نتایج جستجو برای: decitabine

تعداد نتایج: 2165  

2014
B Douglas Smith Charles L Beach Dalia Mahmoud Laura Weber Henry J Henk

BACKGROUND This study examined patient outcomes using real world data for acute myeloid leukemia (AML) patients initiating treatment. METHODS A retrospective, administrative claims-based, comparative analysis was developed to study outcomes for AML patients initiating treatment with decitabine or azacitidine between January 2006 and June 2012. RESULTS Treatment with azacitidine was associat...

2014
Chi T. Viet Dongmin Dang Stacy Achdjian Yi Ye Samuel G. Katz Brian L. Schmidt

Cisplatin resistance in head and neck squamous cell carcinoma (HNSCC) reduces survival. In this study we hypothesized that methylation of key genes mediates cisplatin resistance. We determined whether a demethylating drug, decitabine, could augment the anti-proliferative and apoptotic effects of cisplatin on SCC-25/CP, a cisplatin-resistant tongue SCC cell line. We showed that decitabine treatm...

2017
Xue Wang Jun Wang Yong Yu Tonghui Ma Ping Chen Bing Zhou Ran Tao

Multiple sclerosis (MS) is an autoimmune disease characterized by the dysregulated immune response including innate and adaptive immune responses. Increasing evidence has proven the importance of epigenetic modification in the progression of MS. Recent studies revealed that low-dose decitabine (Dec, 5-Aza-2'-deoxycytidine), which incorporates into replicating DNA and inhibits DNA methylation, c...

Journal: :PLoS ONE 2009
Ruth Halaban Michael Krauthammer Mattia Pelizzola Elaine Cheng Daniela Kovacs Mario Sznol Stephan Ariyan Deepak Narayan Antonella Bacchiocchi Annette Molinaro Yuval Kluger Min Deng Nam Tran Wengeng Zhang Mauro Picardo Jan J. Enghild

Decitabine, an epigenetic modifier that reactivates genes otherwise suppressed by DNA promoter methylation, is effective for some, but not all cancer patients, especially those with solid tumors. It is commonly recognized that to overcome resistance and improve outcome, treatment should be guided by tumor biology, which includes genotype, epigenotype, and gene expression profile. We therefore t...

Journal: :Blood 2012
Pearlly Yan David Frankhouser Mark Murphy Hok-Hei Tam Benjamin Rodriguez John Curfman Michael Trimarchi Susan Geyer Yue-Zhong Wu Susan P Whitman Klaus Metzeler Alison Walker Rebecca Klisovic Samson Jacob Michael R Grever John C Byrd Clara D Bloomfield Ramiro Garzon William Blum Michael A Caligiuri Ralf Bundschuh Guido Marcucci

The outcome of older (≥ 60 years) acute myeloid leukemia (AML) patients is poor, and novel treatments are needed. In a phase 2 trial for older AML patients, low-dose (20 mg/m(2) per day for 10 days) decitabine, a DNA hypomethylating azanucleoside, produced 47% complete response rate with an excellent toxicity profile. To assess the genome-wide activity of decitabine, we profiled pretreatment an...

Journal: :Haematologica 2014
Haiyang Yun Frederik Damm Damian Yap Adrian Schwarzer Anuhar Chaturvedi Nidhi Jyotsana Michael Lübbert Lars Bullinger Konstanze Döhner Robert Geffers Samuel Aparicio R Keith Humphries Arnold Ganser Michael Heuser

Hypomethylating agents are widely used in patients with myelodysplastic syndromes and unfit patients with acute myeloid leukemia. However, it is not well understood why only some patients respond to hypomethylating agents. We found previously that the effect of decitabine on hematopoietic stem cell viability differed between Mll5 wild-type and null cells. We, therefore, investigated the role of...

2017
Yousef Zakharia Varun Monga Umang Swami Aaron D. Bossler Michele Freesmeier Melanie Frees Mirza Khan Noah Frydenlund Rithu Srikantha Marion Vanneste Michael Henry Mohammed Milhem

Introduction Epigenetic modifications play an important role in progression and development of resistance in V600EBRAF positive metastatic melanoma. Therefore, we hypothesized that the action of vemurafenib (BRAF inhibitor) can be made more effective by combining with low dose decitabine (a DNA methyltransferase inhibitor). The primary objective of this phase lb study was to determine the dose ...

Journal: :Cancer research 2015
Michelle L Stewart Pablo Tamayo Andrew J Wilson Stephanie Wang Yun Min Chang Jong W Kim Dineo Khabele Alykhan F Shamji Stuart L Schreiber

Decitabine, a cancer therapeutic that inhibits DNA methylation, produces variable antitumor response rates in patients with solid tumors that might be leveraged clinically with identification of a predictive biomarker. In this study, we profiled the response of human ovarian, melanoma, and breast cancer cells treated with decitabine, finding that RAS/MEK/ERK pathway activation and DNMT1 express...

Journal: :Oncology letters 2016
Kai Ding Rong Fu Hui Liu Deepak Anil Nachnani Zong-Hong Shao

Thrombocytopenia is a common, often fatal complication experienced by patients with myelodysplastic syndromes (MDS). 5-aza-2'-deoxycytidine (decitabine) has been used to treat MDS patients with thrombocytopenia with a response rate of 45-50%. However, the mechanism of its effects on megakaryocytes remains unclear. In the present study, the effect of decitabine on megakaryocyte maturation was in...

Journal: :Blood 2011
Matko Kalac Luigi Scotto Enrica Marchi Jennifer Amengual Venkatraman E Seshan Govind Bhagat Netha Ulahannan Violetta V Leshchenko Alexis M Temkin Samir Parekh Benjamin Tycko Owen A O'Connor

Interactions between histone deacetylase inhibitors (HDACIs) and decitabine were investigated in models of diffuse large B-cell lymphoma (DLBCL). A number of cell lines representing both germinal center B-like and activated B-cell like DLBCL, patient-derived tumor cells and a murine xenograft model were used to study the effects of HDACIs and decitabine in this system. All explored HDACIs in co...

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