HER2 Support Group Forums - View Single Post

R.B. · 07-08-2006, 02:16 PM

Re previous posts - omega six pathways cox 2 etc

Blood supply to tumour new vessel growth and cox 2

and a link to an extensive list of trials on the subject on just one search. A common factor in a wide range of cancers?

PGE2 is a product of omega six. Omega three and six fats are included as building blocks in cell membranes. They are included essentially in the proportions ingested

Lets call omega threes white and sixes red, think of it as a rather odd football game. My understanding is that when the body sends out an alert, infection, insect bite etc. the team manager will just ask for a number of players (lets say 100 for illustrative purposes). So 100 players will come off the bench (the membrane). The number of red and white players on the bench is dependent on the number you have chosen by eating them. Lots of omega six = lots of red players on the bench. Alert, players come off bench, red swamp whites in numbers. The result is a red type game. Inflamation and not enough white players for a "fair game" and to keep the red in check, and come to an end of the game. The result can be permenant low level inflamtion between the main games.

From what I read it appears that over time the team manager has just got used to assuming that the red and white teams will always be balanced, and has never learned to balance the teams when they are not. The mangager just ask who ever is sitting there to join the game and becuse we eat more white than reds in general terms the game is always skewed towards the reds.

So it is down to us to make sure that the players are within reasonable limits balanced enough to provide a balanced game.

It is obviously much more comlex than this I am simply trying to explain my limited and rather amateur understanding of why altering the balance of intake of fats can influence the shape of the game.

http://www.ncbi.nlm.nih.gov/entrez/q...m_uid=11688844

RB

http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum

1: Ann Clin Lab Sci. 2001 Oct;31(4):325-48.Click here to read Links
Review: molecular pathology of cyclooxygenase-2 in cancer-induced angiogenesis.

* Fosslien E.

Department of Pathology, College of Medicine, University of Illinois at Chicago, 60612, USA. efosslie@uic.edu

Cancer-induced angiogenesis is the result of increased expression of angiogenic factors, or decreased expression of anti-angiogenic factors, or a combination of both events. For instance, in colon cancer, the malignant cells, the stromal fibroblasts, and the endothelial cells all exhibit strong staining for cyclooxygenase-2 (COX-2), the rate-controlling enzyme in prostaglandin (PG) synthesis. In various cancer tissues, vascular endothelial growth factor (VEGF) and transforming growth factor beta (TGF-beta) co-localize with COX-2. Strong COX-2 and VEGF expression is highly correlated with increased tumor microvascular density (MCD); new vessels proliferate in areas of the tumor that express COX-2. Moreover, high MVD is a predictor of poor prognosis in breast and cervical cancers. COX-2 and VEGF expression are elevated in breast and prostate cancer tissues and their cell-lines. In vitro, PGE2 induces VEGE Supernatants of cultured cells from breast, prostate, and squamous cell cancers contain angiogenic proteins such as COX-2 and VEGF that induce in vitro angiogenesis. A selective COX-2 inhibitor, NS-398, restores tumor cell apoptosis, reduces microvascular density, and reduces tumor growth of PC-3 prostate carcinoma cells xenografted into nude mice. The COX-2 produced by a malignant tumor and COX-2 produced by the surrounding host tissue both contribute to new vessel formation, which explains how selective COX-2 inhibition reduces tumor growth where the tumor COX-2 gene has been silenced by methylation.

PMID: 11688844 [PubMed - indexed for MEDLINE]

07-08-2006, 02:16 PM	#13
R.B. Senior Member Join Date: Mar 2006 Posts: 1,843	Re previous posts - omega six pathways cox 2 etc Blood supply to tumour new vessel growth and cox 2 and a link to an extensive list of trials on the subject on just one search. A common factor in a wide range of cancers? PGE2 is a product of omega six. Omega three and six fats are included as building blocks in cell membranes. They are included essentially in the proportions ingested Lets call omega threes white and sixes red, think of it as a rather odd football game. My understanding is that when the body sends out an alert, infection, insect bite etc. the team manager will just ask for a number of players (lets say 100 for illustrative purposes). So 100 players will come off the bench (the membrane). The number of red and white players on the bench is dependent on the number you have chosen by eating them. Lots of omega six = lots of red players on the bench. Alert, players come off bench, red swamp whites in numbers. The result is a red type game. Inflamation and not enough white players for a "fair game" and to keep the red in check, and come to an end of the game. The result can be permenant low level inflamtion between the main games. From what I read it appears that over time the team manager has just got used to assuming that the red and white teams will always be balanced, and has never learned to balance the teams when they are not. The mangager just ask who ever is sitting there to join the game and becuse we eat more white than reds in general terms the game is always skewed towards the reds. So it is down to us to make sure that the players are within reasonable limits balanced enough to provide a balanced game. It is obviously much more comlex than this I am simply trying to explain my limited and rather amateur understanding of why altering the balance of intake of fats can influence the shape of the game. http://www.ncbi.nlm.nih.gov/entrez/q...m_uid=11688844 RB http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum 1: Ann Clin Lab Sci. 2001 Oct;31(4):325-48.Click here to read Links Review: molecular pathology of cyclooxygenase-2 in cancer-induced angiogenesis. * Fosslien E. Department of Pathology, College of Medicine, University of Illinois at Chicago, 60612, USA. efosslie@uic.edu Cancer-induced angiogenesis is the result of increased expression of angiogenic factors, or decreased expression of anti-angiogenic factors, or a combination of both events. For instance, in colon cancer, the malignant cells, the stromal fibroblasts, and the endothelial cells all exhibit strong staining for cyclooxygenase-2 (COX-2), the rate-controlling enzyme in prostaglandin (PG) synthesis. In various cancer tissues, vascular endothelial growth factor (VEGF) and transforming growth factor beta (TGF-beta) co-localize with COX-2. Strong COX-2 and VEGF expression is highly correlated with increased tumor microvascular density (MCD); new vessels proliferate in areas of the tumor that express COX-2. Moreover, high MVD is a predictor of poor prognosis in breast and cervical cancers. COX-2 and VEGF expression are elevated in breast and prostate cancer tissues and their cell-lines. In vitro, PGE2 induces VEGE Supernatants of cultured cells from breast, prostate, and squamous cell cancers contain angiogenic proteins such as COX-2 and VEGF that induce in vitro angiogenesis. A selective COX-2 inhibitor, NS-398, restores tumor cell apoptosis, reduces microvascular density, and reduces tumor growth of PC-3 prostate carcinoma cells xenografted into nude mice. The COX-2 produced by a malignant tumor and COX-2 produced by the surrounding host tissue both contribute to new vessel formation, which explains how selective COX-2 inhibition reduces tumor growth where the tumor COX-2 gene has been silenced by methylation. PMID: 11688844 [PubMed - indexed for MEDLINE]