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Oncogenomics is a relatively new sub-field of genomics that applies high throughput technologies to characterize genes associated with cancer. Oncogenomics is synonymous with "cancer genomics". Cancer is a genetic disease caused by accumulation of mutations to DNA leading to unrestrained cell proliferation and neoplasm formation. The goal of oncogenomics is to identify new oncogenes or tumor suppressor genes that may provide new insights into cancer diagnosis, predicting clinical outcome of cancers, and new targets for cancer therapies. The success of targeted cancer therapies such as Gleevec, Herceptin, and Avastin raised the hope for oncogenomics to elucidate new targets for cancer treatment. Besides understanding the underlying genetic mechanisms that initiates or drives cancer progression, one of the main goals of oncogenomics is to allow for the development of personalized cancer treatment. Cancer develops due to an accumulation of mutations in DNA. These mutations accumulate randomly, and thus, different DNA mutations and mutation combinations exist between different individuals with the same type of cancer. Thus, identifying and targeting specific mutations which have occurred in an individual patient may lead to increased efficacy of cancer therapy. The completion of the Human Genome Project has greatly facilitated the field of oncogenomics and has increased the abilities of researchers to find cancer causing genes. In addition, the sequencing technologies now available for sequence generation and data analysis have been applied to the study of oncogenomics. With the amount of research conducted on cancer genomes and the accumulation of databases documenting the mutational changes, it has been predicted that the most important cancer-causing mutations, rearrangements, and altered expression levels will be cataloged and well characterized within the next decade. Cancer research may look either on the genomic level at DNA mutations, the epigenetic level at methylation or histone modification changes, the transcription level at altered levels of gene expression, or the protein level at altered levels of protein abundance and function in cancer cells. Oncogenomics focuses on the genomic, epigenomic, and transcript level alterations in cancer. ==History== The genomics era became established with success in the 1990s, due to the generation of DNA sequences of many organisms. In the 21st century, the completion of the Human Genome Project at the Wellcome Trust Sanger Institute paved the way for many new endeavors for studying the functional genomics and examining the genomes which characterize different diseases. Cancer has been one of the main focuses. Reasons why access to whole cancer genome sequencing is so important to cancer (or cancer genome) research: #The mutations present in the cancer genome are the direct cause of disease and they define the tumor phenotype. #As a result of the access to both diseased and normal tissue samples from the same patient, and the fact that most cancer genomic mutations represent somatic events, we are able to confidently identify the mutations specific to cancer. #In cancer, mutations within the genome are progressive and in some cancer cases changes related to disease stage, development of metastasis, and drug resistance are distinguishable. The first cancer genome was sequenced in 2008 by Timothy J. Ley ''et. al''.〔 This study sequenced a typical Acute Myeloid Leukaemia (AML) genome and it normal counterpart genome obtained from the same patient's skin. When comparing the two sequences these researchers discovered 10 genes which contained acquired mutations: *2 of these mutations were previously thought to contribute to tumor progression, and they were: * *an internal tandem duplication of the FLT3 receptor tyrosine kinase gene, which constitutively activates kinase signaling, and is associated with a poor prognosis * *a four base insertion in exon 12 of the NPM1 gene (NPMc) * * *Both of these are common in AML tumors (found in about 25-30% of them), and they are both thought to contribute to the progression of the disease rather than to actually cause it directly. *The remaining 8 were new mutations and all were single base changes: * *4 of the genes were found to be in families that are strongly associated with cancer pathogenesis (PTPRT, CDH24, PCLKC, and SLC15A1) * *the other four were not found to have any previous association with cancer pathogenesis, but they had potential functions in metabolic pathways that suggested mechanisms by which they could act to promote cancer (KNDC1, GPR124, EB12, GRINC1B) All of these genes are involved in pathways known to contribute to cancer pathogenesis, but before this study most of these genes would not have been candidates for targeted gene therapy based on the prior understanding of cancer. Thus the results of this study were successful in showing the importance of whole cancer genome sequencing techniques in identifying somatic mutations involved in cancer. This study also showed the importance of parallel sequencing of the patient's normal genome to determine which mutations/variants were inherited or acquired. This technique is important in the identification of the true somatic mutations. 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Oncogenomics」の詳細全文を読む スポンサード リンク
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