This very informative article seems to be saying the same thing in a more technical and indierct way.
http://edrv.endojournals.org/cgi/content/full/26/3/331
When I saw the straight line graph between CPY19 the gene encoding aromatase and cox a light went on.
Aromatase is the oestrogen percusor.
The article has a good schematic and some interesting thoughts on flavanoids etc as aromatase inhibitors.
And what is COX 1 and 2 made from omega six. Excess six in cell membranes causal to dietary intake must equal greater expression at call out via PGE 2 etc.
RB
ABSTRACT
http://edrv.endojournals.org/cgi/con...ll/26/3/331/F4
B. Aromatase gene expression
Over the past two decades, knowledge of the biochemistry, molecular biology, and regulation of aromatase has increased greatly. The aromatase gene, designated CYP19, encodes the cytochrome P450arom, and this gene is located on chromosome 15q21.1. The coding region is approximately 30 kb in size, and the regulatory region is approximately 93 kb (9, 15). The aromatase gene consists of 10 exons, and its full-length cDNA of 3.4 kb encodes for a protein of 503 amino acids. The aromatase protein is a glycosylated cytochrome P450 protein with a molecular mass of approximately 58,000 Da (16). The regulation of aromatase is complex in various tissues, and several tissue-specific promoter regions have been identified upstream from the CYP19 gene (9, 17, 18)...................
The increased expression of aromatase cytochrome P450arom observed in breast cancer tissues is associated with a switch in the major promoter region used in gene expression, with promoter PII being the predominant promoter used in breast cancer tissues (24). As a result of the use of the alternate promoter, the regulation of estrogen biosynthesis switches from one controlled primarily by glucocorticoids and cytokines to a promoter regulated through cAMP-mediated pathways (24). Prostaglandin E2 (PGE2) increases intracellular cAMP levels and stimulates estrogen biosynthesis (24), whereas other autocrine factors such as IL-1ß do not appear to act via PGE2 (25).
Local production of PGE2 via the cyclooxygenase isozymes (constitutive COX-1 isozyme and inducible COX-2 isozyme) can influence estrogen biosynthesis and estrogen-dependent breast cancer. This biochemical mechanism may explain epidemiological observations of the beneficial effects of nonsteroidal antiinflammatory drugs (NSAIDs) on breast cancer (26, 27, 28, 29). Investigations using human breast cancer patient specimens demonstrated a strong linear correlation between CYP19 expression and the sum of COX-1 and COX-2 expression (30). Gene expression analysis for CYP19, COX-1, and COX-2 were performed in 20 human breast cancer specimens and in five normal control breast tissue samples. A positive correlation was observed between CYP19 expression and the greater extent of breast cancer cellularity (Fig. 4AGo), in agreement with literature reports showing that aromatase levels were higher in tumors than in normal tissue. Furthermore, a positive linear correlation was observed between COX-2 expression breast cancer cellularity in each sample. Linear regression analysis using a bivariate model shows a strong linear association between CYP19 expression and the sum of COX-1 and COX-2 expression (Fig. 4BGo). Similar correlations between CYP19 expression and COX-2 expression in breast cancer patient specimens have been confirmed in other laboratories (31).