Posts tagged ‘cancer research’
Researchers at Mount Sinai Hospital’s Lunenfeld-Tanenbaum Research Institute have made a new discovery regarding how normal cells communicate and control their growth. The novel findings have the potential to better inform the selection of cancer drug therapies in clinical trials, and to improve drug resistance in cancer patients.
Published in the prestigious journal Nature today, researchers in Dr. Anthony Pawson’s lab at the Lunenfeld-Tanenbaum Research Institute studied a cell growth trigger that is initiated by a protein which is often mutated in cancer. This protein, called epithelial growth factor receptor (EGFR), sits on the cell surface, and sends signals inside cells to control processes such as cell survival and expansion. The protein is an important target for cancer drug therapies.
Using targeted mass spectrometry, a cutting-edge technology, scientists in Dr. Pawson’s lab tracked the assembly of multiple proteins into signaling complexes from the moment the EGFR signal is turned ‘on’, to when the cell signal turns ‘off’. In cancer, the ‘off’ signal is often defective, leading to uncontrolled cell growth.
Researchers have identified many genetic markers for familial breast cancers, but not for sporadic breast cancer, which accounts for 80 per cent of all cases. Sambasivarao Damaraju, a professor with the Faculty of Medicine & Dentistry and a researcher at the Cross Cancer Institute, worked with his team to scan the DNA of about 7,200 Alberta women, including those who have had sporadic breast cancer and those who have not had cancer. Their genomes were scanned from DNA isolated from blood.
The results? Women who had sporadic breast cancer frequently had a genetic marker on chromosome 4, a marker that has never been associated with familial breast cancer cases.
University of Montreal researchers have discovered a novel molecular mechanism that can potentially slow the progression of some cancers and other diseases of abnormal growth. In the May 23 edition of the prestigious journal Cell, scientists from the University of Montreal explain how they found that the anti-cancer and anti-proliferative drug rapamycin slows down or prevents cells from dividing.
“Cells normally monitor the availability of nutrients and will slow down or accelerate their growth and division accordingly. A key monitor of nutrients is a protein called the Target of Rapamycin (TOR), but we do not know the details of how this protein feeds signals downstream to control growth” says Dr. Stephen Michnick, senior author and a University of Montreal biochemistry professor. He adds that, “we were surprised to find that TOR hooks up to a circuit that controls the exit of cells from division which in turn modulates the RNA message that codes for a key cell cycle regulator called B-cyclin”.
Work by McMaster’s Mick Bhatia has been selected by the Canadian Cancer Society as part of the organization’s top 10 cancer research breakthroughs of 2012.
The heat shock protein-90 co-chaperone, Cyclophilin 40, promotes ALK-positive, anaplastic large cell lymphoma viability and its expression is regulated by the NPM-ALK oncoprotein.
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