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Chinese Journal of Cancer Research 2016年第1期28卷 29-49页

作者： Qiu Rao Qiu-Yuan Xia Liang Cheng Xiao-Jun Zhou Department of Pathology Jinling Hospital Nanjing University School of Medicine Nanjing China Department of Pathology and Laboratory Indiana University School of Medicine Indianapolis IN USA

Renal cell carcinoma （RCC） compromises multiple types and has been emerging dramatically over the recent several decades. Advances and consensus have been achieved targeting common RCCs, such as clear cell carcinoma, papillary RCC and chromophobe RCC. Nevertheless, little is known on the characteristics of several newly-identified RCCs, including clear cell （tubulo） papillary RCC, Xpl 1 translocation RCC, t（6;11） RCC, succinate dehydrogenase （SDH）-deficient RCC, acquired cystic disease- associated RCC, hereditary leiomyomatosis RCC syndrome-associated RCC, ALK translocation RCC, thyroid-like follicular RCC, tubulocystic RCC and hybrid oncocytic/chromophobe tumors （HOCT）. In current review, we will collect available literature of these newly-described RCCs, analyze their clinical pathologic characteristics, discuss their morphologic and immunohistologic features, and finally summarize their molecular and genetic evidences. We expect this review would be beneficial for the understanding of RCCs, and eventually promote clinical management strategies.

关键词： Renal cell carcinoma (RCC) renal tumor immunohistochemistry molecular genetics

molecular genetics of cancer and tumorigenesis:Drosophila models

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Journal of genetics and Genomics 2011年第10期38卷 429-430页

作者： Wu-Min Deng Department of Biological Science Florida State University Tallahassee FL 32306-4295 USA

Why do some cells not respond to normal control of cell division and become tumorous？ Which signals trigger some tumor cells to migrate and colonize other tissues？ What genetic factors are responsible for tumorigenesis and cancer development？ What environmental factors play a role in cancer formation and progression？ In how many ways can our bodies prevent and restrict the growth of cancerous cells？ How can we identify and deliver effective drugs to fight cancer？ In the fight against cancer, which kills more people than any other disease, these and other questions have long interested researchers from a diverse range of fields. To answer these questions and to fight cancer more effectively,

关键词： molecular genetics cancer and tumorigenesis Drosophila

molecular genetics of Brugada syndrome

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Frontiers in Biology 2010年第4期5卷 339-347页

作者： Tie KE Xin TU Shuoyan ZHANG Yuhua LIAO Qing K.WANG Key Laboratory of molecular Biophysics of the Ministry of Education College of Life Science and Technology and Center for Human Genome ResearchHuazhong University of Science and TechnologyWuhan 430074China Cardio-X Institute Huazhong University of Science and TechnologyWuhan 430074China Institute of Cardiology Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430074China Center for Cardiovascular genetics Cleveland ClinicClevelandOH 44195USA

Brugada syndrome(BrS)is a life-threatening cardiac rhythm disorder characterized by persistent STsegment elevation in leads V1–V3 and right bundle branch block on electrocardiograms(ECG),and by syncope and sudden death from ventricular tachycardia(VT)and ventricular fibrillation(VF).BrS is responsible for nearly 4%of sudden cardiac deaths and considered to be the most common cause of natural death in males younger than 50 years in some Asian *** the first diseasecausing gene for BrS(the cardiac sodium channel gene SCN5A)was identified in 1998,extensive investigations on both clinical and basic aspects of BrS have occurred ***5A mutations remain the most common cause of BrS;nearly 300 SCN5A mutations have been identified and are responsible for 20%–30%of BrS *** genetic testing is available for ***,seven other disease-causing genes for BrS have been identified and include GPD1L(BrS2),CACNA1C(Cav1.2,BrS3),CACNB2(Cavβ2,BrS4),SCN1B(Navβ1,BrS5),KCNE3(MiRP2,BrS6),SCN3B(Navβ3,BrS7),and HCN4(BrS8).This article will briefly review the progress made over the past decade in our understanding of the clinical,genetic and molecular aspects of BrS.

关键词： Brugada syndrome molecular genetics arrhythmia sudden death SCN5A ion channel

Gallbladder cancer epidemiology, pathogenesis and molecular genetics: Recent update

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World Journal of Gastroenterology 2017年第22期23卷 3978-3998页

作者： Aarti Sharma Kiran Lata Sharma Annapurna Gupta Alka Yadav Ashok Kumar Department of Surgical Gastroenterology Sanjay Gandhi Post Graduate Institute of Medical Sciences Department of Biochemistry and Medical genetics John Buhler Research Centre University of Manitoba

Gallbladder cancer is a malignancy of biliary tract which is infrequent in developed countries but common in some specific geographical regions of developing countries. Late diagnosis and deprived prognosis are major problems for treatment of gallbladder carcinoma. The dramatic associations of this orphan cancer with various genetic and environmental factors are responsible for its poorly defined pathogenesis. An understanding to the relationship between epidemiology, molecular genetics and pathogenesis of gallbladder cancer can add new insights to its undetermined pathophysiology. Present review article provides a recent update regarding epidemiology, pathogenesis, and molecular genetics of gallbladder cancer. We systematically reviewed published literature on gallbladder cancer from online search engine Pub Med(http://***/pubmed). Various keywords used for retrieval of articles were Gallbladder, cancer Epidemiology, molecular genetics and bullion operators like AND, OR, NOT. Cross references were manually searched from various online search engines(http://***/pubmed,https://***/, http://***/***). Most of the articles published from 1982 to 2015 in peer reviewed journals have been included in this review.

关键词： Gallbladder cancer Epidemiology molecular genetics Pathogenesis

Clinic, neuropathology and molecular genetics of frontotemporal dementia: a mini-review

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Translational Neurodegeneration 2013年第1期2卷 43-51页

作者： Xiao-dong Pan Xiao-chun Chen Department of Neurology Union Hospital of Fujian Medical University29 Xinquan RoadFuzhou 350001China Key Laboratory of Brain Aging and Neurodegenerative Disease Fujian Institute of GeriatricsUnion Hospital of Fujian Medical University29 XinquanRoadFuzhou 350001China Centre of Neurobiology Fujian Medical University88 Jiaotong RoadFuzhou 350001China

Frontotemporal lobar degeneration(FTLD)represents a group of clinically,neuropathologically and genetically heterogeneous disorders with plenty of overlaps between the neurodegenerative mechanism and the clinical *** is pathologically characterized by the frontal and temporal lobar *** dementia(FTD)clinically presents with abnormalities of behavior and personality and language impairments *** clinical spectrum of FTD encompasses distinct canonical syndromes:behavioural variant of FTD(bvFTD)and primary progressive *** later includes nonfluent/agrammatic variant PPA(nfvPPA or PNFA),semantic variant PPA(svPPA or SD)and logopenic variant PPA(lvPPA).In addition,there is also overlap of FTD with motor neuron disease(FTD-MND or FTD-ALS),as well as the parkinsonian syndromes,progressive supranuclear palsy(PSP)and corticobasal syndrome(CBS).The FTLD spectrum disorders are based upon the predominant neuropathological proteins(containing inclusions of hyperphosphorylated tau or ubiquitin protein,e.g transactive response(TAR)DNA-binding protein 43 kDa(TDP-43)and fusedin-sarcoma protein in neurons and glial cells)into three main categories:(1)microtubule-associated protein tau(FTLD-Tau);(2)TAR DNA-binding protein-43(FTLD-TDP);and(3)fused in sarcoma protein(FTLD-FUS).There are five main genes mutations leading clinical and pathological variants in FTLD that identified by molecular genetic studies,which are chromosome 9 open reading frame 72(C9ORF72)gene,granulin(GRN)gene,microtubule associated protein tau gene(MAPT),the gene encoding valosin-containing protein(VCP)and the charged multivesicular body protein 2B(CHMP2B).In this review,recent advances on the different clinic variants,neuroimaging,genetics,pathological subtypes and clinicopathological associations of FTD will be discussed.

关键词： bvFTD Nonfluent/agrammatic variant Semantic variant Logopenic variant molecular genetics MAPT GRN C9ORF72

molecular genetics of gastric adenocarcinoma in clinical practice

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World Journal of Medical genetics 2014年第3期4卷 58-68页

作者： Margaret Cho Ogechukwu Eze Ruliang Xu Department of Pathology New York University Langone Medical Center New York NY 10016 United States

The molecular genetics of gastric carcinoma(GC) dictates their biology and clinical behavior. The two morphologically distinct types of gastric carcinoma by Lauren classification, i.e., intestinal and diffuse cell types, have a significant difference in clinical outcome. These two types of GC have different molecular pathogenetic pathways with unique genetic alterations. In addition to environmental and other etiologies, intestinal type GC is associated with Helicobacter pylori(H. pylori) infection and involves a multistep molecular pathway driving the normal epithelium to intestinal metaplasia, dysplasia, and malignant transformation by chromosomal and/or microsatellite instability(MSI), mutation of tumor suppressor genes, and loss of heterozygosity among others. Diffuse type shows no clear causal relationship with H. pylori infection, but is commonly associated with deficiency of cell-cell adhesion due to mutation of the E-cadherin gene(CDH1), and a manifestation of the hereditary gastric cancer syndrome. Thus, detection of CDH1 mutation or loss of expression of E-cadherin may aid in early diagnosis or screening of diffuse type GC. Detection of certain genetic markers, for example, MSI and matrix metalloproteinases, mayprovide prognostic information, particularly for intestinal type. The common genetic alterations may offer therapeutic targets for treatment of GC. Polymorphisms in Thymidylate synthase to metabolize 5-fluorouracil, glutathione S-transferase for degradation of Cisplatin, and amplification/overexpression of human epidermal growth factor receptor 2 targeted by monoclonal antibody Trastuzumab, are a few examples. P13K/Akt/mT OR pathway, c-Met pathways, epidermal growth factor receptor, insulin-like growth factor receptor, vascular endothelial growth factor receptor fibroblast growth factor receptor, and micro RNAs are several potential therapeutic biomarkers for GC under investigation.

关键词： molecular genetics Lauren classification Intestinal type gastric cancer Diffuse type gastric cancer molecular Biomarker

Recent advances in the molecular genetics of resin biosynthesis and genetic engineering strategies to improve defenses in conifers

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Journal of Forestry Research 2003年第2期14卷 171-179页

作者：唐巍 O-23 E.S.King Village2900 Ligon St.North Carolina State University

Since the first terpenoid synthase cDNA was obtained by the reverse genetic approach from grand fir, great progress in the molecular genetics of terpenoid formation has been made with angiosperms and genes encoding a monoterpene synthase, a sesquiterpene synthase, and a diterpene synthase. Tree killing bark beetles and their vectored fungal pathogens are the most destructive agents of conifer forests worldwide. Conifers defend against attack by the constitutive and inducible production of oleoresin that accumulates at the wound site to kill invaders and both flush and seal the injury. Although toxic to the bark beetle and fungal pathogen, oleoresin also plays a central role in the chemical ecology of these boring insects. Recent advances in the molecular genetics of terpenoid biosynthesis provide evidence for the evolutionary origins of oleoresin and permit consideration of genetic engineering strategies to improve conifer defenses as a component of modern forest biotechnology. This review described enzymes of resin biosynthesis, structural feathers of genes genomic intron and exon organization, pathway organization and evolution, resin production and accumulation, interactions between conifer and bark beetle, and engineering strategies to improve conifer defenses.

关键词： Genetic engineering strategies Resin biosynthesis Bark beetles Genomics molecular genetics

molecular genetics公司签订里夫脱河谷热病毒疫苗的研制合同

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生物技术通报 1986年第5期 18-18页

作者：郝慧斌

美国医学协会传染病研究所签定了170万美元的合同,在3年时间内研制出一种用于里夫脱河谷热病毒(Rift Valley Fever Virus)的重组体DNA疫苗。该病毒引起一种在中东和非洲流行于牲畜和人类的热病。 molecular genetics公司(明内通卡,明尼... 详细信息

美国医学协会传染病研究所签定了170万美元的合同,在3年时间内研制出一种用于里夫脱河谷热病毒(Rift Valley Fever Virus)的重组体DNA疫苗。该病毒引起一种在中东和非洲流行于牲畜和人类的热病。 molecular genetics公司(明内通卡,明尼苏达州)和该协会根据以前的一个合同从1982年至1984年对该病毒进行过研究。在此期间合同支付额总计为108.5万美元。新合同将以以前所做的工作为基础。

关键词：美元热病本位币里夫 molecular genetics 河谷

Therapy of gastric mucosa associated lymphoid tissue lymphoma

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World Journal of Gastroenterology 2007年第26期13卷 3554-3566页

作者： Andrea Morgner Renate Schmelz Christian Thiede Manfred Stolte Stephan Miehlke Medical DepartmentⅠ University HospitalTechnical University DresdenGermany Institute for Pathology Academic Teaching Hospital BayreuthBayreuthGermany

Gastric mucosa associated lymphoid tissue （MALT） lymphoma has recently been incorporated into the World Health Organization （WHO） lymphoma classification, termed as extranodal marginal zone B-cell lymphoma of MALT-type. In about 90% of cases this lymphoma is associated with H pylori infection which has been dearly shown to play a causative role in lymphomagenesis. Although much knowledge has been gained in defining the clinical features, natural history, pathology, and molecular genetics of the disease in the last decade, the optimal treatment approach for gastric MALT lymphomas, especially locally advanced cases, is still evolving. In this review we focus on data for the therapeutic, stage dependent management of gastric MALT lymphoma. Hence, the role of eradication therapy, surgery, chemotherapy and radiotherapy is critically analyzed. Based on these data, we suggest a therapeutic algorithm that might help to better stratify patients for optimal treatment success.

关键词： Gastric lymphoma Mucosa-associatedlymphoid tissue H pylori Eradication Radiation Surgery Chemotherapy molecular genetics

Genetic and molecular changes in ovarian cancer

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Cancer Biology & Medicine 2016年第2期13卷 236-247页

作者： Robert L Hollis Charlie Gourley Edinburgh Cancer Research UK Centre MRC Institute of Genetics and Molecular Medicine University of Edinburgh

Epithelial ovarian cancer represents the most lethal gynecological malignancy in the developed world, and can be divided into five main histological subtypes: high grade serous, endometrioid, clear cell, mucinous and low grade serous. These subtypes represent distinct disease entities, both clinically and at the molecular level. molecular analysis has revealed significant genetic heterogeneity in ovarian cancer, particularly within the high grade serous subtype. As such, this subtype has been the focus of much research effort to date, revealing molecular subgroups at both the genomic and transcriptomic level that have clinical ***, stratification of ovarian cancer patients based on the underlying biology of their disease remains in its infancy. Here, we summarize the molecular changes that characterize the five main ovarian cancer subtypes, highlight potential opportunities for targeted therapeutic intervention and outline priorities for future research.

关键词： ovarian cancer molecular genetics histological subtypes molecular subgrouping ovary