Dec. 3, 2007 McGill University researchers have uncovered the crucial role played by the enzyme focal adhesion kinase (FAK) in the onset of breast cancer.
Using transgenic mice with pre-existing cancers, the McGill team was able to disable the function of FAK in the mammary gland. "When we did that, we basically blocked tumour progression in our mouse model," said Dr. Muller, Professor of Biochemistry at McGill, Canada Research Chair in Molecular Oncology and a researcher with the Molecular Oncology Group at the McGill University Health Centre (MUHC). "This shows that FAK, which was already linked to tumour growth in skin carcinomas, is very critical for tumour progression from a pre-malignant to a malignant state in the mammary tumour system."
Dr. Muller and his team made a similar breakthrough with an earlier discovery in 2004, when they showed that the protein beta1-integrin was similarly critical in the initiation of tumour growth and development of breast cancer in genetically engineered mice.
Likewise, when this gene was blocked, cancerous tumours ceased to grow. The current discovery about FAK is an exciting sequel to the earlier research, says Dr. Muller, because, unlike beta1-integrin, kinase enzymes are eminently "druggable" with current technology.
Dr. Muller cautions that this study -- like the Beatson Institute's earlier research linking FAK to tumour progression in skin carcinomas -- is still preliminary. "However, developing an FAK inhibitor would certainly add another weapon to the arsenal for dealing with breast cancer," he said.
The research, led by Dr. William Muller -- along with colleagues from McGill and the Beatson Institute for Cancer Research in Scotland -- was published the week of November 26 in the Proceedings of the National Academy of Sciences (PNAS). The study's first author is Dr. Hicham Lahlou, a post-doctoral fellow in Dr. Muller's lab.
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