Saturday, December 22, 2012
The Cancer Genome Atlas (TCGA) is a project to catalogue genetic mutations responsible for cancer, using genome analysis techniques started in 2005. TCGA represents an effort in the War on Cancer that is applying recently developed high-throughput genome analysis techniques and is seeking to improve our ability to diagnose, treat, and prevent cancer through a better understanding of the molecular basis of this disease. In 2006 the National Cancer Institute and the National Human Genome Research Institute selected people and laboratories that will participate in this project. The goal of the project was to provide systematic, comprehensive genomic characterization and sequence analysis of three types of human cancers: glioblastoma multiforme, lung, and ovarian cancer. The project is unique in terms of the size of the patient cohort interrogated (scheduled are 500 patient samples, far more than most genomics studies), and the number of different techniques used to analyze the patient samples. Techniques that are being used include gene expression profiling, copy number variation profiling, SNP genotyping, genome wide DNA methylation profiling, microRNA profiling, and exon sequencing of at least 1,200 genes. Recently the group organizing the TCGA announced that they would sequence the entire genomes of some tumors and at least 6,000 candidate genes and microRNA sequences. This targeted sequencing is actively being performed by all three sequencing centers using hybrid-capture technology. A gene list is available on the TCGA website. In phase II, TCGA will perform whole exon sequencing on 80% of the cases and whole genome sequencing on 80% of the cases used in the project. TCGA has expanded in 2009 from a pilot to a large scale project. Over the next 5 years TCGA will provide genomic characterization and sequence analysis on 20-25 different tumor types. In FY 2010 a number of new centers have been funded to characterize these new tumor types. There are Genome Characterization Centers (GCCs) and Genome Data Analysis Centers (GDACs) funded to move this project into the next phase. The fact that the RFA for the expanded phase of TCGA included the specific funding of these analysis cores reflects the growing need for dedicated funding to bioinformatics in these large scale programs.
Tuesday, October 2, 2012
Thursday, September 27, 2012
Sunday, September 23, 2012
Monday, September 10, 2012
Siddhartha Mukherjee's fascination with cancer is rooted not just in how to fight it, but in where it originated. Discovering almost nothing on the subject, the cancer physician and researcher wrote "Emperor of All Maladies: A Biography of Cancer," that explores the history of the disease that causes one quarter of all American deaths.
Saturday, May 26, 2012
Molecular target identification for translational medicine: the anticancer topoisomerase I inhibitors.
Dr. Pommier received his MD and PhD degrees from the University of Paris, France and has been at the NIH since 1981. Dr. Pommier is a member of the Molecular Target steering committee at the NCI. He received an NIH Merit Award for his role in elucidating the function of topoisomerase enzymes as targets for anticancer drugs and Federal Technology Transfer Awards for studies on HIV-1 integrase and DNA topoisomerase inhibitors. Dr. Pommier is a program committee member of the American Association for Cancer Research, Senior Editor for Cancer Research, and associate editor for Cancer Research, Molecular Pharmacology, Leukemia, The Journal of Experimental Therapeutics and Oncology, The International Journal of Oncology, and Drug Resistance Updates. Dr. Pommier holds several patents for inhibitors of DNA topoisomerases I and II and HIV-1 integrase inhibitors
Friday, March 23, 2012
Macroscopic Analysis of the Disease
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In recent years the study of the diseases has advanced in complexity focused in molecular and laboratory studies, perhaps this valuable advances the medical exercise are guided in more of the cases by an accurate clinical examination. For the correct identification of the patterns given for each disease the clinician need a deep background in general pathology and in the identification of a correct diagnosis.
Tuesday, March 6, 2012
Ground-breaking UK-led research has unravelled the complete genetic code of the most common type of hereditary breast cancer for the first time.
Scientists from the Breakthrough Breast Cancer Research Centre at The Institute of Cancer Research (ICR) have fully sequenced the DNA of two breast cancers caused by a faulty BRCA1 gene. Surprisingly, changes in the genetic code of the two tumours looked almost entirely different from one another. This information can now help scientists identify better treatment strategies for patients with a faulty BRCA1 gene.
The study today also produced preliminary results identifying three new breast cancer genes – DAPK3, TMEM135 and GATA4. These are tumour suppressor genes which, when mutated, could be involved in causing breast cancer or driving its growth. The results are published today online in the Journal of Pathology.
Hereditary breast cancer accounts for up to 10% of all breast cancers, or around 4,500 cases in the UK each year. The most common cause is a faulty BRCA1 gene. Women with a BRCA1 mutation have around up to 85 per cent risk of developing breast cancer during their lifetime. BRCA1 breast cancers are usually aggressive and typically do not benefit from targeted drugs such as tamoxifen and Herceptin (trastuzumab).
Study co-author, Professor Jorge Reis-Filho, from the Breakthrough Breast Cancer Research Centre at the ICR, said: “This research has big implications for how we treat hereditary breast cancer in the future. We often consider patients with a faulty BRCA gene as one group but our work shows that each tumour can look very different from each other genetically. Now we understand this, we can start to identify the best treatment strategies to save more lives of hereditary breast cancer patients.”
The scientists looked at two tumours, both caused by a faulty BRCA1 gene, with one classified as hormone receptor negative and one hormone receptor positive. They then tracked all of the genetic mutations in both of the tumours and found only one similarity in addition to the initial BRCA1 fault. All of the additional genetic alterations were different. The hormone receptor negative tumour had around twice as many mutations as the other, underlining the differences that have occurred in their DNA.
Based on the alterations found in these two cases, the scientists scanned the genome of another group of breast cancers and identified three genes that were found to be altered in several other tumours. Although these genes have not previously been linked to breast cancer, the results suggest they may drive the identification of additional subtypes of breast cancer.
Study co-author Dr Rachael Natrajan, from the Breakthrough Breast Cancer Research Centre at the ICR, said: “It is exciting to find new genes which could be involved in causing and driving breast cancer. Now these have been identified we have to do more work to find out the role that they play. Ultimately, this knowledge could help us develop new treatments that target the specific defects of each patient’s disease.”
The UK-led study also included teams from the Institut Curie in France, the University Medical Center Utrecht in the Netherlands, and The Cancer Research UK London Research Institute and the University of Nottingham in the UK.