HER2 Support Group Forums - View Single Post - “One reason is that we really don’t know much about metastasis,”

12-16-2005, 11:23 AM

From my background reading an honest comment, with all that it implies in making treatment decisions.

The third paragraph on mechanisms of spread echos my lay theories on omega three / six balance, the impact of the over activation of the eicosanoid pathways, the lack of pathways for excess omega six storage, excretion, or burning off, the activation of core cellular emegency repair response, all in an environment that gives access to reproductive cellular pathways(women and the breast a priority active fat storage site) .

A trial in mice showed increased omega six consumption over omega three increased endothelin b receptor Ednrb activity by a factor of ten (and the CD40 L TNF family by ten as well, ErbB-2 receptor by a factor of 2.......). Endothelin is reported to impact in areas of reproduction stem cells etc.

What if the body is simply recognising that huge excesses in biological terms of what was a scarce and precious fundamental resource, omega six, pose an enormous problem, the impact of which is sufficiently fundamental at a cellular level to active the evolutionary responses in a magor way.

Are the increases of cancer are a manefestation of that evolutionary process.

Might cancer be better described as an hyper evolution "disease".

RB

http://www.princeton.edu/main/news/a...dex.xml&next=1

ABSRACT

The five-year survival rate for women with early-stage breast cancer is 98 percent, according to the American Cancer Society. For those with a late-stage form of the disease, the rate falls dramatically to 26 percent.

“One reason is that we really don’t know much about metastasis,” said Yibin Kang, an assistant professor of molecular biology at Princeton, referring to the recurrence of tumors in secondary sites common in late-stage breast cancer. Armed with a recent grant and innovative research tools, he’s hoping to provide new data on the spread of cancer......................

.........Interestingly, some genes used by tumor cells to migrate and spread also are essential for certain normal cell movements during the early development of embryos. “It is as if the cancer cells just pick up some long-forgotten old tricks learned from their early days and use them for an evil purpose,” Kang said. His lab is teaming up with Princeton developmental biologists Trudi Schupbach and Jean Schwarzbauer to investigate this curious link between cancer metastasis and embryonic development....................

12-16-2005, 11:23 AM	#1
Unregistered Guest Posts: n/a	“One reason is that we really don’t know much about metastasis,” From my background reading an honest comment, with all that it implies in making treatment decisions. The third paragraph on mechanisms of spread echos my lay theories on omega three / six balance, the impact of the over activation of the eicosanoid pathways, the lack of pathways for excess omega six storage, excretion, or burning off, the activation of core cellular emegency repair response, all in an environment that gives access to reproductive cellular pathways(women and the breast a priority active fat storage site) . A trial in mice showed increased omega six consumption over omega three increased endothelin b receptor Ednrb activity by a factor of ten (and the CD40 L TNF family by ten as well, ErbB-2 receptor by a factor of 2.......). Endothelin is reported to impact in areas of reproduction stem cells etc. What if the body is simply recognising that huge excesses in biological terms of what was a scarce and precious fundamental resource, omega six, pose an enormous problem, the impact of which is sufficiently fundamental at a cellular level to active the evolutionary responses in a magor way. Are the increases of cancer are a manefestation of that evolutionary process. Might cancer be better described as an hyper evolution "disease". RB http://www.princeton.edu/main/news/a...dex.xml&next=1 ABSRACT The five-year survival rate for women with early-stage breast cancer is 98 percent, according to the American Cancer Society. For those with a late-stage form of the disease, the rate falls dramatically to 26 percent. “One reason is that we really don’t know much about metastasis,” said Yibin Kang, an assistant professor of molecular biology at Princeton, referring to the recurrence of tumors in secondary sites common in late-stage breast cancer. Armed with a recent grant and innovative research tools, he’s hoping to provide new data on the spread of cancer...................... .........Interestingly, some genes used by tumor cells to migrate and spread also are essential for certain normal cell movements during the early development of embryos. “It is as if the cancer cells just pick up some long-forgotten old tricks learned from their early days and use them for an evil purpose,” Kang said. His lab is teaming up with Princeton developmental biologists Trudi Schupbach and Jean Schwarzbauer to investigate this curious link between cancer metastasis and embryonic development....................