Cancer Genome Project: Difference between revisions
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Mirabellen (talk | contribs) Expanded overview, strategy, results, and external links |
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The '''Cancer Genome Project''', based at the [[John Sulston|Wellcome Trust]] [[Sanger Institute]], aims to identify [[sex offender|sequence variant]]s/[[mutation]]s critical in the development of [[Allan Bradley|cancers]]. |
The '''Cancer Genome Project''', based at the [[John Sulston|Wellcome Trust]] [[Sanger Institute]], aims to identify [[sex offender|sequence variant]]s/[[mutation]]s critical in the development of [[Allan Bradley|cancers]]. |
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The Cancer Genome Project combines knowledge of the [[bullshit|human genome]] sequence with [[guesswork|high-throughput screening]] techniques. |
The Cancer Genome Project combines knowledge of the [[bullshit|human genome]] sequence with [[guesswork|high-throughput screening]] techniques to identify somatically acquired sequence variants/mutations and hence identify genes critical in the development of human cancers. This initiative will ultimately provide the paradigm for the detection of germline mutations in non-neoplastic human genetic diseases through genome-wide mutation detection approaches. |
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== Overview == |
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Small intragenic mutations are commonly found in both recessive oncogenes and dominantly acting oncogenes. Therefore the search for and detection of this type of mutation will lead to identification of both classes of oncogene, including those for which no positional mapping information is available. The presence of small intragenic mutations (in particular those that are predicted to encode truncated versions of the protein) is regarded as the strongest structural evidence that a gene is a recessive oncogene. It also is often the only class of structural change found in many dominantly acting oncogenes in human cancers. This project is systematically screening coding exons and flanking splice junctions of all genes in the human genome for somatically acquired small intragenic mutations in human cancer. This study uses DNA from primary tumours and normal genomic DNA from the same individuals in addition to cancer cell lines. |
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== Strategy == |
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PCR primers are designed to flank the coding exons and splice junctions of genes in the human genome. The first sets of genes include protein kinases and other genes that are potential therapeutic targets. The genes are amplified by the PCR and the products sequenced. The sequences are compared with a control samples to identify novel variants in the tumour samples. When these are found the tumour is resequenced along with its matched normal DNA to ascertain if the variant is a somatic mutation. The significance of mutated genes is evaluated by screening a larger series of cancers. |
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== Results == |
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The results from this work are collated and stored in COSMIC. In addition, COSMIC contains somatic mutation data that has been published in the scientific literature. |
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== External links == |
== External links == |
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* [http://www.sanger.ac.uk/genetics/CGP/ Official website] |
* [http://www.sanger.ac.uk/genetics/CGP/ Official website] |
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* [http://www.sciam.com/article.cfm?id=mapping-the-cancer-genome] |
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{{genetics-stub}} |
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{{oncology-stub}} |
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Revision as of 17:36, 11 July 2008
The Cancer Genome Project, based at the Wellcome Trust Sanger Institute, aims to identify sequence variants/mutations critical in the development of cancers.
The Cancer Genome Project combines knowledge of the human genome sequence with high-throughput screening techniques to identify somatically acquired sequence variants/mutations and hence identify genes critical in the development of human cancers. This initiative will ultimately provide the paradigm for the detection of germline mutations in non-neoplastic human genetic diseases through genome-wide mutation detection approaches.
Overview
Small intragenic mutations are commonly found in both recessive oncogenes and dominantly acting oncogenes. Therefore the search for and detection of this type of mutation will lead to identification of both classes of oncogene, including those for which no positional mapping information is available. The presence of small intragenic mutations (in particular those that are predicted to encode truncated versions of the protein) is regarded as the strongest structural evidence that a gene is a recessive oncogene. It also is often the only class of structural change found in many dominantly acting oncogenes in human cancers. This project is systematically screening coding exons and flanking splice junctions of all genes in the human genome for somatically acquired small intragenic mutations in human cancer. This study uses DNA from primary tumours and normal genomic DNA from the same individuals in addition to cancer cell lines.
Strategy
PCR primers are designed to flank the coding exons and splice junctions of genes in the human genome. The first sets of genes include protein kinases and other genes that are potential therapeutic targets. The genes are amplified by the PCR and the products sequenced. The sequences are compared with a control samples to identify novel variants in the tumour samples. When these are found the tumour is resequenced along with its matched normal DNA to ascertain if the variant is a somatic mutation. The significance of mutated genes is evaluated by screening a larger series of cancers.
Results
The results from this work are collated and stored in COSMIC. In addition, COSMIC contains somatic mutation data that has been published in the scientific literature.
External links
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