Potent Anti-Tumor Gene Tested in Mice Produces Remission
Definitions:
Hematopoietic stem cells- The bone marrow cells that produce all blood and immune system cells.
melanoma- An oftentimes deadly type of skin cancer characterized by a black or dark brown-pigmented tumor.
Summary:
In the year of 2010 alone, more than 68,000 patients have been diagnosed with melanoma while 9000 deaths were affiliated with it. Current treatments for metastatic melanoma are toxic and unsuccessful as many of the patients die withing 6-12 months of diagnose.
The Indiana School of Medicine tested a new T cell receptor gene into the hematopoietic stem cells of mice. What this specific gene does is that it detects a certain protein that is affiliated and found on the surface of melanoma. It is then cloned and sent back into the hosts. The results show that the transplantations of the genetically modified hematopoietic stem cells resulted in an immune system towards melanoma and eradicated all of the mice subject's tumors. This new gene may be a new approach towards this kind of skin cancer.
Discussion:
I chose this article because cancer is one of the most devastating disease and that it is the cause of many deaths around the world. I also found it interesting as this new gene may be a novel method to treat melanoma. Ive always thought of cancer as a complex and unbeatable disease that will never be cured. However, with the discovering and testing of the new T receptor gene, it not only paves the way for new trials in usage of humans, but also gives hope that this new discovery may be a cure for cancer.
Questions:
If this gene eradicated all of the mice's tumor cells, how can it be incorporated into destroying human tumor cells?
Will this gene cause any unwanted side effects when clinically tried in humans?
Citations:
Article and Picture: Ha, Sung P. "Gene therapy for metastic melanoma in mice produces complete
remission." Science Daily. Science News, 18 Nov. 2010. Web. 19 Nov. 2010. <http://www.sciencedaily.com/releases/2010/11/101118124206.htm>.