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https://www.readbyqxmd.com/read/29445424/promoter-methylation-of-dna-damage-repair-ddr-genes-in-human-tumor-entities-rbbp8-ctip-is-almost-exclusively-methylated-in-bladder-cancer
#1
Jolein Mijnes, Jürgen Veeck, Nadine T Gaisa, Eduard Burghardt, Tim C de Ruijter, Sonja Gostek, Edgar Dahl, David Pfister, Sebastian C Schmid, Ruth Knüchel, Michael Rose
Background: Genome-wide studies identified pan-cancer genes and shared biological networks affected by epigenetic dysregulation among diverse tumor entities. Here, we systematically screened for hypermethylation of DNA damage repair (DDR) genes in a comprehensive candidate-approach and exemplarily identify and validate candidate DDR genes as targets of epigenetic inactivation unique to bladder cancer (BLCA), which may serve as non-invasive biomarkers. Methods: Genome-wide DNA methylation datasets (2755 CpG probes of n = 7819 tumor and n = 659 normal samples) of the TCGA network covering 32 tumor entities were analyzed in silico for 177 DDR genes...
2018: Clinical Epigenetics
https://www.readbyqxmd.com/read/29435332/more-is-less-less-is-more-or-does-it-really-matter-the-curious-case-of-impact-of-azacitidine-administration-schedules-on-outcomes-in-patients-with-myelodysplastic-syndromes
#2
Rory M Shallis, Amer M Zeidan
Myelodysplastic syndromes (MDS) encompass a diverse group of hematologic disorders characterized by ineffective and malignant hematopoiesis, peripheral cytopenias and significantly increased risk of progression to acute myeloid leukemia (AML). The hypomethylating agents (HMA) azacitidine and decitabine induce meaningful clinical responses in a significant subset of patients with MDS. Though never compared directly with decitabine, only azacitidine has improved overall survival (OS) compared to conventional care in a randomized trial in patients with higher-risk MDS...
2018: BMC Hematology
https://www.readbyqxmd.com/read/29423093/combination-of-a-hypomethylating-agent-and-inhibitors-of-parp-and-hdac-traps-parp1-and-dnmt1-to-chromatin-acetylates-dna-repair-proteins-down-regulates-nurd-and-induces-apoptosis-in-human-leukemia-and-lymphoma-cells
#3
Benigno C Valdez, Yang Li, David Murray, Yan Liu, Yago Nieto, Richard E Champlin, Borje S Andersson
Combination of drugs that target different aspects of aberrant cellular processes is an efficacious treatment for hematological malignancies. Hypomethylating agents (HMAs) and inhibitors of poly(ADP-ribose) polymerases (PARPis) and histone deacetylases (HDACis) are clinically active anti-tumor drugs. We hypothesized that their combination would be synergistically cytotoxic to leukemia and lymphoma cells. Exposure of AML and lymphoma cell lines to the combination of the PARPi niraparib (Npb), the HMA decitabine (DAC) and the HDACi romidepsin (Rom) or panobinostat (Pano) synergistically inhibited cell proliferation by up to 70% via activation of the ATM pathway, increased production of reactive oxygen species, decreased mitochondrial membrane potential, and activated apoptosis...
January 9, 2018: Oncotarget
https://www.readbyqxmd.com/read/29423052/mage-a11-is-activated-through-tfcp2-zeb1-binding-sites-de-methylation-as-well-as-histone-modification-and-facilitates-escc-tumor-growth
#4
Shina Liu, Fei Liu, Weina Huang, Lina Gu, Lingjiao Meng, Yingchao Ju, Yunyan Wu, Juan Li, Lihua Liu, Meixiang Sang
Recently, we have reported that the product of Melanoma Antigens Genes (MAGE) family member MAGE-A11 is an independent poor prognostic marker for esophageal squamous cell carcinoma (ESCC). However, the reason how MAGE-A11 is activated in ESCC progression still remains unclear. In the current study, we demonstrated that DNA methylation and the subsequent histone posttranslational modifications play crucial roles in the regulation of MAGE-A11 in ESCC progression. We found that the methylation rate of TFCP2/ZEB1 binding site on MAGE-A11 promoter in ESCC tissues and cells is higher than the normal esophageal epithelial tissues and cells...
January 9, 2018: Oncotarget
https://www.readbyqxmd.com/read/29404266/necrotizing-fungal-gingivitis-in-a-patient-with-acute-myelogenous-leukemia-visible-yet-obscure
#5
Prajwal Boddu, Pei-Ling Chen, Priyadharsini Nagarajan, Victor G Prieto, Alex Won, Mark Chambers, Steven Kornblau
Oral fungal infections present with atypical and varied manifestations, and distinguishing them from other entities including leukemic infiltration can be diagnostically challenging. In this report, we describe a 62 year old female with acute myeloid leukemia who presented, towards the end of her second treatment cycle of decitabine in a prolonged neutropenic state, with a month of painful, necrotic-appearing marginal gingival lesions. She was duly initiated on empiric broad spectrum antifungal treatment but did not show a clinical response with the appearance of new skin lesions concerning for progressive fungemia...
January 2018: Journal of Oral and Maxillofacial Surgery, Medicine, and Pathology
https://www.readbyqxmd.com/read/29402783/monoclonal-gammopathy-responsive-to-decitabine-given-for-acute-myeloid-leukemia-in-a-frail-patient
#6
Pasquale Niscola, Benedetta Neri, Luciana Morino, Paolo de Fabritiis
No abstract text is available yet for this article.
January 17, 2018: Acta Haematologica
https://www.readbyqxmd.com/read/29397843/-comparison-of-decitabine-rigimen-and-traditional-chemotherapy-regimen-in-treatment-of-patients-with-intermediate-or-high-risk-myelodysplastic-syndrome
#7
Qian-Peng Zhang, Yong-Sheng Han, Xiang Wan, Guang-Yu Sun
OBJECTIVE: To compare the clinical efficacy and relevant adverse reactions of homebred decitabine regimen and traditional chemotherapy regimen in treatment of patients with intermediate or high-risk myelodysplastic syndrome (MDS). METHODS: Forty-eight patients suffered from newly diagnosed intermediate or high-risk MDS from December 2011 to December 2016 were analyzed retrospectively. Among them 29 patients were treated by traditional chemotherapy regimen, and 19 patients were treated by decitabine regimen [15 mg/(m2·d), ivgtt, d1-5]...
February 2018: Zhongguo Shi Yan Xue Ye Xue za Zhi
https://www.readbyqxmd.com/read/29397824/-clinical-efficacy-of-decitabine-combined-with-or-without-cytarabine-based-low-dose-regimen-for-senile-patients-with-acute-myeloid-leukemia
#8
Hong-Wei Zhou, Min-Hang Zhou, Zhi-Hong Wang, Peng-Fei Li, Mo Liu, Yu DU, Yi-Bing Yao, Chao-Jin Peng, Yu Jing, Jun-Zhong Sun
OBJECTIVE: To investigate the therapeutic effectiveness and side effects of decitabine combined with or without cytarabine-based low dose regimen for acute myeloid leukemia in geratic patients. METHODS: Clinical data of 8 geratic patients (aged over 70 years) suffered from acute myeloid leukemia from September 2009 to March 2012 were analyzed retrospectively, including age, sex, peripheral blood and bone marrow characteristics and so on. These patients were treated by an 1-hour intravenous infusion of decitabine 20 mg/m2 per day for 5 consecutive days every 4 weeks combined with or without low dose regimen dominantly consisting of cytarabine 20 mg per day as subcutaneous injection for seven consecutive days...
February 2018: Zhongguo Shi Yan Xue Ye Xue za Zhi
https://www.readbyqxmd.com/read/29383097/efficacy-of-decitabine-loaded-gelatinases-stimuli-nanoparticles-in-overcoming-cancer-drug-resistance-is-mediated-via-its-enhanced-demethylating-activity-to-transcription-factor-ap-2-epsilon
#9
Yi-Dong Hong, Jian Zhang, Ming Zhuang, Wei Li, Puy-Uan Wu, Ru-Tian Li, Nan Hu, Bao-Xiang Bian, Zi-Yan Song, Feng-Lei Wu
Hypermethylation of the transcription factor AP-2 epsilon (TFAP2E) gene affects 5-fluorouridine (5-FU) resistance in gastric cancer (GC) patients. The epigenetic inhibitor 5-Aza-2'-deoxycytidine (DAC), which reverses DNA methylation by targeting DNA methyltransferases (DNMTs), has potential to sensitize GC to 5-FU. Nevertheless, DNA demethylation only DAC transiently occurs since DAC is unstable in aqueous solutions, which limits its potential. Here we developed intelligent nanoparticles (NPs) comprising gelatinase with polyethylene glycol (PEG) and poly-ε-caprolactone) (PCL) to specifically deliver DAC (DAC-TNPs) to tumors...
December 29, 2017: Oncotarget
https://www.readbyqxmd.com/read/29373959/sequential-decitabine-and-carboplatin-treatment-increases-the-dna-repair-protein-xpc-increases-apoptosis-and-decreases-proliferation-in-melanoma
#10
Timothy Budden, Andre van der Westhuizen, Nikola A Bowden
BACKGROUND: Melanoma has two key features, an over-representation of UV-induced mutations and resistance to DNA damaging chemotherapy agents. Both of these features may result from dysfunction of the nucleotide excision repair pathway, in particular the DNA damage detection branch, global genome repair (GGR). The key GGR component XPC does not respond to DNA damage in melanoma, the cause of this lack of response has not been investigated. In this study, we investigated the role of methylation in reduced XPC in melanoma...
January 26, 2018: BMC Cancer
https://www.readbyqxmd.com/read/29368096/decitabine-augments-cytotoxicity-of-cisplatin-and-doxorubicin-to-bladder-cancer-cells-by-activating-hippo-pathway-through-rassf1a
#11
Madhuram Khandelwal, Vivek Anand, Sandeep Appunni, Amlesh Seth, Prabhjot Singh, Sandeep Mathur, Alpana Sharma
Genetic abnormalities and epigenetic alterations both play vital role in initiation as well as progression of cancer. Whereas genetic mutations cannot be reversed, epigenetic alterations such as DNA methylation can be reversed by the application of DNA methyltransferase inhibitor decitabine. Epigenetic silencing of RASSF1A and involvement of hippo pathway both have been shown to involve in chemo-resistance. Purpose of this study was to observe the effect of combination treatment of decitabine with cisplatin or doxorubicin on bladder cancer cells involving hippo pathway through RASSF1A...
January 24, 2018: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/29341428/epigenetic-silencing-of-tap1-in-aldefluor-breast-cancer-stem-cells-contributes-to-their-enhanced-immune-evasion
#12
Mohammad Sultan, Dejan Vidovic, Arianne S Paine, Thomas T Huynh, Krysta M Coyle, Margaret L Thomas, Brianne M Cruickshank, Cheryl A Dean, Derek R Clements, Youra Kim, Kristin Lee, Shashi A Gujar, Ian C Weaver, Paola Marcato
Avoiding detection and destruction by immune cells is key for tumor initiation and progression. The important role of cancer stem cells (CSC) in tumor initiation has been well established, yet their ability to evade immune detection and targeting is only partly understood. To investigate the ability of breast CSCs to evade immune detection we identified a highly tumorigenic population in a spontaneous murine mammary tumor based on increased aldehyde dehydrogenase (ALDH) activity. We performed tumor growth studies in immunocompetent and immunocompromised mice...
January 17, 2018: Stem Cells
https://www.readbyqxmd.com/read/29339403/a-phase-1-study-of-azacitidine-combined-with-chemotherapy-in-childhood-leukemia-a-report-from-tacl-consortium
#13
Weili Sun, Timothy Triche, Jemily Malvar, Paul Gaynon, Richard Sposto, Xiaojing Yang, Henrique Bittencourt, Andrew E Place, Yoav Messinger, Chris Fraser, Luciano Dalla-Pozza, Bodour Salhia, Peter Jones, Alan S Wayne, Lia Gore, Todd M Cooper, Gangning Liang
Growing evidence indicates that aberrant DNA hypermethylation is associated with leukemogenesis, chemotherapy resistance, and relapse. DNA methyltransferase inhibitors such as azacitidine and decitabine have been shown to reverse drug resistance and prime leukemia cells to cytotoxic agents in vitro. Here we report the first pediatric phase 1 study using azacitidine in sequence with chemotherapy in patients with relapsed/refractory leukemia. Fourteen patients were enrolled, twelve with acute myeloid leukemia (AML) and two with acute lymphoblastic leukemia (ALL)...
January 16, 2018: Blood
https://www.readbyqxmd.com/read/29339097/safety-and-preliminary-efficacy-of-venetoclax-with-decitabine-or-azacitidine-in-elderly-patients-with-previously-untreated-acute-myeloid-leukaemia-a-non-randomised-open-label-phase-1b-study
#14
Courtney D DiNardo, Keith W Pratz, Anthony Letai, Brian A Jonas, Andrew H Wei, Michael Thirman, Martha Arellano, Mark G Frattini, Hagop Kantarjian, Relja Popovic, Brenda Chyla, Tu Xu, Martin Dunbar, Suresh K Agarwal, Rod Humerickhouse, Mack Mabry, Jalaja Potluri, Marina Konopleva, Daniel A Pollyea
BACKGROUND: Elderly patients (aged ≥65 years) with acute myeloid leukaemia have poor outcomes and no effective standard-of-care therapy exists. Treatment with hypomethylating agents such as azacitidine and decitabine is common, but responses are modest and typically short-lived. The oral anti-apoptotic B-cell lymphoma 2 protein inhibitor, venetoclax, has shown promising single-agent activity in patients with relapsed or refractory acute myeloid leukaemia and preclinical data suggested synergy between hypomethylating agents and venetoclax, which led to this combination phase 1b study...
January 12, 2018: Lancet Oncology
https://www.readbyqxmd.com/read/29331774/the-synergy-of-vitamin-c-with-decitabine-activates-tet2-in-leukemic-cells-and-significantly-improves-overall-survival-in-elderly-patients-with-acute-myeloid-leukemia
#15
Huihui Zhao, Huayuan Zhu, Jiayu Huang, Yu Zhu, Ming Hong, Han Zhu, Jingjing Zhang, Shan Li, Lijia Yang, Yun Lian, Shuai Wang, Jianping Mao, Yaoyu Chen, Jianyong Li, Sixuan Qian
BACKGROUND: Decitabine is widely used in the treatment of acute myeloid leukemia (AML) in elderly patients. Low-dose Vitamin C has also been indicated to induce DNA demethylation at the cellular level. However, little is known whether low-dose Vitamin C has a synergistic effect with decitabine in clinic. METHODS: The effect of combined low-dose Vitamin C and decitabine on cell proliferation, the cell cycle, apoptosis and the expression level and activity of TET2 was investigated in HL60 and NB4 human leukemic cells...
January 2, 2018: Leukemia Research
https://www.readbyqxmd.com/read/29318382/mir-29-silencing-modulates-the-expression-of-target-genes-related-to-proliferation-apoptosis-and-methylation-in-burkitt-lymphoma-cells
#16
Luciano Mazzoccoli, Marcela Cristina Robaina, Alexandre Gustavo Apa, Martin Bonamino, Luciana Wernersbach Pinto, Eduardo Queiroga, Carlos E Bacchi, Claudete Esteves Klumb
PURPOSE: Burkitt lymphoma (BL) is a B-cell lymphoma frequently diagnosed in children. It is characterized by MYC translocations, which lead to the constitutive expression of the MYC oncogene. MYC contributes to miR-29 repression through an E-box MYC binding site on the miR-29b-1/miR-29a promoter region. We evaluated the role of miR-29a/b/c and their predicted targets in BL pathogenesis. METHODS: Mature sequences of miR-29a/b/c were transfected to the BL cell lines BL41 and Raji, and evaluated for DNMT3B, MCL1, BIM, CDK6, AKT and TCL1 protein expression as well as for MCL-1 and CDK6 mRNA expression...
January 9, 2018: Journal of Cancer Research and Clinical Oncology
https://www.readbyqxmd.com/read/29305415/histone-modifier-gene-mutations-in-peripheral-t-cell-lymphoma-not-otherwise-specified
#17
Meng-Meng Ji, Yao-Hui Huang, Jin-Yan Huang, Zhao-Fu Wang, Di Fu, Han Liu, Feng Liu, Christophe Leboeuf, Li Wang, Jing Ye, Yi-Ming Lu, Anne Janin, Shu Cheng, Wei-Li Zhao
Due to heterogeneous morphological and immunophenotypic features, approximately 50% of peripheral T-cell lymphomas are unclassifiable and categorized as peripheral T-cell lymphomas, not otherwise specified, presenting aggressive disease course and poor clinical outcome. Identification of actionable biomarkers is urgently needed to develop better therapeutic strategies. Epigenetic alterations play a crucial role in tumor progression. Histone modifications, particularly methylation and acetylation, are generally involved in chromatin state regulation...
January 5, 2018: Haematologica
https://www.readbyqxmd.com/read/29295935/estrogen-dependent-epigenetic-regulation-of-soluble-epoxide-hydrolase-via-dna-methylation
#18
Yang-Ming Yang, Dong Sun, Sharath Kandhi, Ghezal Froogh, Jian Zhuge, Weihua Huang, Bruce D Hammock, An Huang
To elucidate molecular mechanisms responsible for the sexually dimorphic phenotype of soluble epoxide hydrolase (sEH) expression, we tested the hypothesis that female-specific down-regulation of sEH expression is driven by estrogen-dependent methylation of the Ephx2 gene. Mesenteric arteries isolated from male, female, ovariectomized female (OV), and OV with estrogen replacement (OVE) mice, as well as the human cell line (HEK293T) were used. Methylation-specific PCR and bisulfite genomic sequencing analysis indicate significant increases in DNA/CG methylation in vessels of female and OVE compared with those of male and OV mice...
January 2, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29295500/decitabine-and-melphalan-fail-to-reactivate-p73-in-p53-deficient-myeloma-cells
#19
Pierre-Samuel Gillardin, Géraldine Descamps, Sophie Maiga, Benoit Tessoulin, Hanane Djamai, Benedetta Lucani, David Chiron, Philippe Moreau, Steven Le Gouill, Martine Amiot, Catherine Pellat-Deceunynck, Agnès Moreau-Aubry
(1) Background: TP53 deficiency remains a major adverse event in Multiple Myeloma (MM) despite therapeutic progresses. As it is not possible to target TP53 deficiency with pharmacological agents, we explored the possibility of activating another p53 family member, p73, which has not been well studied in myeloma. (2) Methods: Using human myeloma cell lines (HMCLs) with normal or abnormal TP53 status, we assessed TP73 methylation and expression. (3) Results: Using microarray data, we reported that TP73 is weakly expressed in 47 HMCLs and mostly in TP53 wild type (TP53wt) HMCLs (p = 0...
December 23, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29284705/immunotherapy-of-mds-you-can-run-but-you-can-t-hide
#20
Ephraim J Fuchs
The hypomethylating agent decitabine induces expression of the cancer testis antigen NY-ESO-1 in the myeloid cells of patients with myelodysplastic syndrome (MDS).  MDS patients treated with decitabine and an NY-ESO-1 vaccine developed NY-ESO-1-specific T cell responses directed against their abnormal myeloid cells, raising hopes for combinatorial immunotherapy of this disease.
December 28, 2017: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
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