检索结果-南通市图书馆

Epigenetic reduction of DNA repair in progression to gastrointestinal cancer

World Journal of Gastrointestinal Oncology 2015年第5期7卷 30-46页

作者： carol bernstein Harris bernstein Department of Cellular and Molecular Medicine College of Medicine University of Arizona

Deficiencies in DNA repair due to inherited germ-line mutations in DNA repair genes cause increased risk of gastrointestinal(GI) cancer. In sporadic GI cancers, mutations in DNA repair genes are relatively rare. However, epigenetic alterations that reduce expression of DNA repair genes are frequent in sporadic GI cancers. These epigenetic reductions are also found in field defects that give rise to cancers. Reduced DNA repair likely allows excessive DNA damages to accumulate in somatic cells. Then either inaccurate translesion synthesis past the un-repaired DNA damages or error-prone DNA repair can cause mutations. Erroneous DNA repair can also cause epigenetic alterations(i.e., epimutations, transmitted through multiple replication cycles). Some of these mutations and epimutations may cause progression to cancer. Thus, deficient or absent DNA repair is likely an important underlying cause of cancer. Whole genome sequencing of GI cancers show that between thousands to hundreds of thousands of mutations occur in these cancers. Epimutations that reduce DNA repair gene expression and occur early in progression to GI cancers are a likely source of this high genomic instability. Cancer cells deficient in DNA repair are more vulnerable than normal cells to inactivation by DNA damaging agents. Thus, some of the most clinically effective chemotherapeutic agents in cancer treatment are DNA damaging agents, and their effectiveness often depends on deficient DNA repair in cancer cells. Recently, at least 18 DNA repair proteins, each active in one of six DNA repair pathways, were found to be subject to epigenetic reduction of expression in GI cancers. Different DNA repair pathways repair different types of DNA damage. Evaluation of which DNA repair pathway(s) are deficient in particular types of GI cancer and/or particular patients may prove useful in guiding choice of therapeutic agents in cancer therapy.

关键词： Epigenetic DNA damage DNA repair DNA repair deficiency disorders Epimutation Genomicinstability Germ-line mutation MicroRNAs Precancerousconditions Gastrointestinal cancer

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Epigenetic field defects in progression to cancer

引用

World Journal of Gastrointestinal Oncology 2013年第3期5卷 43-49页

作者： carol bernstein Valentine Nfonsam Anil Ramarao Prasad Harris bernstein Department of Cellular and Molecular Medicine College of Medicine University of Arizona Department of Surgery College of Medicine University of Arizona Department of Pathology College of Medicine University of Arizona

A field defect is a field of pre-malignant tissue in which a new cancer is likely to arise. Field defects often appear to be histologically normal under the microscope. Recent research indicates that cells within a field defect characteristically have an increased frequency of epigenetic alterations and these may be fundamentally important as underlying factors in progression to cancer. However, understanding of epigenetic field defects is at an early stage, and the work of Katsurano et al published this year, is a key contribution to this field. One question examined by Katsurano et al was how early could the formation of an epigenetic field defect be de-tected in a mouse colitis model of tumorigenesis. They highlighted a number of measurable epigenetic altera-tions, detected very early in normal appearing tissue undergoing histologically invisible tumorigenesis. They also documented the increasing presence of the epigenetic alterations at successive times during progression to cancer. In this commentary, we offer a perspective on the changes they observed within a broader sequence of epigenetic events that occur in progressionto cancer. In particular, we highlight the likely central role of epigenetic deficiencies in DNA repair gene expression that arise during progression to cancer.

关键词： Field defect Epigenetics Tumorigenesis Carcinogenesis DNA damage DNA repair Colon cancer Mouse Human

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

引用

World Journal of Gastrointestinal Oncology 2014年第7期6卷 225-243页

作者： Anil R Prasad Shilpa Prasad Huy Nguyen Alexaner Facista Cristy Lewis Beryl Zaitlin Harris bernstein carol bernstein Department of Pathology Northwest Medical Center Tucson AZ 85741 United States Department of Pathology College of Medicine University of Arizona Tucson AZ 85724 United States College of Arts and Sciences Boston University Boston MA 2215 United States Department of Cellular and Molecular Medicine College of Medicine University of Arizona Tucson AZ 85724 United States Matrix Solutions Inc. Alberta T2R 0V2 Canada

AIM:To investigate the close parallels between our novel diet-related mouse model of colon cancer and human colon ***:Twenty-two wild-type female mice(ages 6-8 wk)were fed the standard control diet(AIN-93G)and an additional 22 female mice(ages 6-8 wk)were fed the control diet supplemented with 0.2%deoxycho-lic acid[diet+deoxycholic acid(DOC)]for 10 ***-mors occurred in the colons of mice fed diet+DOC and showed progression to colon cancer[adenocarcinoma(AC)].This progression is through the stages of tubular adenoma(TA),TA with high grade dysplasia or ad-enoma with sessile serrated morphology,intramucosal AC,AC stage T1,and AC stage *** mouse tumors were compared to human tumors at the same stages by histopathological *** of the small and large intestines of mice and humans were evaluated for glandular architecture,cellular and nuclear morphology including cellular orientation,cellular and nuclear atyp-ia,pleomorphism,mitotic activity,frequency of goblet cells,crypt architecture,ulceration,penetration of crypts through the muscularis mucosa and presence of malignant crypts in the muscularis *** addition,preserved colonic tissues from genetically similar male mice,obtained from a prior experiment,were analyzed by *** male mice had been fed the control diet or diet+*** molecular markers were evaluated:8-OH-dG,DNA repair protein ERCC1,autophagy protein beclin-1 and the nuclear location of beta-catenin in the stem cell region of ***,male mice fed diet+DOC plus 0.007%chlorogenic acid(diet+DOC+CGA)were evaluated for ERCC1,beclin-1 and nuclear location of ***:Humans with high levels of diet-relatedDOC in their colons are at a substantially increased riskof developing colon *** mice fed diet+DOChad levels of DOC in their colons comparable to that ofhumans on a high fat *** 22 mice without addedDOC in their diet had no colonic tumors while 20 ofthe 22 mice(91%)fed diet+DOC deve

关键词： Diet Deoxycholate Mouse model Colon cancer Histology Chlorogenic acid 8-OH-dG Beclin 1 Beta-catenin

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Bile acids as endogenous etiologic agents in gastrointestinal cancer

引用

World Journal of Gastroenterology 2009年第27期15卷 3329-3340页

作者： Harris bernstein carol bernstein Claire M Payne Katerina Dvorak Department of Cell Biology and Anatomy College of Medicine and Arizona Cancer Center University of ArizonaTucson Arizona 85724 United States Department of Cell Biology and Anatomy College of Medicine University of ArizonaTucson Arizona 85724 United States Hematology/Oncology Southern Arizona Veterans Affairs Health Care System Tucson Arizona 85723 United States

Bile acids are implicated as etiologic agents in cancer of the gastrointestinal (GI) tract, including cancer of the esophagus, stomach, small intestine, liver, biliary tract, pancreas and colon/rectum. Deleterious effects of bile acid exposure, likely related to carcinogenesis, include: induction of reactive oxygen and reactive nitrogen species; induction of DNA damage; stimulation of mutation; induction of apoptosis in the short term, and selection for apoptosis resistance in the long term. These deleterious effects have, so far, been reported most consistently in relation to esophageal and colorectal cancer, but also to some extent in relation to cancer of other organs. In addition, evidence is reviewed for an association of increased bile acid exposure with cancer risk in human populations, in specific human genetic conditions, and in animal experiments. A model for the role of bile acids in GI carcinogenesis is presented from a Darwinian perspective that offers an explanation for how the observed effects of bile acids on cells contribute to cancer development.

关键词： Bile acids Cancer Adenocarcinoma Esophagus Stomach Small intestine Pancreas Colon Apoptosis DNA damage

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Cancer and age related colonic crypt deficiencies in cytochrome c oxidase Ⅰ

引用

World Journal of Gastrointestinal Oncology 2010年第12期2卷 429-442页

作者： carol bernstein Alexander Facista Huy Nguyen Beryl Zaitlin Nadia Hassounah Cristy Loustaunau Claire Margaret Payne Bhaskar Banerjee Steve Goldschmid V Liana Tsikitis Robert Krouse Harris bernstein Department of Cell Biology and Anatomy College of MedicineUniversity of ArizonaTucsonAZ 85724United State Schulich School of Civil Engineering University of CalgaryCalgary Alberta T2L 1M3Canada Department of Cell Biology and Anatomy College of MedicineUniversity of ArizonaTucsonAZ 85724United States Biomedical Diagnostics and Research Inc TucsonAZ 85719United States Department of Medicine College of MedicineUniversity of ArizonaTucsonAZ 85724United States Department of Surgery College of MedicineUniversity of ArizonaTucsonAZ 85724United States Southern Arizona Veterans Affairs Health Care System TucsonAZ 85723United States

AIM: To investigate whether defi ciency of expressionof cytochrome c oxidase I (CcOI) in colonic crypts is associated with colon ***: The pattern and level of expression of CcOI in non-neoplastic colonic crypts,and in dysplastic tissues,was assessed using standard immunohis-tochemical *** were obtained from individuals undergoing colonoscopies for screening purposes or for a medically indicated *** samples were also obtained from surgical colonic *** from resections were taken from colonic mucosa 1 and 10 cm from tumors and from the tumors *** were evaluated for frequency of crypts with reduced or absent expression of *** most crypts the loss was apparent throughout the entire crypt,while in a small minority the loss was *** strong immunoreactivity using this monoclonal antibody makes the scoring *** percent of crypts with reduced or absent expression of CcOI or (infrequent) segmented loss of expression was then *** analyses were performed using SPSS statistical package ***: The average frequency of CcOI deficient crypts (CcOI-DC) is low in individuals between 20 and 39 years of age,with 0.48% ± 0.40% CcOI-DC for women and 1.80% ± 0.35% for ***-DC increases after age 40 years,so that between the ages of 40 and 44 years the average frequency of CcOI- DC goes up to 5.89% ± 0.84% in women and 2.15% ± 1.27% in *** 80-84 years of age,the average frequency of CcOI-DC goes up in women to 15.77% ± 0.97% and in men to 22.6% ± 0.65%.The increases in CcOI-DC from ages 40-44 years compared to 80-84 years in women and men are significantly different with P < *** women over age 60 years,deficiency of CcOI expression is greater in those women who have had a cancer in their *** frequency of CcOI-DC,measured in men,increased in tissues adjacent to colon cancer,being 4.03% ± 0.27% in individuals free of neoplasia in the age range 55-64 yearsand 14.13% ± 0.

关键词： Cytochrome c oxidase Aging Colon crypts Colorectal cancer Focal lesions

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Abstracts from the 15th International Myopia Conference

引用

Eye and Vision 2016年第1期3卷 211-221页

作者： Alexandra Benavente-Perez Ann Nour Tobin Ansel Kathleen Abarr Luying Yan Keisha Roden David Troilo Chanyi Lu Miaozhen Pan Min Zheng Jia Qu Xiangtian Zhou Christine F. Wildsoet Fan Lu Jie Chen Jinhua Bao Liang Hu Qinmei Wang Zibing Jin Frances Rucker Stephanie Britton Stephan Hanowsky Molly Spatcher Hui-Ying Kuo Ching-Hsiu Ke I-Hsin Kuo Chien-Chun Peng Han-Yin Sun Ian G. Morgan Jeremy A. Guggenheim Rupal L. Shah Cathy Williams Jinglei Yang Peter S. Reinach Sen Zhang Wenfeng Sun Bo Liu Fen Li Xiaoqing Li Aihua Zhao Tianlu Chen Wei Jia Jun Jiang Haoran Wu Kazuo Tsubota Hiroko Ozawa Hidemasa Torii Shigemasa Takamizawa Toshihide Kurihara Kazuno Negishi Klaus Graef Daniel Rathbun Frank Schaeffel Ladan Ghodsi William K. Stell Machelle T. Pardue Ranjay Chakraborty Han na Park Curran S. Sidhu P. Michael Iuvone Michael J Collins Nethrajeith Srinvasalu Sally A. McFadden Paul N. Baird Pablo Artal Pauline Cho SW Cheung Pei-Chang Wu Quan V. Hoang Duk C. Lee Erica G. Landis Michael A. Bergen Curran Sidhu Samer Hattar Richard A. Stone Ravi Metlapally Ruiqin Li Qinglin Xu Hong Zhong Chenglin Pan Weizhong Lan Xiaoning Li Ling Chen Zhikuan Yang Scott A. Read Seang-Mei Saw Shi-Jun Weng Xiao-Hua Wu Kang-Wei Qian Yun-Yun Li Guo-Zhong Xu Furong Huang Xiong-Li Yang Yong-Mei Zhong Earl L Smith, III Baskar Arumugam Li-Fang Hung Lisa A. Ostrin Klaus Trier Monica Jong Brien A. Holden Thomas Chuen Lam Samantha Shan Bing Zuo Dennis Yan-yin Tse Jingfang Bian King-Kit Li Quan Liu Chi-ho To Timothy J. Gawne John T. Siegwart, Jr. Alexander H. Ward Thomas T. Norton Yan Zhang Yue Liu carol Ho Eileen Phan Abraham Hang Emily Eng Christine Wildsoet Department of Biological Sciences SUNY College of Optometry New York NY 10036 USA School of Optometry and Ophthalmology and Eye Hospital Wenzhou Medical University Wenzhou Zhejiang 325027 China Center for Eye Disease & Development School of Optometry & Vision Science Program University of California Berkeley Berkeley CA 94720-2020 USA Wenzhou Medical University Wenzhou Zhejiang 325027 China Biomedical Science and Disease New England College of Optom Boston MA USA School of Optometry Chung Shan Medical University Taichung City 402 Taiwan Institute of Medicine Chung Shan Medical University Taichung City 402 Taiwan Division of Biochemistry and Molecular Biology Research School of Biology Australian National University Canberra Australia State Key Laboratory of Ophthalmology and Division of Preventive Ophthalmology Zhongshan Ophthalmic Center Sun Yat-Sen University Guangzhou China School of Optometry & Vision Sciences Cardiff University Cardiff UK School of Social and Community Medicine University of Bristol Bristol UK School of and Eye Hospital Wenzhou Medical University Wenzhou Zhejiang 325027 China State Key Laboratory Cultivation Base and Key Laboratory of Vision Science Ministry of Health and Zhejiang Provincial Key Laboratory of Ophthalmology and Optometry Wenzhou Zhejiang 325027 People’s Republic of China Shanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine Shanghai Jiao Tong University Affiliated Sixth People’s Hospital Shanghai 200233 China Eye Hospital of Wenzhou Medical University Wenzhou Zhejiang 325027 China Department of Ophthalmology Keio University School of Medicine Shinjuku-ku Tokyo 160-8582 Japan General Medicine Ichikawa Medical Center Urayasu City Chiba 279-0001 Japan Ophthalmic Research Institute University of Tuebingen 72076 Tuebingen Germany bernstein Center for Computational Neuroscience Tuebingen 72076 Tuebingen Germany Werner Reichardt Centre for Integrative Neuroscience Otfried-Mueller-Straße 25 Tueb

To assess the peripheral refractive changes that occur when eye growth decelerates in *** We measured peripheral refraction and on-axis vitreous chamber depth on a total of 53 marmosets;36 treated monocularly for 12 weeks 9 hrs/day(26 with-5 D contact lenses,10 with+5 D)and 17 untreated *** the 26 marmosets treated with-5 D,10 wore contact lenses 9 hrs/day without interruptions and were mea-sured at the end of 10 weeks of treatment(T10)and after 4 weeks of recovery(R14).Eight had both contact lenses removed for 30 mins twice/day(mid-morning and mid-afternoon)during the first four weeks of treatment(early interruption group)and eight had the lenses removed during the second four weeks of treatment(late interruption group).The two interruption groups were measured after 4,8 and 12 weeks of treatment only(T4,T8,T12).

关键词： removed treatment untreated

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：