Latest Ataxia telangiectasia mutated Stories
DNA damage repair is highly complex. UZH researchers have now discovered another piece in the puzzle for the removal of extremely dangerous DNA lesions.
A novel drug may help increase the effectiveness of radiation therapy for the most deadly form of brain cancer.
Researchers at Moffitt Cancer Center have found that a deficiency in an important anti-tumor protein, p53, can slow or delay DNA repair after radiation treatment.
Leading ATM and ATM parts supplier TestLink has recently released the 2012 training schedule for three specialised NCR ATM engineer training courses. (PRWEB)
The expression of p53 and Mdm2 is closely related. In an article published this week in the Cancel Cell review, Robin Fahraeus and his collaborators from Inserm Unit 940 ("Therapeutic Targets for Cancer"), demonstrate that cellular response to DNA damage requires involvement from the protein kinase ATM so that Mdm2 can positively or negatively control protein p53.
It is widely known that mutations in the breast cancer susceptibility 1 (BRCA1) gene significantly increase the chance of developing breast and ovarian cancers, but the mechanisms at play are not fully understood.
DNA damage sensor also responds to oxidative harm outside the nucleus
Scientists at Dana-Farber Cancer Institute have uncovered the mechanism behind a promising new approach to cancer treatment: damaging cancer cells' DNA with potent drugs while simultaneously preventing the cells from repairing themselves.
New work by MIT cancer biologists shows that the interplay between two key genes that are often defective in tumors determines how cancer cells respond to chemotherapy.
A tightly controlled system of checks and balances ensures that a powerful tumor suppressor called p53 keeps a tight lid on unchecked cell growth but doesn't wreak havoc in healthy cells.
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