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  • 1
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    A comprehensive catalogue of somatic mutations from a human cancer genome (2009)
    Nature Publishing Group (NPG)
    Details
    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
    Published by Nature Publishing Group (NPG)
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  • 2
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    Systematic identification of genomic markers of drug sensitivity in cancer cells (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-03-31
    Description: Clinical responses to anticancer therapies are often restricted to a subset of patients. In some cases, mutated cancer genes are potent biomarkers for responses to targeted agents. Here, to uncover new biomarkers of sensitivity and resistance to cancer therapeutics, we screened a panel of several hundred cancer cell lines--which represent much of the tissue-type and genetic diversity of human cancers--with 130 drugs under clinical and preclinical investigation. In aggregate, we found that mutated cancer genes were associated with cellular response to most currently available cancer drugs. Classic oncogene addiction paradigms were modified by additional tissue-specific or expression biomarkers, and some frequently mutated genes were associated with sensitivity to a broad range of therapeutic agents. Unexpected relationships were revealed, including the marked sensitivity of Ewing's sarcoma cells harbouring the EWS (also known as EWSR1)-FLI1 gene translocation to poly(ADP-ribose) polymerase (PARP) inhibitors. By linking drug activity to the functional complexity of cancer genomes, systematic pharmacogenomic profiling in cancer cell lines provides a powerful biomarker discovery platform to guide rational cancer therapeutic strategies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3349233/" 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/PMC3349233/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garnett, Mathew J -- Edelman, Elena J -- Heidorn, Sonja J -- Greenman, Chris D -- Dastur, Anahita -- Lau, King Wai -- Greninger, Patricia -- Thompson, I Richard -- Luo, Xi -- Soares, Jorge -- Liu, Qingsong -- Iorio, Francesco -- Surdez, Didier -- Chen, Li -- Milano, Randy J -- Bignell, Graham R -- Tam, Ah T -- Davies, Helen -- Stevenson, Jesse A -- Barthorpe, Syd -- Lutz, Stephen R -- Kogera, Fiona -- Lawrence, Karl -- McLaren-Douglas, Anne -- Mitropoulos, Xeni -- Mironenko, Tatiana -- Thi, Helen -- Richardson, Laura -- Zhou, Wenjun -- Jewitt, Frances -- Zhang, Tinghu -- O'Brien, Patrick -- Boisvert, Jessica L -- Price, Stacey -- Hur, Wooyoung -- Yang, Wanjuan -- Deng, Xianming -- Butler, Adam -- Choi, Hwan Geun -- Chang, Jae Won -- Baselga, Jose -- Stamenkovic, Ivan -- Engelman, Jeffrey A -- Sharma, Sreenath V -- Delattre, Olivier -- Saez-Rodriguez, Julio -- Gray, Nathanael S -- Settleman, Jeffrey -- Futreal, P Andrew -- Haber, Daniel A -- Stratton, Michael R -- Ramaswamy, Sridhar -- McDermott, Ultan -- Benes, Cyril H -- 086357/Wellcome Trust/United Kingdom -- 1U54HG006097-01/HG/NHGRI NIH HHS/ -- P41GM079575-02/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Mar 28;483(7391):570-5. doi: 10.1038/nature11005.〈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/22460902" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line, Tumor ; Cell Survival/drug effects ; Drug Resistance, Neoplasm/drug effects/*genetics ; *Drug Screening Assays, Antitumor ; Gene Expression Regulation, Neoplastic/genetics ; Genes, Neoplasm/*genetics ; Genetic Markers/*genetics ; Genome, Human/*genetics ; Genomics ; Humans ; Indoles/pharmacology ; Neoplasms/*drug therapy/*genetics/pathology ; Oncogene Proteins, Fusion/genetics ; Pharmacogenetics ; Phthalazines/pharmacology ; Piperazines/pharmacology ; Poly(ADP-ribose) Polymerase Inhibitors ; Proto-Oncogene Protein c-fli-1/genetics ; RNA-Binding Protein EWS/genetics ; Sarcoma, Ewing/drug therapy/genetics/pathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Signatures of mutation and selection in the cancer genome (2010)
    Nature Publishing Group (NPG)
    Details
    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
    Published by Nature Publishing Group (NPG)
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  • 4
    Electronic Resource
    Electronic Resource
    Electrophoretic karyotype of the amylolytic yeast Lipomyces starkeyi and cloning, sequencing and chromosomal localization of its TRP1 gene (1996)
    Springer
    Current genetics 30 (1996), S. 83-88 
    Details
    ISSN: 1432-0983
    Keywords: Key wordsLipomyces starkeyi ; Electrophoretic karyotype ; CHEF ; TRP1
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract  The genome of the amylolytic yeast strain Lipomyces starkeyi NCYC 1436 was analysed using contour-clamped homogeneous electric field gel electrophoresis (CHEF). The banding pattern under a variety of running conditions indicating the presence of 11 different chromosome-sized DNA molecules. The sizes of these chromosome bands were determined by comparison with chromosomes from standard strains of Schizosaccharomyces pombe and Saccharomyces cerevisiae. The chromosomal bands were estimated to be within the range 0.7–2.8 Mb, with the genome (excluding mitochondrial DNA) estimated at 15 Mb. The molecular cloning of the TRP1 gene, isolated from a genomic library of this strain, is also reported: the gene was present on a 6.5-kb Sau3A DNA fragment, and complemented the trpC gene of E. coli. The DNA sequence was determined (EMBL accession No. Z68292) and compared to other tryptophan biosynthetic genes encoding N-(5′-phosphoribosyl) anthranilate isomerase (PRAI) activity. The gene was also used as a probe in hybridization studies, and by this means, its chromosomal location was identified.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002940050104
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  • 5
    Electronic Resource
    Electronic Resource
    Localization of glucoamylase genes of Saccharomyces cerevisiae by pulsed field gel electrophoresis (1990)
    Springer
    Antonie van Leeuwenhoek 58 (1990), S. 49-55 
    Details
    ISSN: 1572-9699
    Keywords: glucoamylase ; STA ; PFGE ; CHEF
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The chromosomal locations of four glucoamylase-specifying genes in the yeastSaccharomyces cerevisiae have been determined. Chromosomes were separated by pulsed field gel electrophoresis and blots were probed with radiolabelledSTA2 and marker DNA from specific yeast chromosomes. The three genes encoding extracellular glucoamylases,STA1 (DEX2), STA2 (DEX1) andSTA3 (DEX3) are located on chromosomes IV, II and XIV, respectively.SGA, specifying the sporulation-specific glucoamylase, was positioned on chromosome IX.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02388079
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