Mammography a malignant breast tumor before (L) and (R) 16 weeks of the aromatase inhibitor. We learn more from breast cancer, that it is more complicated.Paul k. Commean / Washington University School of medicineThe deeper researchers diving a in the genetics of breast cancer, the more complicated their discoveries. And the latest and deepest, dive is no exception.
Scientists under the direction of Matthew Ellis at Washington University in St. Louis, Missouri, the whole genome of 50 patients of breast cancer have tumors with matching DNA from the same patients healthy cells sequenced, to determine, genomic changes only in cancer cells. Their results, research in Orlando, Florida, presented today at the annual meeting of the American Association for cancer show that these types of cancer genetic fingerprints are very different; the 1,700 mutations found a total, and most were only for individual patients tumors, and only three to 10% or more. The genomic changes were also all types, from single nucleotide variations and frame shifts translocations, and deletes.
"The results are complex and somewhat alarming, because the problem does make you sit and which breast cancer is to rethink," says Ellis, head of the breast cancer program at the University of Siteman Cancer Center.
Still, he says, there is reason for optimism - not least because careful analysis of the data, combined with what is already known about the functions of the affected genes, provides a wealth of new therapeutic possibilities.
The sheer volume of scientists enterprise is impressive: they sequenced and one analyzes more than ten trillion bases, with a supercomputer Hadron Collider at CERN, Europe's leading physics laboratory in Geneva makes Switzerland the similar to the large. The tumors sequenced with average 30-fold coverage, estrogen-receptor positive breast cancer. They came from the participants known two clinical trials of estrogen lowering drugs as aromatase inhibitor. Patients with breast cancer who are not on these drugs have significantly worse results, although the molecular basis for this is poorly understood. The scientists hope that by the genome sequences of estrogen-sensitive tumors (26 of the 50) compared to estrogen resistant cancers (24), notes on the pathological basis of the difference could find them.
It was at least an Association - for the breast cancer tumor suppressor gene MAP3K1, the protein product that accelerates programmed cell death. Mutations that can disable this gene cells that should die to keep living. MAP3K1 were mutations in about 10% of cancers, and the aromatase-inhibitor sensitive, more favourable, nature of the disease, in particular in the same cancer, seemed previously mutation in a gene called PIK3CA described are mapped.
This was one of the two mutations already associated with breast cancer, which often occurred in the 50 tumors: PIK3CA was found in 43% of the samples and the TP53 tumor suppressor turned is approximately 15%. All in all, about half had the cancer a combination of these three mutations - left half with cancers from different constellations of much less common mutations.
Ellis says, that the complexity of the results indicates that when it comes to the development of Therapeutics"clearly the only way to front the genome-first approach." "No single blockbuster drug is answer resistance the problem of endocrine therapy".
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He adds that also treatments for pathological mechanisms by relatively rare mutations caused because breast cancer is so common, could benefit many thousands of women
"The fact that they sequenced have cancer in a clinical study, that is, what really significant," says Samuel Aparicio, breast cancer researcher at the University of British Columbia and the BC Cancer Agency in Vancouver, Canada. This is because data from clinical trials are scientists of to genomic findings on detailed data to allow, for example, survival. "You know exactly what happened to patients," says Aparicio.
Ellis, for its part, says that he has already begun his next step: repeat the experiment on at least 1000 more tumors. "It's complicated, and we do need many more often to see how it all works", he says. "But we certainly to start the methodology to determine it."
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