In a November 1, 2015 press release from the University of Oxford, it was announced that Oxford scientists have identified an Achilles heel of certain cancer cells, namely mutations in a gene called SETD2. Their findings will be presented to the National Cancer Research Institute conference in Liverpool, UK, on Monday, November 2, 2015. It is well known that mutations drive cancer cell growth and resistance to treatment. However, these mutations can also become a weak point for a tumor. The Oxford research team found that this is the case for cancer cells with mutations in a key cancer gene called SETD2. Study author Dr. Timothy Humphrey said “Mutations in SETD2 are frequently found in kidney cancer and some childhood brain tumors, so we were excited when we discovered that a new drug we were studying specifically killed cancer cells with this mutation.” The normal human SETD2 gene codes for a histone demthyltransferase that is specific for lysine-36 of histone H3, and methylation of this residue is associated with active chromatin. This protein also contains a novel transcriptional activation domain and has been found associated with hyper-phosphorylated RNA polymerase II. The SETD2 gene is located on the short arm of chromosome 3 and has been shown to play a tumour suppressor role in human cancer The Liverpool presentation will discuss how Dr. Humphrey and his team showed that cancer cells with a mutated SETD2 gene are killed by a drug called AZD1775 that inhibits a protein called WEE1 (image). The WEE1 protein was first discovered by British Nobel Prize winner Sir Paul Nurse.
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