The protein p53 suppresses tumor development by potently inducing tumor cell death, making it an obvious target for anticancer therapeutics. However, this therapeutic approach is confounded by the fact that genetic mutations cause loss or inactivation of p53 in approximately 50% of human cancers.
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A CSIRO research team has pinpointed the genetic difference between red (or black) and white grapes - a discovery which could lead to the production of new varieties of grapes and ultimately new wines.
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In his paper, to be published in The EMBO Jorunal, Dr Surrallùs describes how proteins of the Fanconi/BRCA pathway recognise the presence of genetic mutations in order to repair them. The researchers also found that alteration of this mechanism makes tumour cells much more sensitive to certain drugs. This discovery will make it possible to develop strategies to make tumours more vulnerable to chemotherapy.
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Yale School of Medicine researchers have identified a rare defect in a single gene that poses a substantial risk for metabolic syndrome and early heart disease, the leading cause of death worldwide.
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Researchers at The University of Texas at San Antonio (UTSA), The University of Texas Health Science Center at San Antonio (UTHSC) and The University of Hawaii (UH) have found that Assisted Reproductive Technologies (ARTs) do not increase the risk of genetic mutations in developing fetuses. Results of the study in mice will be released in this week's journal, Proceedings of the National Academy of Sciences.
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Every day for 10 years, a seemingly heart-healthy 53-year-old woman experienced rapid and irregular heartbeats. She had no personal or family history of hypertension or hyperthyroidism. She did not suffer from myocardial or coronary artery disease, or any abnormalities of the heart as best doctors and medical science could determine. Yet, she complained of heart palpitations and dizziness nearly to the point of fainting.
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When cells become cancerous, they also become 100 times more likely to genetically mutate than regular cells, researchers have found. The findings may explain why cells in a tumor have so many genetic mutations, but could also be bad news for cancer treatments that target a particular gene controlling cancer malignancy.
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A study led by researchers at Dana-Farber Cancer Institute and Broad Institute of the Massachusetts Institute of Technology and Harvard University provides the first demonstration of a practical method of screening tumors for cancer-related gene abnormalities that might be treated with "targeted" drugs.
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Certain patients suffering from multiple myeloma, a difficult-to-treat cancer of the plasma cells, may respond positively to a drug that shows potential to extend their survival rates by as much as six months, according to researchers at the Mayo Clinic Cancer Center.
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