Canadian scientists have discovered a gene that suppresses the growth of many cancerous tumours.
The researchers from British Columbia (BC) say the discovery could improve treatments for many cancer patients.
The research team at the BC Cancer Agency conducted studies on mice which revealed that when the gene HACE1 was inactivated, spontaneous late-stage cancer developed.
The researchers first became interested in HACE1 several years ago, when they discovered that the gene, common to all humans, was effectively turned off in certain tumours, such as those caused by breast cancer, lung cancer and lymphoma.
That discovery led to the suspicion that HACE1, when working properly, in some way protects tissue from developing tumours.
They carried out tests on mice to test that hypothesis and found when mice without the HACE1 gene were exposed to environmental triggers for cancer, such as ultraviolet radiation, lung carcinogens and other genetic alterations, there was a surge in tumour development.
The mice developed breast, lung and liver cancers, as well as lymphomas, melanomas and sarcomas; when the HACE1 gene was reintroduced via injection into the mice, tumour growth was halted.
Dr. Poul Sorensen, senior scientist at the agency says the discovery of the gene is very exciting because it clearly has implications for a wide range of cancers, and provides a novel link between cellular stress and cancer.
Dr. Sorensen, says if scientists can learn how to reactivate HACE1 or block cancer cells from inactivating the gene, it may be possible to improve treatments for many cancer patients.
Sorensen says it has long been suspected that cancer is caused by a combination of genetic and environmental factors working together and their results give an insight into how the disease takes root when a single gene is inactivated.
The study is published in the current issue of the journal Nature Medicine and was conducted in collaboration with Dr. Josef Penninger of the Institute of Molecular Biotechnology of the Austrian Academy of Sciences.