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  • 1
    Publication Date: 2009-12-18
    Description: All cancers carry somatic mutations. A subset of these somatic alterations, termed driver mutations, confer selective growth advantage and are implicated in cancer development, whereas the remainder are passengers. Here we have sequenced the genomes of a malignant melanoma and a lymphoblastoid cell line from the same person, providing the first comprehensive catalogue of somatic mutations from an individual cancer. The catalogue provides remarkable insights into the forces that have shaped this cancer genome. The dominant mutational signature reflects DNA damage due to ultraviolet light exposure, a known risk factor for malignant melanoma, whereas the uneven distribution of mutations across the genome, with a lower prevalence in gene footprints, indicates that DNA repair has been preferentially deployed towards transcribed regions. The results illustrate the power of a cancer genome sequence to reveal traces of the DNA damage, repair, mutation and selection processes that were operative years before the cancer became symptomatic.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3145108/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3145108/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pleasance, Erin D -- Cheetham, R Keira -- Stephens, Philip J -- McBride, David J -- Humphray, Sean J -- Greenman, Chris D -- Varela, Ignacio -- Lin, Meng-Lay -- Ordonez, Gonzalo R -- Bignell, Graham R -- Ye, Kai -- Alipaz, Julie -- Bauer, Markus J -- Beare, David -- Butler, Adam -- Carter, Richard J -- Chen, Lina -- Cox, Anthony J -- Edkins, Sarah -- Kokko-Gonzales, Paula I -- Gormley, Niall A -- Grocock, Russell J -- Haudenschild, Christian D -- Hims, Matthew M -- James, Terena -- Jia, Mingming -- Kingsbury, Zoya -- Leroy, Catherine -- Marshall, John -- Menzies, Andrew -- Mudie, Laura J -- Ning, Zemin -- Royce, Tom -- Schulz-Trieglaff, Ole B -- Spiridou, Anastassia -- Stebbings, Lucy A -- Szajkowski, Lukasz -- Teague, Jon -- Williamson, David -- Chin, Lynda -- Ross, Mark T -- Campbell, Peter J -- Bentley, David R -- Futreal, P Andrew -- Stratton, Michael R -- 077012/Z/05/Z/Wellcome Trust/United Kingdom -- 088340/Wellcome Trust/United Kingdom -- 093867/Wellcome Trust/United Kingdom -- England -- Nature. 2010 Jan 14;463(7278):191-6. doi: 10.1038/nature08658. Epub 2009 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016485" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Cell Line, Tumor ; DNA Damage/genetics ; DNA Mutational Analysis ; DNA Repair/genetics ; Gene Dosage/genetics ; Genes, Neoplasm/*genetics ; Genome, Human/*genetics ; Humans ; Loss of Heterozygosity/genetics ; Male ; Melanoma/etiology/genetics ; MicroRNAs/genetics ; Mutagenesis, Insertional/genetics ; Mutation/*genetics ; Neoplasms/etiology/*genetics ; Polymorphism, Single Nucleotide/genetics ; Precision Medicine ; Sequence Deletion/genetics ; Ultraviolet Rays
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2009-12-18
    Description: Cancer is driven by mutation. Worldwide, tobacco smoking is the principal lifestyle exposure that causes cancer, exerting carcinogenicity through 〉60 chemicals that bind and mutate DNA. Using massively parallel sequencing technology, we sequenced a small-cell lung cancer cell line, NCI-H209, to explore the mutational burden associated with tobacco smoking. A total of 22,910 somatic substitutions were identified, including 134 in coding exons. Multiple mutation signatures testify to the cocktail of carcinogens in tobacco smoke and their proclivities for particular bases and surrounding sequence context. Effects of transcription-coupled repair and a second, more general, expression-linked repair pathway were evident. We identified a tandem duplication that duplicates exons 3-8 of CHD7 in frame, and another two lines carrying PVT1-CHD7 fusion genes, indicating that CHD7 may be recurrently rearranged in this disease. These findings illustrate the potential for next-generation sequencing to provide unprecedented insights into mutational processes, cellular repair pathways and gene networks associated with cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2880489/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2880489/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pleasance, Erin D -- Stephens, Philip J -- O'Meara, Sarah -- McBride, David J -- Meynert, Alison -- Jones, David -- Lin, Meng-Lay -- Beare, David -- Lau, King Wai -- Greenman, Chris -- Varela, Ignacio -- Nik-Zainal, Serena -- Davies, Helen R -- Ordonez, Gonzalo R -- Mudie, Laura J -- Latimer, Calli -- Edkins, Sarah -- Stebbings, Lucy -- Chen, Lina -- Jia, Mingming -- Leroy, Catherine -- Marshall, John -- Menzies, Andrew -- Butler, Adam -- Teague, Jon W -- Mangion, Jonathon -- Sun, Yongming A -- McLaughlin, Stephen F -- Peckham, Heather E -- Tsung, Eric F -- Costa, Gina L -- Lee, Clarence C -- Minna, John D -- Gazdar, Adi -- Birney, Ewan -- Rhodes, Michael D -- McKernan, Kevin J -- Stratton, Michael R -- Futreal, P Andrew -- Campbell, Peter J -- 077012/Wellcome Trust/United Kingdom -- 077012/Z/05/Z/Wellcome Trust/United Kingdom -- 088340/Wellcome Trust/United Kingdom -- 093867/Wellcome Trust/United Kingdom -- P50 CA070907/CA/NCI NIH HHS/ -- P50CA70907/CA/NCI NIH HHS/ -- England -- Nature. 2010 Jan 14;463(7278):184-90. doi: 10.1038/nature08629. Epub 2009 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016488" target="_blank"〉PubMed〈/a〉
    Keywords: Carcinogens/toxicity ; Cell Line, Tumor ; DNA Copy Number Variations/drug effects/genetics ; DNA Damage/genetics ; DNA Helicases/genetics ; DNA Mutational Analysis ; DNA Repair/genetics ; DNA-Binding Proteins/genetics ; Exons/genetics ; Gene Expression Regulation, Neoplastic/drug effects ; Genome, Human/drug effects/genetics ; Humans ; Lung Neoplasms/*etiology/*genetics ; Mutagenesis, Insertional/drug effects/genetics ; Mutation/drug effects/*genetics ; Promoter Regions, Genetic/genetics ; Sequence Deletion/genetics ; Small Cell Lung Carcinoma/*etiology/*genetics ; Smoking/*adverse effects ; Tobacco/*adverse effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2010-01-08
    Description: Clear cell renal cell carcinoma (ccRCC) is the most common form of adult kidney cancer, characterized by the presence of inactivating mutations in the VHL gene in most cases, and by infrequent somatic mutations in known cancer genes. To determine further the genetics of ccRCC, we have sequenced 101 cases through 3,544 protein-coding genes. Here we report the identification of inactivating mutations in two genes encoding enzymes involved in histone modification-SETD2, a histone H3 lysine 36 methyltransferase, and JARID1C (also known as KDM5C), a histone H3 lysine 4 demethylase-as well as mutations in the histone H3 lysine 27 demethylase, UTX (KMD6A), that we recently reported. The results highlight the role of mutations in components of the chromatin modification machinery in human cancer. Furthermore, NF2 mutations were found in non-VHL mutated ccRCC, and several other probable cancer genes were identified. These results indicate that substantial genetic heterogeneity exists in a cancer type dominated by mutations in a single gene, and that systematic screens will be key to fully determining the somatic genetic architecture of cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820242/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820242/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dalgliesh, Gillian L -- Furge, Kyle -- Greenman, Chris -- Chen, Lina -- Bignell, Graham -- Butler, Adam -- Davies, Helen -- Edkins, Sarah -- Hardy, Claire -- Latimer, Calli -- Teague, Jon -- Andrews, Jenny -- Barthorpe, Syd -- Beare, Dave -- Buck, Gemma -- Campbell, Peter J -- Forbes, Simon -- Jia, Mingming -- Jones, David -- Knott, Henry -- Kok, Chai Yin -- Lau, King Wai -- Leroy, Catherine -- Lin, Meng-Lay -- McBride, David J -- Maddison, Mark -- Maguire, Simon -- McLay, Kirsten -- Menzies, Andrew -- Mironenko, Tatiana -- Mulderrig, Lee -- Mudie, Laura -- O'Meara, Sarah -- Pleasance, Erin -- Rajasingham, Arjunan -- Shepherd, Rebecca -- Smith, Raffaella -- Stebbings, Lucy -- Stephens, Philip -- Tang, Gurpreet -- Tarpey, Patrick S -- Turrell, Kelly -- Dykema, Karl J -- Khoo, Sok Kean -- Petillo, David -- Wondergem, Bill -- Anema, John -- Kahnoski, Richard J -- Teh, Bin Tean -- Stratton, Michael R -- Futreal, P Andrew -- 077012/Wellcome Trust/United Kingdom -- 077012/Z/05/Z/Wellcome Trust/United Kingdom -- 082359/Wellcome Trust/United Kingdom -- 088340/Wellcome Trust/United Kingdom -- 093867/Wellcome Trust/United Kingdom -- England -- Nature. 2010 Jan 21;463(7279):360-3. doi: 10.1038/nature08672. Epub 2010 Jan 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20054297" target="_blank"〉PubMed〈/a〉
    Keywords: Carcinoma, Renal Cell/*genetics/pathology ; Cell Hypoxia/genetics ; Chromatin/metabolism ; Gene Expression Regulation, Neoplastic ; *Genes, Neurofibromatosis 2 ; Histone Demethylases ; Histone-Lysine N-Methyltransferase/*genetics ; Histones/*metabolism ; Humans ; Kidney Neoplasms/*genetics/pathology ; Mutation/genetics ; Nuclear Proteins/*genetics ; Oxidoreductases, N-Demethylating/*genetics ; Sequence Analysis, DNA
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2010-02-19
    Description: The cancer genome is moulded by the dual processes of somatic mutation and selection. Homozygous deletions in cancer genomes occur over recessive cancer genes, where they can confer selective growth advantage, and over fragile sites, where they are thought to reflect an increased local rate of DNA breakage. However, most homozygous deletions in cancer genomes are unexplained. Here we identified 2,428 somatic homozygous deletions in 746 cancer cell lines. These overlie 11% of protein-coding genes that, therefore, are not mandatory for survival of human cells. We derived structural signatures that distinguish between homozygous deletions over recessive cancer genes and fragile sites. Application to clusters of unexplained homozygous deletions suggests that many are in regions of inherent fragility, whereas a small subset overlies recessive cancer genes. The results illustrate how structural signatures can be used to distinguish between the influences of mutation and selection in cancer genomes. The extensive copy number, genotyping, sequence and expression data available for this large series of publicly available cancer cell lines renders them informative reagents for future studies of cancer biology and drug discovery.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3145113/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3145113/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bignell, Graham R -- Greenman, Chris D -- Davies, Helen -- Butler, Adam P -- Edkins, Sarah -- Andrews, Jenny M -- Buck, Gemma -- Chen, Lina -- Beare, David -- Latimer, Calli -- Widaa, Sara -- Hinton, Jonathon -- Fahey, Ciara -- Fu, Beiyuan -- Swamy, Sajani -- Dalgliesh, Gillian L -- Teh, Bin T -- Deloukas, Panos -- Yang, Fengtang -- Campbell, Peter J -- Futreal, P Andrew -- Stratton, Michael R -- 077012/Z/05/Z/Wellcome Trust/United Kingdom -- 088340/Wellcome Trust/United Kingdom -- 093867/Wellcome Trust/United Kingdom -- P01 CA155258/CA/NCI NIH HHS/ -- England -- Nature. 2010 Feb 18;463(7283):893-8. doi: 10.1038/nature08768.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20164919" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line, Tumor ; Chromosome Fragile Sites/*genetics ; Chromosomes, Human/genetics ; DNA Copy Number Variations/genetics ; DNA Mutational Analysis ; *Gene Deletion ; Gene Dosage/genetics ; Genes, Neoplasm/*genetics ; Genes, Recessive/*genetics ; Genome, Human/*genetics ; *Homozygote ; Humans ; Models, Genetic ; Neoplasms/*genetics ; Oligonucleotide Array Sequence Analysis ; Physical Chromosome Mapping ; Reproducibility of Results ; Selection, Genetic/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2011-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McQuatters-Gollop, Abigail -- Reid, Philip C -- Edwards, Martin -- Burkill, Peter H -- Castellani, Claudia -- Batten, Sonia -- Gieskes, Winfried -- Beare, Doug -- Bidigare, Robert R -- Head, Erica -- Johnson, Rod -- Kahru, Mati -- Koslow, J Anthony -- Pena, Angelica -- England -- Nature. 2011 Apr 14;472(7342):E6-7; discussion E8-9. doi: 10.1038/nature09950.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sir Alister Hardy Foundation for Ocean Science, The Laboratory, Citadel Hill, Plymouth, PL1 2PB, UK. abiqua@sahfos.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21490625" target="_blank"〉PubMed〈/a〉
    Keywords: Aquatic Organisms/growth & development/*isolation & purification/metabolism ; Atlantic Ocean ; Bias (Epidemiology) ; Biomass ; Chlorophyll/analysis ; Data Collection/methods ; *Ecosystem ; Fisheries ; Phytoplankton/growth & development/*isolation & purification/metabolism ; Reproducibility of Results ; Seawater/chemistry/microbiology ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2012-06-23
    Description: All cancers carry somatic mutations in their genomes. A subset, known as driver mutations, confer clonal selective advantage on cancer cells and are causally implicated in oncogenesis, and the remainder are passenger mutations. The driver mutations and mutational processes operative in breast cancer have not yet been comprehensively explored. Here we examine the genomes of 100 tumours for somatic copy number changes and mutations in the coding exons of protein-coding genes. The number of somatic mutations varied markedly between individual tumours. We found strong correlations between mutation number, age at which cancer was diagnosed and cancer histological grade, and observed multiple mutational signatures, including one present in about ten per cent of tumours characterized by numerous mutations of cytosine at TpC dinucleotides. Driver mutations were identified in several new cancer genes including AKT2, ARID1B, CASP8, CDKN1B, MAP3K1, MAP3K13, NCOR1, SMARCD1 and TBX3. Among the 100 tumours, we found driver mutations in at least 40 cancer genes and 73 different combinations of mutated cancer genes. The results highlight the substantial genetic diversity underlying this common disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3428862/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3428862/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stephens, Philip J -- Tarpey, Patrick S -- Davies, Helen -- Van Loo, Peter -- Greenman, Chris -- Wedge, David C -- Nik-Zainal, Serena -- Martin, Sancha -- Varela, Ignacio -- Bignell, Graham R -- Yates, Lucy R -- Papaemmanuil, Elli -- Beare, David -- Butler, Adam -- Cheverton, Angela -- Gamble, John -- Hinton, Jonathan -- Jia, Mingming -- Jayakumar, Alagu -- Jones, David -- Latimer, Calli -- Lau, King Wai -- McLaren, Stuart -- McBride, David J -- Menzies, Andrew -- Mudie, Laura -- Raine, Keiran -- Rad, Roland -- Chapman, Michael Spencer -- Teague, Jon -- Easton, Douglas -- Langerod, Anita -- Oslo Breast Cancer Consortium (OSBREAC) -- Lee, Ming Ta Michael -- Shen, Chen-Yang -- Tee, Benita Tan Kiat -- Huimin, Bernice Wong -- Broeks, Annegien -- Vargas, Ana Cristina -- Turashvili, Gulisa -- Martens, John -- Fatima, Aquila -- Miron, Penelope -- Chin, Suet-Feung -- Thomas, Gilles -- Boyault, Sandrine -- Mariani, Odette -- Lakhani, Sunil R -- van de Vijver, Marc -- van 't Veer, Laura -- Foekens, John -- Desmedt, Christine -- Sotiriou, Christos -- Tutt, Andrew -- Caldas, Carlos -- Reis-Filho, Jorge S -- Aparicio, Samuel A J R -- Salomon, Anne Vincent -- Borresen-Dale, Anne-Lise -- Richardson, Andrea L -- Campbell, Peter J -- Futreal, P Andrew -- Stratton, Michael R -- 077012/Z/05/Z/Wellcome Trust/United Kingdom -- 088340/Wellcome Trust/United Kingdom -- 093867/Wellcome Trust/United Kingdom -- 10118/Cancer Research UK/United Kingdom -- CA089393/CA/NCI NIH HHS/ -- P30 CA016672/CA/NCI NIH HHS/ -- WT088340MA/Wellcome Trust/United Kingdom -- Cancer Research UK/United Kingdom -- Chief Scientist Office/United Kingdom -- Department of Health/United Kingdom -- England -- Nature. 2012 May 16;486(7403):400-4. doi: 10.1038/nature11017.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Genome Project, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22722201" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Breast Neoplasms/classification/*genetics/pathology ; Cell Transformation, Neoplastic/*genetics ; Cytosine/metabolism ; DNA Mutational Analysis ; Female ; Humans ; JNK Mitogen-Activated Protein Kinases/metabolism ; Mutagenesis/*genetics ; Mutation/*genetics ; Neoplasm Grading ; Oncogenes/*genetics ; Reproducibility of Results ; Signal Transduction/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2007-06-02
    Description: Worm et al. (Research Articles, 3 November 2006, p. 787) investigated the importance of biodiversity to marine ecosystem services across temporal and spatial scales. In projecting the extent of future fisheries collapse, we argue that the authors inappropriately extrapolated beyond their available observations and used data on marine reserves and fishery closures that are not representative of global fisheries.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holker, Franz -- Beare, Doug -- Dorner, Hendrik -- di Natale, Antonio -- Ratz, Hans-Joachim -- Temming, Axel -- Casey, John -- New York, N.Y. -- Science. 2007 Jun 1;316(5829):1285; author reply 1285.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉European Commission, Directorate General Joint Research Centre, Institute for the Protection and Security of the Citizen, Agriculture and Fisheries Unit, TP 051, 21020, Italy. franz.hoelker@jrc.it〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17540886" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; Conservation of Natural Resources ; *Ecosystem ; *Fisheries ; *Fishes ; Forecasting ; Oceans and Seas ; Population Dynamics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Mutation Research/Environmental Mutagenesis and Related Subjects 252 (1991), S. 172-173 
    ISSN: 0165-1161
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 0921-8777
    Keywords: Ataxia telangiectasia ; Mutation spectra ; Splicing ; Xeroderma pigmentosum
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] We constructed maps for eight chromosomes (1, 6, 9, 10, 13, 20, X and (previously) 22), representing one-third of the genome, by building landmark maps, isolating bacterial clones and assembling contigs. By this approach, we could establish the long-range organization of the maps early in the ...
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