Too technical - I know but if I post the fluffy some will say "no evidence".
There have been a significant number of posts looking for potential EGF iinhibitors and hence I post this here with my usual plea in case anybody of influence reads it for Govt trials on omega three and six and BC and other inflamatory diseases by reference to fat stores in tissus which accurately reflect dietary intake.
To the best of my understanding in essence omega three derivative EPA in inhibits epidermal growth factor (EGF) also known as HER 1.
The tissue was not breast tissue but it does add to the argument for trials to look at actions of omega threes and sixes in breast cancer by refernce to genetic arrays, outcomes, and fat content of breast and gluteal tissue.
20:4 Arachnidonic acid is an omega six derivative.
20:5 EPA is an omega three
RB
Abstracts
mitosis (meye-toh-sis)
Division of a single cell into two identical “daughter” cells. Each daughter cell has an identical number of chromosomes as the parent cell. Mitosis begins when the DNA in the parent cell replicates itself; it ends with two cells having the same genes (see genetics). Most cells in the human body, and all single-celled organisms, reproduce through mitosis. (Compare meiosis.)
http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum
1: Prostaglandins Leukot Essent Fatty Acids. 1999 Oct;61(4):225-34. Related Articles, Links
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Regulation of fatty acid biosynthesis as a possible mechanism for the mitoinhibitory effect of fumonisin B1 in primary rat hepatocytes.
Gelderblom WC, Abel S, Smuts CM, Swanevelder S, Snyman SD.
Programme on Mycotoxins and Experimental Carcinogenesis, Tygerberg, South Africa.
The mitoinhibitory effect of fumonisin B1 (FB1) on the mitogenic response of epidermal growth factor (EGF) was investigated in primary hepatocyte cultures with respect to the alterations in the omega6 fatty acid metabolic pathway. Fatty acid analyses of hepatocytes showed that EGF treatment resulted in a significant decrease in the relative levels of 20:4omega6 (arachidonic acid) and an increase in 18:2omega6 (linoleic acid). Supplementation of the hepatocyte cultures with 20:4omega6 in the absence of EGF resulted in an increase in the total omega6 and omega6/omega3 fatty acid ratio. Addition of 20:5omega3 (eicosapentaenoic acid) resulted in an increase of the relative levels of the long chain omega3 fatty acids at the expense of the omega6 fatty acids. When 20:4omega6 and 20:5omega3 was added in the presence of EGF, the mitogenic response of EGF was increased and decreased respectively. When compared to the fatty acid profiles in the absence of EGF, the decreased mitogenic response coincided with a decrease of total omega6 fatty acids and total polyunsaturated fatty acids (PUFA). In addition, the saturated and mono-unsaturated fatty acids increased and the polyunsaturated/saturated (P/S) fatty acid ratio decreased which implied a more rigid membrane structure. Addition of prostaglandin E2 (PGE2) and prostaglandin E1 (PGE1) stimulated and inhibited the mitogenic response respectively. Ibuprofen, a known cyclooxygenase inhibitor, and FB1 inhibited the EGF-induced mitogenic response in a dose-dependent manner. The mitoinhibitory effect of FB1 on the EGF response was counteracted by the addition of PGE2. FB1 also disrupts the omega6 fatty acid metabolic pathway in primary hepatocytes, resulting in the accumulation of C18:2omega6 in phospatidylcholine and triacylglicerol. The disruption of the omega6 fatty acid metabolic pathway and/or prostaglandin synthesis is likely to be an important event in the mitoinhibitory effect of FB1 on growth factor responses.
PMID: 10574646 [PubMed - indexed for MEDLINE]
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