I am HER2NEU positive, ER-. What I am confused about is this. When you are her2neu + is your survial rate lower? It is so confusing. I had five positive lymph nodes, invasive ductal, and had lumpectomy 5cm tumor.
Now I have an infection in my breast, scared and confused.
Hi Happyrock - Her2+ tumors tend to be more aggressive - but the good news is that there is a good treatment in the form of Herceptin - you should ask to enrol on a trial for this, as it is still only prescribed for advanced bc.
BTW - was your Her2 status diagnosed with the IHC test ? I know that this can give false positives.If so, ask to be retested with the more accurate FISH test.
It is all very confusing at first - you will feel better once your treatment protocol has been worked out.
dx bc Oct 2001
tx - mast, chemo(FEC+taxotere), 25 rads.Now on tamoxifen
Her2NEU positive tumors are more aggressive and thus have worse prognosis. These tumors usually respond to a targeted medication called Herceptin (trastuzumab) in addition to other chemotherapy agents.
Leonardo F - Webmaster Cancer Forums
Disclaimer: this information is for informational purposes only. It is not medical advice.
Hi happyrock. I'm also HER2 positive, ER-, PR+, 8cm tumor, 1 node +. I enrolled in a trial and finished all my treatments this past July '04. My chemo was 4x AC, then 12x Taxol & Herceptin (weekly), then 40x Herceptin alone (weekly). If you decide to go this route, the best advice I will give you is to keep your eye on your ejection fraction (score from MUGA scan). I started out low (55) before chemo even began and slowly declined. When I got to 51 I insisted on being referred to a cardiologist, not because that's a dangerously low number, but because if you fall below 50 you are booted out of the trial and can't finish out the Herceptin. The cardiologist put me on two meds, which I had to have approved by the trial folks, and I did fine and was able to get every last drop of Herceptin! So far all is well and I am considered NED (no evidence of disease).
So are you on antibiotics for your infection? Let us know what treatment plan you decide on. Best of luck to you.
In what is seen as a game changing event for the company, TapImmune (OTCBB: TPIV) announced on Monday that it had signed an Exclusive Agreement with the Mayo Foundation for Education & Research, Rochester, MN, to License a proprietary MHC Class I HER2/neu antigen technology.
"It's a new antigen that we've licensed from the Mayo Clinic and it's an antigen that no one recognized before for the HER2/neu receptor," explained Dr. Glynn Wilson, Chairman & CEO at TapImmune, during an exclusive interview with BioMedReports. "The existing products in the market don't go the same pathway and so they're not as effective; and so we think that with our other approaches to HER2/neu, we'll have a real advantage and give us a leading position in development of a vaccine for HER2/neu -- both for therapeutic and hopefully in the future, prophylactic."
After 20 years of HER2/neu vaccine development the scientific team at the firm feels they have a far greater understanding of the target, and indeed of the needs of cancer immunotherapy.
Early on peptide vaccine studies showed that 'killer' T cells could be generated. At around the same time different peptides were shown to generate 'helper' T cells. To date, however, we have not seen a combined approach that provides a naturally processed killer cell target and a collection of broadly reactive HER2/neu derived helper peptides.
With more than 200,000 women in the U.S. being diagnosed with breast cancer each year, 75 percent of whom test positive for the HER2 receptor, but only 25 percent are eligible candidates for Roche-Genentech's breakthrough drug Herceptin, a $5B a year product and some new drug candidates in late stage clinical development, we still don't have a comprehensive approach.
Observers believe that this is where this collaboration between TapImmune and the Mayo Clinic enters and bridges the gap, making what the scientific team at TapImmune believes will be the broadest and most comprehensive HER2/neu breast cancer platform available.
We know now that killer cell targets absent of T cell 'help' offer only short lived responses and do not generate T cell memory. In addition, scientists have figured out that using so called 'universal' T cell helper peptides does not truly deliver the need for 'locally available' helper peptides. These helper T cells need their antigens for stimulation and targeting in the actual tumor, where they need to function.
Without getting too technical it boils down to this. Killers need both naturally processed targets AND they need T cell help. While helper T cells need stimulation as well, and this has to be accomplished in the same microenvironment of the tumor where these functions are being performed. This means that the helper peptides must be natural targets as well, and they have to be found in the same place and time as the killer cells.
Last edited by Didee; 04-27-2012 at 03:25 PM.
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