EGFR article question

[Cheryl]

I was reading the article that Rhonda4 posted under clinical trials about EGFR expression and relationship of ER+/PR-. My tumor was 75%ER+, but only 4% PR+. Does any amount of positive mean "not negative" or is this very low percentage an "almost negative". Thanks for any insight.
Cheryl

[Cheryl]

Sorry, thought of a couple more questions about this if anyone can help.
First, if this equation causes resistance to Tamoxifen, does it do the same with AI's? Secondly, how does Herceptin factor in here in affecting this delima? And finally, does anyone know the criteria for the patients studied here? Any stage?
Thanks

[Rhonda4]

Cheryl,

I looked up the email address for the senior author of the article. I would email him. Hope this helps.

relledge@breastcenter.tmc.edu

Rhonda

[al from canada]

Cheryl,
The "resistance" to TAM is resulting from "cross-talk" between the ER and EGFR. That resistance apparently doesn't happen with A.I.'s. As well, lapatinib has an ability to reverse TAM resistance.
Regards,
Al

[al from canada]

Cheryl,
Here is a great article on that topic:
http://annonc.oxfordjournals.org/cgi/content/full/14/12/1697

Al

[Becky]

Al

This was an excellent article Thank you for posting it.

Becky

[Gina]

Wow, Al, what a GREAT article!! I had not seen it --as before I got on this site, I was mainly focusing on ER- PR- Her2+++, as it is usually rather aggressive. I don't know if it helps matters any or just further muddies the water, but in actual experience, I have seen that estrogen has an inverse relationship to the her-2, at least in the blood. For instance, for pre-menopausal women who still have their periods..., if you are tracking the serum her-2 along with their estrogen levels..you can see that as long as the estrogen is in normal range, it seems to contain the her-2 or keep it in check some how. However, on the week before a woman's period, a time when estrogen tends to dive, serum her-2 tends to increase and in the presence of known disease, may sometimes actually SPIKE. This correlates with anecdotal evidence from some ER- PR- Her3+++ folks who noted that their tumors seemed to grow faster the week before their cycle and may explain how some of these tumors literally seem to pop up over night as they may experience periods of rapid growth during the times in the cycle (period and ovulation) when estrogen levels drop. This also correlates to studies that recommend various scheduling of surgery strategies, keeping the patient's cycle in mind. In my case, as all my tumors/mets so far have been hormonal negative, keeping my normal estrogen levels by still having my ovaries and my periods has seemed to help me keep the her-2 better controlled, but that is just anecdotal. In the case of a person who is ER positive AND her-2 +++, I really don't have a clue how you walk the tight rope between pushing down the estrogen which tends to increase the her-2 which then, I guess, has to be continuously suppressed with the Herceptin and hopefully, eventually ... other things, such as perhaps oleic acid or whatever any body out there can come up with. Keep these fascinating and data-rich articles coming!! Many THANKS!! Gina

[AlaskaAngel]

Al and All,

The puzzle about what to do for those who are both HER2+++ and ER+ is why I believe that the cutoff at "x" months/year for access to Herceptin by those who already completed chemo and who are both HER2+++ and ER+ is not very intelligent.

It also has never made sense to me that the focus has been on one's ER status with so little comment on their PR status.

AlaskaAngel (HER2+++, ER+, PR+)

[Becky]

Everything I have read about hormonal status focuses on ER and blocking that. This is mostly because ER positive does drive cells to proliferate and divide uncontrollably. PR positive status and only PR positive status tells researchers and doctors nothing.

What I mean by this is that research shows that progesterone will cause a cell or a cancer cell to grow (the individual cell itself) but progesterone can't, by itself, cause uncontrolled division. Therefore, if one was truly only PR+, theoretically, you could not have breast cancer. So, if you are PR+ but ER- and HER 2 neg, something else is causing your cancer to grow and divide uncontrollably (very much like being in the triple negative category in which you could be HER 1 or Her 4 positive or something positive that has not been discovered yet). But PR positive by itself doesn't do it because the cells aren't "thown over the edge".

I am on my second onco (and this one is a keeper) but I have 2 second opinion oncos I go to (probably because my first onco was a waste case) but one of these 4 docs told me that Tamoxifen helped block PR pos receptors as well and that it is excellent to be PR positive. The bad part of being ER neg is what is driving the cancer. For us Her 2 gals, we at least know what the demon is and at least have Herceptin.

Have a nice weekend

Becky