Infection with H. pylori, be it in the gastric mucosa or intracellularly anywhere,...also causes the cox-2 to over-express. Basically, as I see it...if you just take the words gastric mucosa and replace them with breast cancer epithelial cells, you have the same thing going on in a percentage of her-2 mediated breast cancer as you do in stomach cancer...the one cancer that is proven to be caused by a bacterium, H. pylori. I would guess that a fair percentage of her-2 neu bc is caused, at its most basic root, by intracellular h. pylori infection, just as is stomach and other gastric cancers. The her-2 positive cancers most likely to be associated with H. pylori are those that also exhibit c-myc. There is a German article that has already concluded that h. pylori can also cause over-expression of her-2.
I think too many women are dying while we beat around the bush with all the proteomic subtleties of complex cancer bio-chemical cascades.
I think somebody should do a simple study with c-myc her-2 positive folks where intracellular h. pylori infection is taken as a given--as it is NOTORIOUSLY difficult to empirically prove or measure, ask nobel prize winner Dr. Barry Marshall--,
treat them with an antibiotic with a long half -life that disrupts plasmid protein synthesis, like Zithromax, at high enough saturations for long enough time to eradicate the infection, and then, measure response with and with out Herceptin. If the infection is what is causing the her-2 to overexpress in the first place, if you knock out the h. pylori plasmids with the Zithromax, the her-2 levels would return to normal on their own and the herceptin would no longer be required, just as the leptin levels do once the h. pylori infection is eradicated. (Google H. pylori and leptin to read numerous studies to this effect)
Unfortunately, as effective as this trial would be, it would, sadly, present NO CURE, just another control as there is so much h. pylori in our environment now that re-infection is practically inevitable...so the only effective means to something more resembling an actual cure...would be a successful h. pylori vaccine...and fortunately, they are working on one--just not thinking of targeting it to a her-2 breast cancer audience, ...but with each new vaccine, comes another set of problems..so there you go...the proverbial RED QUEEN's race..., but still, it is NOT by chance that the exact same bio-chemicals are turning up in a percentage of her-2 neu breast cancer patients as turn up in cases of gastric cancers and MALT LYMPHOMA. I adhere to a common sense approach to Science...where there is smoke, there is fire. So where you have high levels of her-2, cox-2, leptin, and low levels of glutamate, zinc, ATP, and magnesium, just to name a FEW commonalities...you have intracellular h. pylori infection and most likely certain kinds of her-2 mediated cancer.
You have NO idea, HOW MUCH I WOULD LOVE IT FOR some truly brilliant researcher out there reading this thread to PROVE ME WRONG....smile...but the thing I absolutely don't understand is how all the scientists who have looked at actual samples of her-2 positive breast tumor tissue under microscopes all these years, could not have seen the highly vacuolated cells that accompanied it and why they did not immediately understand what this meant...that is what puzzles me the most...hmmm.
Also, I wonder that if one of the biggest impacts of the omega -3 oils is simply because this type of oil is as equally capable of disrupting plasmid protein synthesis (mechanically gums up the bacterium's ability to reproduce) as do the quinolones and the Zithromax. It is also interesting to note that substances like Venorelbine (Navelbine), mistletoe, noni, aloe vera, and other plants high in alkaloids are also traditionally equally high in quinolones, which essentially are all plasmid protein synthesis inhibitors...what this means is that such substances can prevent certain plasmid carrying organisms, like h. pylori and other bacteria to be incapable of replicating. Once reproduction is halted, the bio-chemical cascade that would normally ensue, inflamation (cox-2), high leptin levels, excessive her-2 would be stopped dead in its tracks. Food for thought.
Best regards,
Gina
"Markedly increased levels of cyclooxygenase-2 (COX-2) mRNA, protein, and prostaglandin E(2) synthesis were detected in HER-2/neu-transformed human mammary epithelial cells (184B5/HER) compared with its nontransformed partner cell line (184B5). HER-2/neu stimulated COX-2 transcription via the Ras --> Raf --> MAPK pathway. The inductive effects of HER-2/neu were mediated, in part, by enhanced binding of AP-1 (c-Jun, c-Fos, and ATF-2) to the cyclic AMP-response element (-59/-53) of the COX-2 promoter. The potential contribution of the transcription factor PEA3 was also investigated. Elevated levels of PEA3 were detected in 184B5/HER cells. A PEA3 site (-75/-72) was identified juxtaposed to the cyclic AMP-response element. HER-2/neu-mediated activation of the COX-2 promoter was blocked by mutagenizing the PEA3 site or overexpressing antisense to PEA3. To determine whether HER-2/neu status was also a determinant of COX-2 expression in vivo, we compared levels of COX-2 protein in HER-2/neu-positive and -negative human breast cancers. Increased amounts of COX-2 were detected in HER-2/neu-positive tumors. Taken together, these results suggest that closely spaced PEA3 and cyclic AMP-response elements are required for HER-2/neu-mediated induction of COX-2 transcription. The clear relationship between HER-2/neu status and COX-2 expression in human breast tumors." Cyclooxygenase-2 is overexpressed in HER-2/neu-positive breast cancer by
Authors:
Subbaramaiah K, Norton L,
Gerald W, Dannenberg AJ.
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