Rock Creek Pharmaceuticals Inc. (fka RCPIQ)

[NukeJohn]

More Links on NF-kB and Cancer



Attached below is an excellent article that discusses the link between NF-kB and Cancer. Those of us who have used Anatabloc understand that it helps regulate the excess activation of NF-kB that causes chronic inflammation.

http://www.lef.org/magazine/mag2006/jul2006_report_nuclear_01.htm

The link below shows how Anatabloc reduces inflammation (via the JAK-STAT pathway). It inhibits NF-kB transcription and this reduces IL-1 and IL-6 which, in turn, reduces C Reactive Protein or CRP.

If you really want to dig deeper and understand what impacts a pharmaceutical version of anatabine citrate might have on those with cancer...read this article (and pay close attention to section 12).

http://naturalsupplementsresearch.org/assets/applets/Inflammation_and_cancer-_how_hot_is_the_link.pdf


Current NF-kB Research (from Life Extension Magazine article)

Here’s what we know in 2011 about the relationship between NF-kB and cancer, courtesy of Dr. Sahdeo Prasad of the Cytokine Research Laboratory at the MD Anderson Cancer Center in Houston:

NF-kB becomes activated in response to a host of factors that account for as much as 95% of all cancers. These triggers include tobacco, stress, dietary components, obesity, alcohol, infections, radiation, and environmental toxins.

NF-kB activation has been linked with the transformation of normal cells into cancer cells (thus NF-kB can be thought of as promoting cancer development).

NF-kB is active at a higher rate in cancer cells than in healthy cells. A developing cancer also increases the amount of active NF-kB.

NF-kB has been linked to the survival of dangerous cancer stem cells, the early “parent” cells of many cancers that are now known to exist in otherwise normal tissues. Cancer stem cells can “self-renew” more successfully than healthy cells.

NF-kB stimulates production of gene products that keep cancer cells from dying naturally through the process of programmed cell death, or apoptosis.

NF-kB also increases production of gene products associated with proliferation, the rapid and repeated cell divisions that give cancers their aggressive growth characteristics.

NF-kB controls expression of gene products linked with invasion, new blood vessel growth (angiogenesis), and metastatic spread of tumors.

Many carcinogens activate NF-kB, but most effective cancer-preventing (chemopreventive) compounds suppress NF-kB activation.

Prasad notes that these observations highlight just how intertwined NF-kB is with cancer growth and metastasis. Others have gone on to point out that, though a powerful nemesis, NF-kB also offers myriad opportunities to intervene powerfully and block cancers in their tracks. As we continue to clarify the close relationship between chronic inflammation and cancer, more and more such opportunities are becoming evident.

One of these days the world will understand.

JMHO,

NJ