Sequencing of complete gene map of lung cancer and skin cancer
British scientists announced that for the first time they have successfully drawn a complete genetic map of lung cancer and skin cancer. John Bell, Dean of the British Academy of Medical Sciences, said that this is a "transformative" progress in cancer research and treatment in the past decade In the "Nature" magazine published on the 17th.
Mike Stratton, the leader of the study and one of the leaders of the British Cancer Genome Project, believes that drawing a complete cancer gene map means that doctors can detect human cancer cells earlier and allow patients to prevent accordingly; and Only a simple blood test is required, and then a "personalized" treatment plan is developed according to the different conditions of each individual; it also allows scientists to develop anti-cancer drugs for specific gene mutations as soon as possible.
Scientists have recorded thousands of mutations in human cells in these two newly drawn maps. It is these mutations that cause the cells to become cancerous and produce cancer.
The head of the British Charity Cancer Research Association, Hapal Kumar, said that the next step will be to find out from these thousands of variants which variant genes actually cause the formation and spread of cancer cells, and which variant genes are incidental, so that we can Find a better way to correct and prevent. Drawing a complete genetic map of cancer cells also helps provide MoT blood samples for healthy people to test whether their DNA may have developed a lesion.
Relevant experts pointed out that although environmental factors have a huge impact on cancer, but basically speaking, cancer is a DNA defect disease. DNA defects can cause genetic mutations (some induced by carcinogens), which can cause some cells to divide uncontrollably and then spread in the body. More and more studies have shown that cancer is not a single disease. Each type of cancer includes a large number of different subspecies categories caused by different types of genetic mutations, which require symptomatic treatment.
The current two maps are the first results of the "Cancer Gene Atlas Project" of the International Cancer Genome Association. The International Cancer Genome Association was established on April 29, 2008. It gathers the power of scientists from 10 members including China, the United States, and the United Kingdom to draw a complete map of human cancer genes. At present, the organization plans to invest 1 billion US dollars in 10 years to study in detail the variant genes that can cause 50 kinds of cancer, and draw a full map of these genes.
The association plans to extract cancer cells from 500 cancer patients of this type and sequence the genes in each cancer research, and then compare the results with the coding of healthy cell genes to determine which variant genes actually cause cancer cells. The formation and spread of which variant genes are sporadic.
If the human cancer gene map is successfully drawn, it is expected to open up a new era of personalized cancer treatment. At that time, the doctor will be able to accurately know the specific genetic factors of the patient's tumor growth and spread, thereby making it easier to choose a treatment method for a specific cancer individual. The plan also helps design new drugs that target cancer cells ’genetic weaknesses
Bio Valley recommends the original source:
Nature advance online publication 16 December 2009 | doi: 10.1038 / nature08658
A comprehensive catalogue of somatic mutations from a human cancer genome
Erin D. Pleasance1, 8, R. Keira Cheetham2, 8, Philip J. Stephens1, David J. McBride1, Sean J. Humphray2, Chris D. Greenman1, Ignacio Varela1, Meng-Lay Lin1, Gonzalo R. Ordó? Ez1, Graham R. Bignell1, Kai Ye3, Julie Alipaz4, Markus J. Bauer2, David Beare1, Adam Butler1, Richard J. Carter2, Lina Chen1, Anthony J. Cox2, Sarah Edkins1, Paula I. Kokko-Gonzales2, Niall A. Gormley2, Russell J. Grocock2, Christian D. Haudenschild5, Matthew M. Hims2, Terena James2, Mingming Jia1, Zoya Kingsbury2, Catherine Leroy1, John Marshall1, Andrew Menzies1, Laura J. Mudie1, Zemin Ning1, Tom Royce4, Ole B. Schulz-Trieglaff2, Anastassia Spiridou2, Lucy A. Stebbings1, Lukasz Szajkowski2, Jon Teague1, David Williamson5, Lynda Chin6, Mark T. Ross2, Peter J. Campbell1, David R. Bentley2, P. Andrew Futreal1 & Michael R. Stratton1,7
1 Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK
2 Illumina Cambridge Ltd, Chesterford Research Park, Little Chesterford, Essex CB10 1XL, UK
3 Departments of Molecular Epidemiology, Medical Statistics and Bioinformatics, Leiden University Medical Center, Einthovenweg 20, 2333 ZC Leiden, the Netherlands
4 Illumina Inc., Corporate Headquarters, 9865 Towne Centre Drive, San Diego, California 92121, USA
5 Illumina Hayward, 25861 Industrial Bvld, Hayward, California 94545, USA
6 Dana-Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115, USA
7 Institute of Cancer Research, Sutton, Surrey SM2 5NG, UK
8 These authors contributed equally to this work.
Correspondence to: P. Andrew Futreal1Michael R. Stratton1,7 Correspondence and requests for materials should be addressed to MRS or PAF
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