Here is an excerpt from another informative article about Dr. James (Jay) Bradner and his research team at Dana-Farber Cancer Institute:
Disrupting a cancer gene
Novel approach scores first success against elusive cancer gene – HARVARD gazette
Scientists at Harvard-affiliated Dana-Farber Cancer Institute have successfully disrupted the function of a cancer gene involved in the formation of most human tumors by tampering with the gene’s “on” switch and growth signals, rather than targeting the gene itself.
The results, achieved in multiple myeloma cells, offer a promising strategy for treating not only myeloma but also many other cancer types driven by the gene MYC, the study authors say. Their findings will appear in the print issue of the journal Cell on Sept. 16. Details of the study are currently available on the journal’s website.
“Cancer is a disease of disregulation of growth genes in a cell, and MYC is a master regulator of these genes,” says James E. Bradner of Dana-Farber and Harvard Medical School (HMS). Bradner is one of the study’s senior authors. Previous attempts to shut down MYC by inhibiting it directly with drug molecules have been notably unsuccessful. “In this study, our idea was to switch MYC off, interfering with its ability to activate the cell-growth program.”
In multiple myeloma, MYC is hyperactive — constantly ordering cells to grow and divide — because it is in the wrong position in the cells’ chromosomes. Instead of its normal, quiet neighborhood, MYC finds itself adjacent to a gene known as the immunoglobulin gene. This busy gene is switched on by bits of DNA known as immunoglobulin enhancers, which normally prompt the cell to begin producing disease-fighting antibodies. In myeloma, the immunoglobulin enhancers act on the out-of-place MYC gene like an impatient finger at a doorbell, repeatedly activating it…
You can read more–and watch a new video about JQ1 research–by going to:
On this new video, I did notice that Dr. Bradner admitted cancer cells can become JQ1 resistant–just like they do when exposed to other anti-cancer therapies.
That seems to be the yet undiscovered magic key–finding a way to switch-off the ability of myeloma cells to build-up resistance to therapy.
Good luck, Dr. Bradner! Our hopes and prayers are with you…
Feel good and keep smiling! Pat