 and p21 have been shown to be required for microtubule damage checkpoints in mitosis and in G1 phase of the cell cycle and they thus help to maintain genetic stability. We present here evidence that p21cip-1/waf-1 deficiency relaxes the G1 phase microtubule checkpoint that is activated by microtubule damage induced with nocodazole. Reduced p21cip-1/waf-

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Schwartz, Gary K. "Development of Cell Cycle Active Drugs for the Treatment of Gastrointestinal Cancers: A New Approach to Cancer Therapy." Journal of Clinical Oncology 23, no. 20 (2005): 4499–508. http://dx.doi.org/10.1200/jco.2005.18.341.

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The cell cycle represents a series of tightly integrated events that allow the cell to grow and proliferate. An essential part of the cell cycle machinery is the cyclin-dependent kinases (CDKs). When activated, the CDKs provide a means for the cell to move from one phase of the cell cycle to the next (G1 to S or G2 to M). The cell cycle serves to protect the cell from genotoxic stress. In the setting of DNA damage, the CDKs are inhibited and the cell undergoes cell-cycle arrest. This provides the cell the opportunity to repair its own damaged DNA before it resumes cell proliferation. If a cell

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Deneka, Alexander Y., Margret B. Einarson, John Bennett, et al. "Synthetic Lethal Targeting of Mitotic Checkpoints in HPV-Negative Head and Neck Cancer." Cancers 12, no. 2 (2020): 306. http://dx.doi.org/10.3390/cancers12020306.

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Head and neck squamous cell carcinomas (HNSCC) affect more than 800,000 people annually worldwide, causing over 15,000 deaths in the US. Among HNSCC cancers, human papillomavirus (HPV)-negative HNSCC has the worst outcome, motivating efforts to improve therapy for this disease. The most common mutational events in HPV-negative HNSCC are inactivation of the tumor suppressors TP53 (>85%) and CDKN2A (>57%), which significantly impairs G1/S checkpoints, causing reliance on other cell cycle checkpoints to repair ongoing replication damage. We evaluated a panel of cell cycle-targeting clinical

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Shivakumar, Latha, John Minna, Toshiyuki Sakamaki, Richard Pestell, and Michael A. White. "The RASSF1A Tumor Suppressor Blocks Cell Cycle Progression and Inhibits Cyclin D1 Accumulation." Molecular and Cellular Biology 22, no. 12 (2002): 4309–18. http://dx.doi.org/10.1128/mcb.22.12.4309-4318.2002.

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ABSTRACT The RASSF1A locus at 3p21.3 is epigenetically inactivated at high frequency in a variety of solid tumors. Expression of RASSF1A is sufficient to revert the tumorigenicity of human cancer cell lines. We show here that RASSF1A can induce cell cycle arrest by engaging the Rb family cell cycle checkpoint. RASSF1A inhibits accumulation of native cyclin D1, and the RASSF1A-induced cell cycle arrest can be relieved by ectopic expression of cyclin D1 or of other downstream activators of the G1/S-phase transition (cyclin A and E7). Regulation of cyclin D1 is responsive to native RASSF1A activi

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Bhutani, Divaya, Siyang Leng, Samuel Pan, et al. "Combination Chemotherapy with Carfilzomib, Bendamustine and Dexamethasone Is Highly Active for Therapy of Newly Diagnosed Multiple Myeloma-Results of Single Center Phase I/II Study." Blood 134, Supplement_1 (2019): 3196. http://dx.doi.org/10.1182/blood-2019-130207.

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Background: Carfilzomib and Bendamustine are currently FDA approved for therapy of relapsed refractory multiple myeloma (MM). Bendamustine, in addition to interference with DNA replication, it can induce inhibition of mitotic checkpoints, inefficient DNA repair, and initiation of a p53-dependent DNA-damaging stress response leading to apoptosis of tumor cells (1). It has previously shown significant activity in relapsed myeloma (2). Carfilzomib is a second generation, irreversible proteasome inhibitor has demonstrated promising activity in first line therapy (3,4). we hypothesized that combini

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Rohatgi, Anjali, Ryan Campbell Massa, William E. Gooding, Tullia C. Bruno, Dario Vignali, and John M. Kirkwood. "A phase II study of anti-PD1 monoclonal antibody (Nivolumab) administered in combination with anti-LAG3 monoclonal antibody (Relatlimab) in patients with metastatic melanoma naive to prior immunotherapy in the metastatic setting." Journal of Clinical Oncology 38, no. 15_suppl (2020): TPS10085. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.tps10085.

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TPS10085 Background: Novel checkpoint inhibitors are a promising treatment for advanced melanoma, as only a fraction of patients have durable responses to current FDA-approved immunotherapy. Lymphocyte activation gene 3 (LAG3) is an inhibitory checkpoint receptor on CD4+ and CD8+ T cells, where engagement results in suppression of T cell activation and proliferation. LAG3 and PD1 are co-expressed on T cells during T cell receptor signaling and are down-regulated after antigen clearance. Persistent stimulation leads to prolonged LAG3 and PD1 expression and to T cell exhaustion, a possible mecha

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Querfeld, Christiane, Ni-Chun Tsai, Joycelynne Palmer, 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 136, Supplement 1 (2020): 20. http://dx.doi.org/10.1182/blood-2020-143354.

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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 (NCT03011814) 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, a

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Honasoge, Avinash, Katherine A. Shelton, and Harald Sontheimer. "Autocrine regulation of glioma cell proliferation via pHe-sensitive K+ channels." American Journal of Physiology-Cell Physiology 306, no. 5 (2014): C493—C505. http://dx.doi.org/10.1152/ajpcell.00097.2013.

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Since the seminal studies of Otto Warburg in the 1920s, it has been widely recognized that cancers grow glycolytically, even in the presence of oxygen. This generates an abundance of protons in a gradient across most solid tumors with an acidic core and an alkaline rim. Whether and how this proton gradient may also serve in an autocrine fashion in these tumors is unclear. We demonstrate that human glioma cells form spheroids that act as a viable three-dimensional tumor model, forming physiologically relevant extracellular pH (pHe) and cell proliferation gradients. Using fluorescent cell cycle

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Mullan, Brendan, Tingting Qin, Ruby Siada, et al. "GENE-17. ATRX LOSS IN GLIOMA RESULTS IN EPIGENETIC DYSREGULATION OF THE G2/M CHECKPOINT AND SENSITIVITY TO ATM INHIBITION." Neuro-Oncology 21, Supplement_6 (2019): vi101. http://dx.doi.org/10.1093/neuonc/noz175.419.

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Abstract Gliomas are a leading cause of cancer mortality in children and adults and new targeted therapies are desperately needed. ATRX is a chromatin remodeling protein that is recurrently mutated in H3F3A-mutant pediatric GBM and IDH-mutant grade 2/3 adult glioma. We previously showed that loss of ATRX in glioma results in tumor growth and additional tumor mutations. However, the mechanism driving these phenotypes has not been fully established. We found that in ChIP-Seq datasets of mouse neuronal precursor cells (NPCs) and experimental models of human glioma cells, ATRX binds and regulates

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Mahadevan, Daruka, Xiaobing Liu, Daniel Oscar Persky, Thomas P. Miller, Matthew S. Squires, and Wenqing Qi. "AT9283, a Novel Pan-Aurora/JAK-2 Kinase Inhibitor Suppresses Tumor Growth In Aggressive B-Cell Non-Hodgkin's Lymphoma." Blood 116, no. 21 (2010): 3930. http://dx.doi.org/10.1182/blood.v116.21.3930.3930.

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Abstract Abstract 3930 Aurora kinases (A and B) are oncogenic serine/threonine kinases that play a central role in regulating the mitotic phase of the eukaryotic cell cycle. Auroras are over-expressed in numerous tumors including aggressive B-cell non-Hodgkin's lymphomas (B-NHL) and are considered validated oncology targets. AT9283 a pan-Aurora/JAK-2 inhibitor has undergone early phase trials in acute and chronic myeloid leukemia with promising anti-tumor activity. Hence, we hypothesized that 1) targeting mitosis with AT9283 would be effective in promoting apoptosis in aggressive B-NHL cell li

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Levitt, Peter S., Min Zhu, Amy Cassano, et al. "Genome Maintenance Defects in Cultured Cells and Mice following Partial Inactivation of the Essential Cell Cycle Checkpoint Gene Hus1." Molecular and Cellular Biology 27, no. 6 (2007): 2189–201. http://dx.doi.org/10.1128/mcb.01763-06.

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ABSTRACT Cell cycle checkpoints are evolutionarily conserved signaling pathways that uphold genomic integrity. Complete inactivation of the mouse checkpoint gene Hus1 results in chromosomal instability, genotoxin hypersensitivity, and embryonic lethality. To determine the functional consequences of partial Hus1 impairment, we generated an allelic series in which Hus1 expression was incrementally reduced by combining a hypomorphic Hus1 allele, Hus1 neo , with either wild-type or null (Hus1 Δ1 ) alleles. Primary Hus1 neo/Δ1 embryonic fibroblasts exhibited spontaneous chromosomal abnormalities an

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Rancourt, Raymond C., Peter C. Keng, Christopher E. Helt, and Michael A. O'Reilly. "The role of p21CIP1/WAF1 in growth of epithelial cells exposed to hyperoxia." American Journal of Physiology-Lung Cellular and Molecular Physiology 280, no. 4 (2001): L617—L626. http://dx.doi.org/10.1152/ajplung.2001.280.4.l617.

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Previous studies have shown that hyperoxia inhibits proliferation and increases the expression of the tumor suppressor p53 and its downstream target, the cyclin-dependent kinase inhibitor p21CIP1/WAF1, which inhibits proliferation in the G1 phase of the cell cycle. To determine whether growth arrest was mediated through activation of the p21-dependent G1 checkpoint, the kinetics of cell cycle movement during exposure to 95% O2 were assessed in the Mv1Lu and A549 pulmonary adenocarcinoma cell lines. Cell counts, 5-bromo-2′-deoxyuridine incorporation, and cell cycle analyses revealed that growth

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Schwartz, Gary K., and Manish A. Shah. "Targeting the Cell Cycle: A New Approach to Cancer Therapy." Journal of Clinical Oncology 23, no. 36 (2005): 9408–21. http://dx.doi.org/10.1200/jco.2005.01.5594.

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The cell cycle represents a series of tightly integrated events that allow the cell to grow and proliferate. Critical parts of the cell cycle machinery are the cyclin-dependent kinases (CDKs), which, when activated, provide a means for the cell to move from one phase of the cell cycle to the next. The CDKs are regulated positively by cyclins and regulated negatively by naturally occurring CDK inhibitors (CDKIs). Cancer represents a dysregulation of the cell cycle such that cells that overexpress cyclins or do not express the CDKIs continue to undergo unregulated cell growth. The cell cycle als

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Barr, Paul M., Kenneth Robert Carson, Joshua Brody, et al. "CheckMate 436: A phase 1-2 study to evaluate safety and efficacy of nivolumab plus brentuximab vedotin in patients with CD30-expressing relapsed/refractory non-Hodgkin lymphomas." Journal of Clinical Oncology 35, no. 15_suppl (2017): TPS7577. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.tps7577.

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TPS7577 Background: Nivolumab (nivo) is a PD-1 immune checkpoint inhibitor that augments T-cell activation and host anti-tumor responses. PD-1 blockade has shown promise in B- and T-cell non-Hodgkin lymphoma (NHL),1 but many patients (pts) with NHL do not respond or progress after response. Combination therapy using anti-tumor agents with complementary mechanisms of action and low immunosuppressive impact may result in more frequent and durable responses. Brentuximab vedotin (BV) is an anti-CD30 antibodydrug conjugate that induces cell cycle arrest and apoptosis, with activity in a range of N

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Graeber, T. G., J. F. Peterson, M. Tsai, K. Monica, A. J. Fornace, and A. J. Giaccia. "Hypoxia induces accumulation of p53 protein, but activation of a G1-phase checkpoint by low-oxygen conditions is independent of p53 status." Molecular and Cellular Biology 14, no. 9 (1994): 6264–77. http://dx.doi.org/10.1128/mcb.14.9.6264-6277.1994.

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It has been convincingly demonstrated that genotoxic stresses cause the accumulation of the tumor suppressor gene p53. One important consequence of increased p53 protein levels in response to DNA damage is the activation of a G1-phase cell cycle checkpoint. It has also been shown that G1-phase cell cycle checkpoints are activated in response to other stresses, such as lack of oxygen. Here we show that hypoxia and heat, agents that induce cellular stress primarily by inhibiting oxygen-dependent metabolism and denaturing proteins, respectively, also cause an increase in p53 protein levels. The p

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Graeber, T. G., J. F. Peterson, M. Tsai, K. Monica, A. J. Fornace, and A. J. Giaccia. "Hypoxia induces accumulation of p53 protein, but activation of a G1-phase checkpoint by low-oxygen conditions is independent of p53 status." Molecular and Cellular Biology 14, no. 9 (1994): 6264–77. http://dx.doi.org/10.1128/mcb.14.9.6264.

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It has been convincingly demonstrated that genotoxic stresses cause the accumulation of the tumor suppressor gene p53. One important consequence of increased p53 protein levels in response to DNA damage is the activation of a G1-phase cell cycle checkpoint. It has also been shown that G1-phase cell cycle checkpoints are activated in response to other stresses, such as lack of oxygen. Here we show that hypoxia and heat, agents that induce cellular stress primarily by inhibiting oxygen-dependent metabolism and denaturing proteins, respectively, also cause an increase in p53 protein levels. The p

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Harb, Wael A., Lee S. Rosen, Ding Wang, et al. "A phase I study of enadenotucirev (EnAd), an oncolytic Ad11/Ad3 chimeric group B adenovirus, in combination with nivolumab in tumors of epithelial origin." Journal of Clinical Oncology 35, no. 15_suppl (2017): TPS3115. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.tps3115.

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TPS3115 Background: EnAd is a tumor-selective chimeric Ad11/Ad3 group B oncolytic adenovirus developed using directed evolution. Phase I clinical studies have identified a well-tolerated systemic dose and regimen for EnAd monotherapy. EnAd shows a high level of selective replication and cell killing for a broad range of carcinoma cell lines with little replication in normal and non-carcinoma cells. Previous studies have shown that after systemic administration there is significant uptake and replication of EnAd in various carcinomas associated with improved CD8+ T-cell tumor infiltration. Thes

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Mohanty, Suchismita, Thai Tran, Natalie Sandoval, et al. "Cyclin D1 Promotes Survival and Chemoresistance By Maintaining ATR and CHEK1 Signaling in TP53-Deficient Mantle Cell Lymphoma Cell Lines." Blood 124, no. 21 (2014): 5197. http://dx.doi.org/10.1182/blood.v124.21.5197.5197.

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Abstract Mantle cell lymphoma (MCL) is a heterogeneous disease, ranging from indolent to aggressive conditions. Prognostic markers that predict aggressive MCL include blastoid cytologic features, high proliferation index (Argatoff et al. 1997), INK4A/ARF locus deletion (Dreyling et al. 1997), TP53 deletion and/or mutations (Greiner et al. 1996), elevated cyclin D1 (CCND1) expression (Rosenwald et al. 2003), and NOTCH1/2 mutations (Kridel et al. 2012, Bea et al. 2013). Among these, TP53 lesions are the most recurrent, suggesting their important role in MCL pathogenesis. In response to DNA damag

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Bono, Petri, Reetta Virtakoivu, Felix Vaura, et al. "Immune activation in first-in-human anti-macrophage antibody (anti-Clever-1 mAb; FP-1305) phase I/II MATINS trial: Part I dose-escalation, safety, and efficacy results." Journal of Clinical Oncology 38, no. 15_suppl (2020): 3097. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.3097.

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3097 Background: The scavenger receptor CLEVER-1 mediates the clearance of “unwanted” self-components and is highly expressed on tumor associated macrophages (TAMs). CLEVER-1 expression is associated with immunotherapy resistance and poor survival in several cancers. Pre-clinical studies demonstrate that CLEVER-1 inhibition increases TAM pro-inflammatory cytokine secretion and antigen presentation reactivating CD8 T cell responses with robust anti-tumor activity. Targeting CLEVER-1 could therefore overcome the immunosuppressive tumor microenvironment and has led to the development of FP-1305,

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Janku, Filip, James Strauss, Raghad Karim, et al. "A phase Ia/Ib dose-escalation study of intravenously administered SB 11285 alone and in combination with nivolumab in patients with advanced solid tumors." Journal of Clinical Oncology 38, no. 15_suppl (2020): TPS3162. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.tps3162.

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TPS3162 Background: Activation of the Stimulator of Interferon Genes (STING) pathway in immune cells in the tumor microenvironment (TME) and tumor cells results in the induction of innate and adaptive immunity and subsequent activation of cytotoxic T cells and NK cells for durable anti-tumor responses. SB 11285 is a novel agonist of the STING pathway leading to the activation of tumor-resident APCs and priming of tumor antigen specific CD8+ T cells. In our preclinical studies using multiple tumor-derived cell lines, SB 11285 has been observed to cause the induction of cytokines, such as INF-b,

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Iuchi, Toshihiko, Ryusuke Hara, Hajime Kageyama, et al. "SPDR-09 CHANGES IN CELL CYCLE-RELATED GENE EXPRESSIONS OF GLIOBLASTOMAS BEFORE AND IMMEDIATELY AFTER CHEMO-RADIATION THERAPY." Neuro-Oncology Advances 1, Supplement_2 (2019): ii7. http://dx.doi.org/10.1093/noajnl/vdz039.033.

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Abstract PURPOSE/OBJECTIVE The molecular responses of glioblastomas (GBMs) to hypofractionated IMRT/TMZ were investigated to elucidate the molecular targets included in the resistance of these tumors to chemo-radiation therapy. MATERIALS /METHODS Phase I study of neo-adjuvant IMRT (72Gy/12Fx.)/TMZ for the treatment of patients with GBMs had been performed previously in our institution. In this trial, stereotactic biopsy of the tumor to confirm the pathological diagnosis prior to treatment was required, and tumor removal was scheduled within 10 days after completion of IMRT/TMZ. Therefore, both

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Pillai, Rathi Narayana, Suresh S. Ramalingam, David P. Carbone, et al. "Randomized, open-label phase Ib/II study of atezolizumab with or without daratumumab in previously treated advanced or metastatic non-small cell lung cancer (NSCLC)." Journal of Clinical Oncology 35, no. 15_suppl (2017): TPS9102. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.tps9102.

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TPS9102 Background: Daratumumab (DARA), a human CD38 monoclonal antibody, is approved for treatment of relapsed/refractory multiple myeloma (RRMM). DARA produces deep clinical responses in RRMM and induces T-cell expansion through reduction of immune suppressive cell populations (CD38+ myeloid-derived suppressor cells and regulatory T and B cells). Atezolizumab (atezo) blocks programmed death-ligand 1 (PD-L1) and was recently approved for metastatic NSCLC that progressed on or during platinum therapy based on data showing improved overall survival (OS) in the atezo vs docetaxel treatment arm.

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Blais, Alexandre, Chris J. C. van Oevelen, Raphaël Margueron, Diego Acosta-Alvear, and Brian David Dynlacht. "Retinoblastoma tumor suppressor protein–dependent methylation of histone H3 lysine 27 is associated with irreversible cell cycle exit." Journal of Cell Biology 179, no. 7 (2007): 1399–412. http://dx.doi.org/10.1083/jcb.200705051.

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The retinoblastoma tumor suppressor protein (pRb) is involved in mitotic exit, promoting the arrest of myoblasts, and myogenic differentiation. However, it is unclear how permanent cell cycle exit is maintained in differentiated muscle. Using RNA interference, expression profiling, and chromatin immunoprecipitations, we show that pRb is essential for cell cycle exit and the differentiation of myoblasts and is also uniquely required to maintain this arrest in myotubes. Remarkably, we also uncover a function for the pRb-related proteins p107 and p130 as enforcers of a G2/M phase checkpoint that

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Yentz, Sarah Elizabeth, Melissa Andrea Reimers, Monika Joshi, et al. "Single-arm phase ib/II study of durvalumab and guadecitabine in advanced kidney cancer (NCT03308396)." Journal of Clinical Oncology 36, no. 6_suppl (2018): TPS711. http://dx.doi.org/10.1200/jco.2018.36.6_suppl.tps711.

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TPS711 Background: Checkpoint inhibitor immunotherapy directed at PD1/PDL1 has shown clinical efficacy in advanced clear cell Renal Cell Cancer (ccRCC). However, only a minority of patients respond to anti-PD1 monotherapy. There is an urgent unmet need to improve response rates including through rational combinations to reverse immune evasion by tumors. The chemokines CXCL9 and CXCL10 in the tumor micro-environment are chemo-attractants for activated NK and Th1 cells and are critical for anti-tumor immunity. Preclinical data from our group showed hypermethylation induced silencing of CXCL9/10

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Ingles Garces, Alvaro Henrique, Maxime Chenard-Poirier, Robert Hugh Jones, et al. "A phase I study of oral SRA737 (formerly CCT245737) given in combination with gemcitabine plus cisplatin or gemcitabine alone in patients with advanced cancer." Journal of Clinical Oncology 35, no. 15_suppl (2017): TPS2613. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.tps2613.

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TPS2613 Background: SRA737 is a highly selective, orally bioavailable small molecule inhibitor of Checkpoint kinase 1 (Chk1), a key cell cycle checkpoint and central regulator of the DNA Damage Response (DDR) network. In cancer cells, replication stress induced by genomic alterations in oncogenes (eg, MYC and RAS) combined with loss of function in tumor suppressors (eg, TP53 and ATM) results in persistent DNA damage and genomic instability. Targeted inhibition of components of the DDR network such as Chk1 by SRA737 may be synthetically lethal to cancer cells. Chk1 is also believed to facilitat

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Joerger, Markus, Anastasios Stathis, Ioannis Metaxas, et al. "A phase I study to assess the safety, pharmacokinetics (PK), pharmacodynamics (PD) and antitumor activities of BAL101553, a novel tumor checkpoint controller (TCC), administered as 48-hour infusion in adult patients with advanced solid tumors." Journal of Clinical Oncology 35, no. 15_suppl (2017): TPS2602. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.tps2602.

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TPS2602 Background: BAL101553 (prodrug of BAL27862), is a novel TCC that promotes tumor cell death by modulating the spindle assembly checkpoint. BAL27862 has shown potent antitumor activity in diverse preclinical tumor models, including models refractory to standard therapies. In a completed Phase 1 study using 2-h IV infusions (Days 1, 8, 15, q28d, NCT01397929 , CDI-CS-001, Lopez et al. JCO 34, 2016 suppl; 2525) dose-limiting vascular effects were observed and appeared Cmax related. The recommended Phase 2 dose for 2-h IV BAL101553 is 30 mg/m2. Vascular toxicity was not observed in an ongoin

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Yang, Jie, Fan Yu, Jinlei Guan, et al. "Knockdown of RNF2 enhances the radiosensitivity of squamous cell carcinoma in lung." Biochemistry and Cell Biology 97, no. 5 (2019): 589–99. http://dx.doi.org/10.1139/bcb-2018-0252.

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A previous study has reported that knockdown of RING finger protein 2 (RNF2) increases the radiosensitivity of esophageal cancer cells both in vitro and in vivo. However, the effect of RNF2 knockdown on radiosensitivity in squamous cell carcinoma (SqCC) remains unknown. For this, NCI-H226 and SK-MES-1 cells were exposed to X-ray irradiation and then RNF2 levels were determined. RNF2 was knocked-down and stable transfectants were selected. Radiosensitivity, cell proliferation, apoptosis, cell cycle, and γ-H2AX foci formation were evaluated. Interaction among ataxia telangiectasia mutated protei

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Krohs, Julika, Dominik Schnerch, Marie Follo, Julia Felthaus, Monika Engelhardt, and Ralph M. Waesch. "The Tumor Suppressor APC/CCdh1 and Its Role In Replication Stress and The Origin Of Genomic Instability." Blood 122, no. 21 (2013): 2489. http://dx.doi.org/10.1182/blood.v122.21.2489.2489.

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Abstract Introduction We have previously proposed that Cdh1 is a tumor suppressor by maintaining genomic stability. We also found Cdh1 downregulated in several tumor cell lines including AML (Oncogene 2008; 27:907-17). Heterozygous Cdh1 knockout mice develop epithelial tumors, myelodysplasia and plasma cell dyscrasias (Nat. Cell Biol. 2008;10:802-11). By analyzing primary AML samples from bone marrow (BM) or peripheral blood (PB) we detected downregulation of Cdh1 in the vast majority of samples when compared to normal CD34+ HSCs. Progression through the cell cycle is tightly regulated by diff

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Wijnen, Rosa, Camilla Pecoraro, Daniela Carbone, et al. "Cyclin Dependent Kinase-1 (CDK-1) Inhibition as a Novel Therapeutic Strategy against Pancreatic Ductal Adenocarcinoma (PDAC)." Cancers 13, no. 17 (2021): 4389. http://dx.doi.org/10.3390/cancers13174389.

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The role of CDK1 in PDAC onset and development is two-fold. Firstly, since CDK1 activity regulates the G2/M cell cycle checkpoint, overexpression of CDK1 can lead to progression into mitosis even in cells with DNA damage, a potentially tumorigenic process. Secondly, CDK1 overexpression leads to the stimulation of a range of proteins that induce stem cell properties, which can contribute to the development of cancer stem cells (CSCs). CSCs promote tumor-initiation and metastasis and play a crucial role in the development of PDAC. Targeting CDK1 showed promising results for PDAC treatment in dif

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Sablina, A. A., G. V. Ilyinskaya, S. N. Rubtsova, L. S. Agapova, P. M. Chumakov, and B. P. Kopnin. "Activation of p53-mediated cell cycle checkpoint in response to micronuclei formation." Journal of Cell Science 111, no. 7 (1998): 977–84. http://dx.doi.org/10.1242/jcs.111.7.977.

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Inactivation of p53 tumor-suppressor leads to genetic instability and, in particular, to accumulation of cells with abnormal numbers of chromosomes. In order to better define the role of p53 function in maintaining genome integrity we investigated the involvement of p53 in the control of proliferation of micronucleated cells resulting from abnormal chromosome segregation. Using cell lines expressing temperature-sensitive (ts) p53 or containing p53 genetic suppressor element (p53-GSE) we showed that inhibition of p53 function increases the frequency of cells with micronuclei. Immunofluorescence

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Itamochi, Hiroaki, Mayumi Nishimura, Nao Oumi, et al. "Checkpoint Kinase Inhibitor AZD7762 Overcomes Cisplatin Resistance in Clear Cell Carcinoma of the Ovary." International Journal of Gynecologic Cancer 24, no. 1 (2014): 61–69. http://dx.doi.org/10.1097/igc.0000000000000014.

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ObjectiveCheckpoint kinase (Chk) inhibitors are thought to increase the cytotoxic effects of DNA-damaging agents and are undergoing clinical trials. The present study was aimed to assess the potential to use the Chk1 and Chk2 inhibitor, AZD7762, with other anticancer agents in chemotherapy to treat ovarian clear cell carcinoma.MethodsFour ovarian clear cell carcinoma cell lines were used in this study. We treated the cells with AZD7762 and anticancer agents, then assessed cell viability, cell cycle distribution, apoptosis, and the expression of protein in apoptotic pathways and molecules downs

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Zivadinovic, Radomir, Aleksandra Petric, Goran Lilic, Vekoslav Lilic, and Biljana Djordjevic. "Persistent human papillomavirus infection in the etiology of cervical carcinoma: The role of immunological, genetic, viral and cellular factors." Srpski arhiv za celokupno lekarstvo 142, no. 5-6 (2014): 378–83. http://dx.doi.org/10.2298/sarh1406378z.

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The aim of this paper was to present the role of human papillomavirus (HPV) in cervical carcinogenesis from several aspects. By explaining the HPV virus lifecycle and structure, its effect on cervical cell cycle and subversion of immune response can be better understood. Early E region of the viral genome encodes proteins that are directly involved in carcinogenesis. The E6 protein binds to p53 protein (product of tumor-suppressor gene) blocking and degrading it, which in turn prevents cell cycle arrest and apoptosis induction. E6 is also capable of telomerase activation, which leads to cell i

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