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Embracing the promise of personalized medicine, Fox Chase Cancer Center is offering a high-tech DNA test that can identify the genetic mutations driving an individual patient's cancer. Via Brian Shields 
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Inhibiting telomerase, an enzyme that rescues malignant cells from destruction by extending the protective caps on the ends of chromosomes, kills tumor cells but also triggers resistance pathways that allow cancer to survive and spread, scientists reported.
"Telomerase is overexpressed in many advanced cancers, but assessing its potential as a therapeutic target requires us to understand what it does and how it does it," said senior author Ronald DePinho, M.D., president of The University of Texas MD Anderson Cancer Center.
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Scientists have for the first time identified several gene mutations that they say sharply increase the chances of autism, and have found that the risk increases with the age of the parents, particularly the father.
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A mutation that allows cells to grow out of control could also provide a new way to target and destroy cancer cells. This potential Achilles’ heel comes from a mutation in a gene called PTEN, which is found in a wide range of cancers.
PTEN is one of many tumor suppressor genes that we have to prevent our cells from growing out of control. If the PTEN gene stops working because of a mutation, it can cause tumours to develop – indeed many tumors have a mutated form of PTEN. However when a door closes, a window opens: the PTEN mutation helps the tumor to grow, but it could also mark it out as a target.
Researchers from the Institute of Cancer Research, London, found that switching off another gene known as NLK (Nemo-like kinase) killed tumor cells that had the PTEN mutation. This makes NLK a good target for drug developers to create a new cancer treatment.
Initially, the researchers took samples of tumor cells with and without the mutation, and switched off genes for important proteins that are used for regulating lots of processes in the cell. To do this they used small interfering RNA (or siRNA) which interfere with the processes of specific genes. These siRNAs block the chain of events that allow a gene to produce a protein, effectively switching it off. By switching off 779 genes individually, they could look for ones where cells with the PTEN mutation died and cells without the mutation survived.
This is how the researchers discovered the powerful effect of switching off the NLK gene. They are not certain how this works but it appears to protect a protein called FOXO1 that can act as a backup tumor suppressor and cause the cancer cell to die. When PTEN is mutated, the FOXO1 protein becomes vulnerable to a process called phosphorylation, which means it is ejected from the cell nucleus and destroyed. NLK is one of the proteins that phosphorylates FOXO1 and so by switching off the NLK gene, FOXO1 is able to do its job.
Via Dr. Stefan Gruenwald
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Numerous cancer types are known to have an influence on human chromosomes, deleting certain portions in order to be able to infect the body. Now, researchers have shown that some of these deleted sections contain clusters of tumor-suppressing genes.
Experts say that this has been suspected for quite some time, but that evidence to prove that this was indeed the case has been lacking. The new investigation looked at a copy-number alteration (CNA), a deletion that occurs on the short arm of chromosome 8 (8p).
The study was carried out on mouse models of human liver cancer. Researchers found that this specific CNA affected a series of genes that work together to counteract tumors as soon as they start evolving.
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Attention scientists: "The Scientist surveyed freely available data, visualization, and analysis portals for cancer genome information to bring you a start-up guide for integrating the approach into your work.
>>Is my favorite gene mutated in cancer? A good starting point is to check for known mutations and other aberrations in your gene of interest..."
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This is a great step forward in the treatment of cancer by Fox Chase Cancer Center. Hopefully in the future, similar offerings will become the standard of care.