نتایج جستجو برای: متیلاسیون p16

تعداد نتایج: 5627  

1999
Eric Poe Xing Yan Nie Yunlong Song Guang-Yu Yang Yuyang Christine Cai Li-Dong Wang Chung S. Yang

The 9p21 gene cluster, harboring growth suppressive genes p14, p15, and p16, is one of the major aberration hotspots in human cancers. It was shown that p14 and p16 play active roles in the p53 and Rb tumor suppressive pathways, respectively, and p15 is a mediator of the extracellular growth inhibition signals. To elucidate specific targets and aberrations affecting this subchromosomal region, ...

Journal: :Molecular vision 2006
Pei-Liang Chen Ya-Wen Cheng Chun-Chi Chiang Sung Huei Tseng Pak Sam Chau Yi-Yu Tsai

PURPOSE A pterygium has long been considered as a degenerative condition. After p53 protein was found to be abnormally expressed in the epithelium, researchers suggested that a pterygium may be a tumor, but additional evidence is required to support this hypothesis. Aberrant methylation of the p16 gene (CDKN2A) promoter and resultant gene silencing play important roles in the pathogenesis of ma...

پایان نامه :وزارت علوم، تحقیقات و فناوری - دانشگاه تربیت مدرس - دانشکده علوم پزشکی 1392

چکیده: سرطان مجاری ادراری-تناسلی یکی از مهمترین علل مرگ و میر در میان زنان سراسر دنیا می باشد. متیلاسیون در موقعیت کربن شماره 5 باز سیتوزین یکی از مهمترین انواع تنظیمات اپی ژنتیکی بوده که روی مولکول دو رشته ای dna اتفاق می افتد. متیلاسیون باز سیتوزین ارتباط تنگاتنگ با تنظیم بیان ژن دارد. وضعیت متیلاسیون dna را با تکنیک بیسولفیت سکوئنسینگ می توان مورد بررسی و مطالعه قرار داد. متیلاسیون dna سبب ...

پایان نامه :وزارت علوم، تحقیقات و فناوری - دانشگاه شهید چمران اهواز - دانشکده علوم 1394

اعتیاد به استفاده اجباری از دارو، بدون توجه به عواقب ناخوشایند آن اطلاق می شود. اعتیاد همانند سایر بیماری های پیچیده رایج، اختلالی چند عاملی و چند ژنی است. در مطالعات بسیاری، تاثیر اعتیاد به مواد مخدر در انسان و مدل های حیوانی مانند موش باعث تغییرات اپی ژنتیکی از جمله متیلاسیونdna گردیده است. تغییرات اپی ژنتیک بوسیله برهمکنش استعدادهای ارثی، محرک محیطی و تماس با مواد مخدر در طولانی مدت بر بیان ...

Journal: :Clinical cancer research : an official journal of the American Association for Cancer Research 2004
Yu Sun Dajun Deng Wei-Cheng You Hua Bai Lian Zhang Jing Zhou Lin Shen Jun-Ling Ma Yu-Quan Xie Ji-You Li

PURPOSE Inactivation of p16 by aberrant methylation of CpG islands is a frequent event in carcinomas and precancerous lesions of various organs, including the stomach. The aim of this study is to investigate the relationship between p16 methylation and malignant transformation of human gastric dysplasia (DYS) based on follow-up endoscopic screening in a high-risk population. EXPERIMENTAL DESI...

2012
Jae Jun Lee Eunkyung Ko Junhun Cho Ha Young Park Jeong Eon Lee Seok Jin Nam Duk-Hwan Kim Eun Yoon Cho

BACKGROUND The p16(INK4a) gene methylation has been reported to be a major tumorigenic mechanism. METHODS We evaluated the methylation status of the p16(INK4a) genes in 231 invasive breast cancer and 90 intraductal carcinoma specimens using a methylation-specific polymerase chain reaction and p16 protein expression using immunohistochemistry. The quantity of cell-free methylated p16(INK4a) DN...

Journal: :Clinical cancer research : an official journal of the American Association for Cancer Research 1997
J Grim A D'Amico S Frizelle J Zhou R A Kratzke D T Curiel

We have previously established the efficacy of adenoviral gene delivery vectors for the treatment of bladder carcinoma in vivo. In the present work, we developed a gene therapy strategy for bladder cancer based on the replacement of the tumor suppressor p16, which is known to be mutated or deleted in a variety of human tumors, including those derived from the bladder. Previous reports have demo...

Journal: :Cancer research 1997
M Schutte R H Hruban J Geradts R Maynard W Hilgers S K Rabindran C A Moskaluk S A Hahn I Schwarte-Waldhoff W Schmiegel S B Baylin S E Kern J G Herman

The Rb/p16 tumor-suppressive pathway is abrogated frequently in human tumors, either through inactivation of the Rb or p16INK4a/CDKN2/MTS1 tumor-suppressor proteins, or through alteration or overexpression of the cyclin D1 or cyclin-dependent kinase 4 oncoproteins. We reported previously that the p16 gene was genetically inactivated in 82% of pancreatic carcinomas. Nearly half of these inactiva...

Journal: :Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 2008
Lisa G Aspinwall Samantha L Leaf Erin R Dola Wendy Kohlmann Sancy A Leachman

Genetic testing for melanoma has yet to enter routine clinical use because of the scarcity of available data on the effect of test reporting. A prospective study of 59 members of Utah CDKN2A/p16 mutation-positive pedigrees was conducted to establish the effect of CDKN2A/p16 genetic test reporting on melanoma early detection intentions and behaviors (total body skin examination and skin self-exa...

Journal: :Cancer research 1995
S Stone P Jiang P Dayananth S V Tavtigian H Katcher D Parry G Peters A Kamb

The p16 gene (P16, MTS1, CDKN2) encodes a negative regulator of the cell cycle. Molecular genetic techniques have been used to explore the role of p16 in normal development and cancer. Two transcripts derived from the p16 gene with distinct protein coding potentials are described. The previously undescribed transcript form has the same exons 2 and 3 as the p16-encoding mRNA but contains a diffe...

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