8 results on '"Andy Jenkinson"'
Search Results
2. Supplementary Glioma Genes from A Hypermutation Phenotype and Somatic MSH6 Mutations in Recurrent Human Malignant Gliomas after Alkylator Chemotherapy
- Author
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Richard Wooster, P. Andrew Futreal, Michael R. Stratton, David N. Louis, Tracy T. Batchelor, Wolf Mueller, Kymberly K. Levine, Jennifer E. Roy, Gregory Riggins, Douglas F. Easton, Andy Yates, Sara Widaa, Sofie West, Jennifer Varian, Calli Tofts, Helen Solomon, Alexandra Small, Rebecca Shepherd, David Richardson, Keiran Raine, Robert Petty, Janet Perry, Andrew Menzies, Richard Lugg, Ross Laman, Vivienne Kosmidou, David Jones, Andy Jenkinson, Jonathon Hinton, Katy Hills, Rachel Harrison, Kelly Halliday, Kristian Gray, Matthew Gorton, Simon Forbes, Ed Dicks, Jennifer Cole, Jody Clements, Adam Butler, Gemma Buck, Lisa Brackenbury, Syd Barthorpe, Tim Avis, Adrian Parker, Sarah O'Meara, Helen Davies, Graham Bignell, Sarah Edkins, Chris Greenman, Jon Teague, Claire Stevens, Philip Stephens, Daniel P. Cahill, Raffaella Smith, and Chris Hunter more...
- Abstract
Supplementary Glioma Genes from A Hypermutation Phenotype and Somatic MSH6 Mutations in Recurrent Human Malignant Gliomas after Alkylator Chemotherapy
- Published
- 2023
- Full Text
- View/download PDF
Catalog
3. Supplementary Glioma Gene Mutations from A Hypermutation Phenotype and Somatic MSH6 Mutations in Recurrent Human Malignant Gliomas after Alkylator Chemotherapy
- Author
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Richard Wooster, P. Andrew Futreal, Michael R. Stratton, David N. Louis, Tracy T. Batchelor, Wolf Mueller, Kymberly K. Levine, Jennifer E. Roy, Gregory Riggins, Douglas F. Easton, Andy Yates, Sara Widaa, Sofie West, Jennifer Varian, Calli Tofts, Helen Solomon, Alexandra Small, Rebecca Shepherd, David Richardson, Keiran Raine, Robert Petty, Janet Perry, Andrew Menzies, Richard Lugg, Ross Laman, Vivienne Kosmidou, David Jones, Andy Jenkinson, Jonathon Hinton, Katy Hills, Rachel Harrison, Kelly Halliday, Kristian Gray, Matthew Gorton, Simon Forbes, Ed Dicks, Jennifer Cole, Jody Clements, Adam Butler, Gemma Buck, Lisa Brackenbury, Syd Barthorpe, Tim Avis, Adrian Parker, Sarah O'Meara, Helen Davies, Graham Bignell, Sarah Edkins, Chris Greenman, Jon Teague, Claire Stevens, Philip Stephens, Daniel P. Cahill, Raffaella Smith, and Chris Hunter more...
- Abstract
Supplementary Glioma Gene Mutations from A Hypermutation Phenotype and Somatic MSH6 Mutations in Recurrent Human Malignant Gliomas after Alkylator Chemotherapy
- Published
- 2023
- Full Text
- View/download PDF
4. Data from A Hypermutation Phenotype and Somatic MSH6 Mutations in Recurrent Human Malignant Gliomas after Alkylator Chemotherapy
- Author
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Richard Wooster, P. Andrew Futreal, Michael R. Stratton, David N. Louis, Tracy T. Batchelor, Wolf Mueller, Kymberly K. Levine, Jennifer E. Roy, Gregory Riggins, Douglas F. Easton, Andy Yates, Sara Widaa, Sofie West, Jennifer Varian, Calli Tofts, Helen Solomon, Alexandra Small, Rebecca Shepherd, David Richardson, Keiran Raine, Robert Petty, Janet Perry, Andrew Menzies, Richard Lugg, Ross Laman, Vivienne Kosmidou, David Jones, Andy Jenkinson, Jonathon Hinton, Katy Hills, Rachel Harrison, Kelly Halliday, Kristian Gray, Matthew Gorton, Simon Forbes, Ed Dicks, Jennifer Cole, Jody Clements, Adam Butler, Gemma Buck, Lisa Brackenbury, Syd Barthorpe, Tim Avis, Adrian Parker, Sarah O'Meara, Helen Davies, Graham Bignell, Sarah Edkins, Chris Greenman, Jon Teague, Claire Stevens, Philip Stephens, Daniel P. Cahill, Raffaella Smith, and Chris Hunter more...
- Abstract
Malignant gliomas have a very poor prognosis. The current standard of care for these cancers consists of extended adjuvant treatment with the alkylating agent temozolomide after surgical resection and radiotherapy. Although a statistically significant increase in survival has been reported with this regimen, nearly all gliomas recur and become insensitive to further treatment with this class of agents. We sequenced 500 kb of genomic DNA corresponding to the kinase domains of 518 protein kinases in each of nine gliomas. Large numbers of somatic mutations were observed in two gliomas recurrent after alkylating agent treatment. The pattern of mutations in these cases showed strong similarity to that induced by alkylating agents in experimental systems. Further investigation revealed inactivating somatic mutations of the mismatch repair gene MSH6 in each case. We propose that inactivating somatic mutations of MSH6 confer resistance to alkylating agents in gliomas in vivo and concurrently unleash accelerated mutagenesis in resistant clones as a consequence of continued exposure to alkylating agents in the presence of defective mismatch repair. The evidence therefore suggests that when MSH6 is inactivated in gliomas, alkylating agents convert from induction of tumor cell death to promotion of neoplastic progression. These observations highlight the potential of large scale sequencing for revealing and elucidating mutagenic processes operative in individual human cancers. (Cancer Res 2006; 66(8): 3987-91) more...
- Published
- 2023
- Full Text
- View/download PDF
5. AutoCSA, an algorithm for high throughput DNA sequence variant detection in cancer genomes
- Author
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Ed Dicks, Michael R. Stratton, Simon A. Forbes, David S. Richardson, Sarah Edkins, Helen Davies, Richard Wooster, C. Mattocks, Phil Stephens, Patrick S. Tarpey, Keiran Raine, Andy Jenkinson, Christopher Greenman, P A Futreal, Rebecca Shepherd, Andy Menzies, Adam Butler, Jon W. Teague, Kristian Gray, and Andrew D. Yates more...
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Statistics and Probability ,High-throughput screening ,DNA Mutational Analysis ,Molecular Sequence Data ,Biology ,Biochemistry ,Genome ,Article ,DNA sequencing ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Neoplasms ,Genetic variation ,medicine ,Humans ,Genetic Predisposition to Disease ,Genetic Testing ,Molecular Biology ,030304 developmental biology ,Genetic testing ,Genetics ,0303 health sciences ,Base Sequence ,medicine.diagnostic_test ,Chromosome Mapping ,Genetic Variation ,Cancer ,DNA, Neoplasm ,medicine.disease ,3. Good health ,Computer Science Applications ,Computational Mathematics ,Computational Theory and Mathematics ,chemistry ,Algorithm ,Algorithms ,Software ,030217 neurology & neurosurgery ,DNA - Abstract
The undertaking of large-scale DNA sequencing screens for somatic variants in human cancers requires accurate and rapid processing of traces for variants. Due to their often aneuploid nature and admixed normal tissue, heterozygous variants found in primary cancers are often subtle and difficult to detect. To address these issues, we have developed a mutation detection algorithm, AutoCSA, specifically optimized for the high throughput screening of cancer samples. Availability: http://www.sanger.ac.uk/genetics/CGP/Software/AutoCSA. Contact: [email protected] more...
- Published
- 2007
- Full Text
- View/download PDF
6. Patterns of somatic mutation in human cancer genomes
- Author
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David N. Louis, Syd Barthorpe, Peter J. Campbell, Richard Wooster, Claire Stevens, Douglas F. Easton, Daniel P. Cahill, Ewan Birney, Keiran Raine, Simon A. Forbes, Gurpreet Bhamra, Jon Hinton, Michael R. Stratton, Tim Avis, Barbara L. Weber, Andy Menzies, Bhudipa Choudhury, Yoke Eng Chiew, Andrew D. Yates, Georgia Chenevix-Trench, Imre Vastrik, Gillian L. Dalgliesh, Andrew G. Nicholson, Alexandra Small, Ed Dicks, Janet Perry, Anthony R. Green, Sarah O’Meara, Raffaella Smith, Rachel Harrison, Bin Tean Teh, Sofie West, Tony Webb, Adam Butler, Sara Widaa, Gemma Buck, Rebecca Shepherd, Jennifer Cole, Sarah Edkins, Jennifer Varian, Peter Goldstraw, Andy Jenkinson, Jon W. Teague, Helen Davies, Sok Kean Khoo, Kris Gray, Suet Yi Leung, Calli Tofts, Dave Richardson, Christopher Greenman, P. Andrew Futreal, Tatiana Mironenko, Jody Clements, David T. Jones, Anna deFazio, Katy Hills, Kelly Halliday, Min-Han Tan, Siu Tsan Yuen, Philip J. Stephens, Christopher I. Hunter, Francis Brasseur, Leendert H. J. Looijenga, Mel Greaves, Esther Schmidt, and Graham R. Bignell more...
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DNA Mutational Analysis ,Molecular Sequence Data ,Genomics ,Biology ,medicine.disease_cause ,Genome ,Article ,Germline mutation ,Neoplasms ,medicine ,Humans ,Amino Acid Sequence ,Genetics ,Mutation ,Multidisciplinary ,Genome, Human ,Cancer ,medicine.disease ,Neoplasm Proteins ,Kataegis ,Human genome ,Carcinogenesis ,Protein Kinases ,Genes, Neoplasm - Abstract
Cancers arise owing to mutations in a subset of genes that confer growth advantage. The availability of the human genome sequence led us to propose that systematic resequencing of cancer genomes for mutations would lead to the discovery of many additional cancer genes. Here we report more than 1,000 somatic mutations found in 274 megabases (Mb) of DNA corresponding to the coding exons of 518 protein kinase genes in 210 diverse human cancers. There was substantial variation in the number and pattern of mutations in individual cancers reflecting different exposures, DNA repair defects and cellular origins. Most somatic mutations are likely to be 'passengers' that do not contribute to oncogenesis. However, there was evidence for 'driver' mutations contributing to the development of the cancers studied in approximately 120 genes. Systematic sequencing of cancer genomes therefore reveals the evolutionary diversity of cancers and implicates a larger repertoire of cancer genes than previously anticipated. more...
- Published
- 2007
7. Mutation analysis of 24 known cancer genes in the NCI-60 cell line set
- Author
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Andy Jenkinson, Janet Perry, Jennifer Varian, Michael R. Stratton, Tony Webb, Claire Stevens, Tim Avis, Alex Small, Lisa Brackenbury, Kristian Gray, David S. Richardson, Kelly Halliday, Thomas Santarius, Ogechi Ikediobi, Graham R. Bignell, Syd Barthorpe, Keiran Raine, Calli Tofts, Andrew Menzies, Jennifer Cole, Sarah Edkins, Rachel Harrison, Sarah O’Meara, Raffaella Smith, Jody Clements, Helen Davies, Rebecca Shepherd, Helen Solomon, Tatiana Mironenko, Adrian Parker, David T. Jones, John N. Weinstein, Christopher I. Hunter, Katy Hills, William C. Reinhold, P. Andrew Futreal, Vivienne Kosmidou, Jonathan Hinton, Adam Butler, Jon W. Teague, Andrew D. Yates, Philip J. Stephens, Gemma Buck, Richard Lugg, Ed Dicks, Simon A. Forbes, Richard Wooster, Sara Widaa, and Sofie West more...
- Subjects
Neuroblastoma RAS viral oncogene homolog ,Cancer Research ,Sequence analysis ,DNA Mutational Analysis ,medicine.disease_cause ,Article ,Cell Line, Tumor ,medicine ,PTEN ,Humans ,HRAS ,Genetics ,Mutation ,biology ,Gene Expression Profiling ,Homozygote ,Cancer ,Exons ,medicine.disease ,Oncology ,biology.protein ,KRAS ,RNA Splice Sites ,Carcinogenesis ,Gene Deletion ,Genes, Neoplasm - Abstract
The panel of 60 human cancer cell lines (the NCI-60) assembled by the National Cancer Institute for anticancer drug discovery is a widely used resource. The NCI-60 has been characterized pharmacologically and at the molecular level more extensively than any other set of cell lines. However, no systematic mutation analysis of genes causally implicated in oncogenesis has been reported. This study reports the sequence analysis of 24 known cancer genes in the NCI-60 and an assessment of 4 of the 24 genes for homozygous deletions. One hundred thirty-seven oncogenic mutations were identified in 14 (APC, BRAF, CDKN2, CTNNB1, HRAS, KRAS, NRAS, SMAD4, PIK3CA, PTEN, RB1, STK11, TP53, and VHL) of the 24 genes. All lines have at least one mutation among the cancer genes examined, with most lines (73%) having more than one. Identification of those cancer genes mutated in the NCI-60, in combination with pharmacologic and molecular profiles of the cells, will allow for more informed interpretation of anticancer agent screening and will enhance the use of the NCI-60 cell lines for molecularly targeted screens. [Mol Cancer Ther 2006;5(11):2606–12] more...
- Published
- 2006
8. A Hypermutation Phenotype and Somatic MSH6 Mutations in Recurrent Human Malignant Gliomas after Alkylator Chemotherapy
- Author
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Claire Stevens, Jody Clements, Katy Hills, Ross Laman, Jennifer E. Roy, David S. Richardson, Jennifer Cole, Sarah Edkins, Christopher Greenman, Kelly Halliday, Sofie West, Helen Davies, Matthew Gorton, Sara Widaa, Richard Wooster, Adam Butler, Richard Lugg, Raffaella Smith, Tracy T. Batchelor, Lisa Brackenbury, Jon W. Teague, Gregory J. Riggins, Andy Jenkinson, Adrian Parker, Syd Barthorpe, Christopher I. Hunter, Simon A. Forbes, Michael R. Stratton, Wolf Mueller, Douglas F. Easton, Janet Perry, Jennifer Varian, Sarah O’Meara, David N. Louis, Helen Solomon, David T. Jones, Ed Dicks, Rachel Harrison, P. Andrew Futreal, Rebecca Shepherd, Philip J. Stephens, Keiran Raine, Tim Avis, Kristian Gray, Gemma Buck, Daniel P. Cahill, Andrew D. Yates, Vivienne Kosmidou, Jonathon Hinton, Robert Petty, Andrew Menzies, Graham R. Bignell, Calli Tofts, Alexandra Small, and Kymberly K. Levine more...
- Subjects
Male ,Cancer Research ,Somatic cell ,Mutagenesis (molecular biology technique) ,Somatic hypermutation ,Biology ,medicine.disease_cause ,Article ,Germline mutation ,medicine ,Temozolomide ,Humans ,Antineoplastic Agents, Alkylating ,Aged ,Mutation ,Brain Neoplasms ,Glioma ,Middle Aged ,MSH6 ,DNA-Binding Proteins ,Dacarbazine ,Oncology ,Cancer research ,DNA mismatch repair ,Female ,Neoplasm Recurrence, Local ,Protein Kinases ,medicine.drug - Abstract
Malignant gliomas have a very poor prognosis. The current standard of care for these cancers consists of extended adjuvant treatment with the alkylating agent temozolomide after surgical resection and radiotherapy. Although a statistically significant increase in survival has been reported with this regimen, nearly all gliomas recur and become insensitive to further treatment with this class of agents. We sequenced 500 kb of genomic DNA corresponding to the kinase domains of 518 protein kinases in each of nine gliomas. Large numbers of somatic mutations were observed in two gliomas recurrent after alkylating agent treatment. The pattern of mutations in these cases showed strong similarity to that induced by alkylating agents in experimental systems. Further investigation revealed inactivating somatic mutations of the mismatch repair gene MSH6 in each case. We propose that inactivating somatic mutations of MSH6 confer resistance to alkylating agents in gliomas in vivo and concurrently unleash accelerated mutagenesis in resistant clones as a consequence of continued exposure to alkylating agents in the presence of defective mismatch repair. The evidence therefore suggests that when MSH6 is inactivated in gliomas, alkylating agents convert from induction of tumor cell death to promotion of neoplastic progression. These observations highlight the potential of large scale sequencing for revealing and elucidating mutagenic processes operative in individual human cancers. (Cancer Res 2006; 66(8): 3987-91) more...
- Published
- 2006
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