کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8536784 | 1560917 | 2018 | 78 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Nucleosidic DNA demethylating epigenetic drugs - A comprehensive review from discovery to clinic
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
BSCDLT5-Aza-CdRSAEMTDDnmtDACtmaxAZAEFsTTPTSGCDADFSMDS5-AzacytidineAMLRFSDNA hypermethylationORRCCRCMMLdCKAzanucleosidesCmaxDNA methyltransferase inhibitorsAUC - AUCDNA methyltransferase - DNA متیل ترانسفرازPFs - PF هاt1/2 - t1 / 2Nucleoside analogs - آنالوگهای هسته ایBED - بسترprogression-free survival - بقا بدون پیشرفتdisease-free survival - بقاء بدون بیماریEvent-free survival - بقاء بدون وقفهoverall survival - بقای کلBest supportive care - بهترین مراقبت های حمایتیMaximum tolerated dose - حداکثر دوز قابل تحملmaximum observed plasma concentration - حداکثر غلظت پلاسما مشاهده شدهGene silencing - خاموشی ژنDOR - دردCombinatorial therapy - درمان ترکیبیdose-limiting toxicities - دوز محدود کننده سمیتBiologically effective dose - دوز موثر زیستیdeoxycytidine kinase - دگزوسی سیتیدین کینازcomplete remission - رمی کاملtime to maximum plasma concentration - زمان به حداکثر غلظت پلاسماTime to progression - زمان به پیشرفتrelapse-free survival - زنده ماندن بدون عودmyelodysplastic syndrome - سندرم میلودیسپلاستیکcytidine deaminase - سیتیدین دامینازserious adverse events - عوارض جانبی جدیPharmacodynamics - فارماکودینامیکPharmacokinetics - فارماکوکینتیکacute myeloid leukemia - لوسمی حاد میلوئیدی یا به اختصار AMLAcute lymphoblastic leukemia - لوسمی لنفوبلاستیک حادchronic myelomonocytic leukemia - لوسمی میلوومونوسیتی مزمنduration of response - مدت زمان پاسخDrug resistance - مقاومت داروییarea under the curve - منطقه تحت منحنیoverall response rate - نرخ پاسخ کلیALL - همهTumor suppressor gene - ژن سرکوب کننده تومور
موضوعات مرتبط
علوم پزشکی و سلامت
داروسازی، سم شناسی و علوم دارویی
داروشناسی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
DNA methylation plays a pivotal role in the etiology of cancer by mediating epigenetic silencing of cancer-related genes. Since the relationship between aberrant DNA methylation and cancer has been understood, there has been an explosion of research at developing anti-cancer therapies that work by inhibiting DNA methylation. From the discovery of first DNA hypomethylating drugs in the 1980s to recently discovered second generation pro-drugs, exceedingly large number of studies have been published that describe the DNA hypomethylation-based anti-neoplastic action of these drugs in various stages of the pre-clinical investigation and advanced stages of clinical development. This review is a comprehensive report of the literature published in past 40â¯years, on so far discovered nucleosidic DNA methylation inhibitors in chronological order. The review will provide a complete insight to the readers about the mechanisms of action, efficacy to demethylate and re-express various cancer-related genes, anti-tumor activity, cytotoxicity profile, stability, and bioavailability of these drugs. The review further presents the far known mechanisms of primary and secondary resistance to azanucleoside drugs. Finally, the review highlights the ubiquitous role of DNA hypomethylating epi-drugs as chemosensitizers and/or priming agents, and recapitulate the combinatorial cancer preventive effects of these drugs with other epigenetic agents, conventional chemo-drugs, or immunotherapies. This comprehensive review analyzes the beneficial characteristics and drawbacks of nucleosidic DNA methylation inhibitors, which will assist the pre-clinical and clinical researchers in the design of future experiments to improve the therapeutic efficacy of these drugs and circumvent the challenges in the path of successful epigenetic therapy.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Pharmacology & Therapeutics - Volume 188, August 2018, Pages 45-79
Journal: Pharmacology & Therapeutics - Volume 188, August 2018, Pages 45-79
نویسندگان
Khushboo Agrawal, Viswanath Das, Pankhuri Vyas, Marián Hajdúch,