Me Too!!
 

Hi I'm also Triple Positive and would'nt consider it rare at all.

I would be very interested in knowing how the PR receptor figured into all this. I read Dr. Lee's book (can't recall the name) a few years ago. He felt that the PR receptor played just as much of a role, if not a greater one than the ER receptor. However, my PR receptor status was not tested or not listed -- although am not sure why. When I asked I was given the explanation--there was no need since there was no treatment directed towards it--either way. In retrospect, I am wondering if they did know and whatever it was indicated that Tamoxifen would be less effective but they wanted to go ahead and offer me Tamoxifen, which they did.
However, by the time I was ready to start hormonal treatment, I/we (husband and I) had read enough that made me a bit uneasy about Tamoxifen. It was my husband, who has his PhD in biological chemistry and previously did cancer research, who suggested to my onc that perhaps the failure rate of Herceptin (which was around 30%) was being seen in those who were also Her2+ My onc thought that was an interesting possibility which later, according to research findings, turned out to be the case.
Because of that possibility (before it was known), I refused Tamoxifen. It turned out that that was the only way I could get an aromatase inhibitor. I was then offered Arimidex. I asked for Femara but my luck didn't go that far--would only approve Arimidex. That was 5+ years ago.
As far as being 'rare' -- it wasn't only being Her2+ and ER+ that was rare for me. I also had a rare presentation of IBC (in nipple only) and main type (or at least what was found in area biopsied) turned out to be not only lobular (which 12 to15% have) but a rare variant of that--pleomorphic invasive lobular which, if I recall correctly, only 5% have (although instead of 5% that may have been 1 to 2% asa well). Whatever--most of what I had going on was rare--which, I guess, was a good thing because on that basis (or at least that was what he wrote as a rationale) allowed me to get Herceptin out-of-protocol.
I was stage II at the time--however, even that is somewhat debatable--may have been stage IV from the start--depending on who (oncologist or cancer facility) evaluates. (Path report from biopsy said stage II. After mastectomy they wrote stage IIb. However, in addition to having advanced bc that path report stated I had a separate tumor in nipple w/dermal lymphatics which he said meant I had IBC. I then asked, that if I had IBC isn't that more advanced than stage II? He then changed my charts to read stage III. Another 2nd opinion dr told me that what they listed as staging was not what was important--it was the treatment that was important. In retrospect--made us wonder, if perhaps, I was stage IV from the start, not only because of ALL (in addition I also had high grade dcis with extensive comedo necrosis and the nipple also had 'Pagetian' spreadO,I had going on, but because tumor markers were elevated as well. The early scans found many enlarged retroperitoneal/aortocaval nodes (largest being 2.5 cm, lengthwise--never biopsied) and a lesion in the liver (never biopsied). There were also remaining axillary lymph enlarged nodes matted together, according to scan report. (Path report stated only 12 were removed; 9 of those were positive).
So, reading 'between the lines' it sure seemed like I had more than stage II or III...I guess at this point that isn't as relevant since I am still around to write about it...

Re: Rare? Her2+, ER+, PR+
 

Just thought I'd bump this thread as there has been discussion recently about triple pos.
Jenny

Re: Rare? Her2+, ER+, PR+
 

My mom was diagnosed triple positive too, 3 1/2 years ago. It's not rare, about 20 % of all breast tumors are triple positive. There are 4 subtypes according the ER, Pr and Her2 receptors. I found this article

http://ww5.komen.org/BreastCancer/Su...astCancer.html

it explains well the four subtypes. The progonosis of triple positve breast cancer is poorer than Hr pos and Her2 neg, but is better compared to the other two subtypes. The ER+ receptor are a good thing because it counterbalances the Her2 neu pos receptor. At one of our first visit the onco said this type of tumor though very aggressive (it grows faster than the other types) tend to respond well to treatments, and there are plenty of treaments. Endocrine therapy, Targeted therapy, and as a last resort Chemiotherapy. The downside, as said before, is the fact that this type of tumor has a high ki67 score, which means that the cells grow faster, thus the cancer must always be under greater check in order to change therapy as soon as possible when the prior one fails.

Re: Rare? Her2+, ER+, PR+
 

kykeon22,

I think you should reread that article. The four subtypes of BC are listed in order of better prognosis -

Luminal A (ER+ and or PR+, Her 2 -)
Luminal B (ER + and or PR+/ Her 2 +)
Triple Negative
Her 2neu+ ( ER/PR - Her 2 +)

Triple + is not 20% of all BC - from what I understand, it is about 10% of the 25% of the Her2+ BC - thereby making us a very small subsect. The article even says 6 - 19%.

And for most of us triple+s, chemotherapy was not a "last resort" - it was an intregal part of our treatment.

I'm sure some of our statistic brainiacs with better math skills than I can chime in here.

all the best
caya

Re: Rare? Her2+, ER+, PR+
 

I usually estimate that 55-60% of breast cancer is ER+her2-
10-13% or so is her2+ER-
9-12% or so is triple +
15-22% is triple negative

This is not exact as they usually estimate that about 66% of bc is ER+, 34% ER- But then, ER testing is not that exact either and her2 testing when not done in central laboratories can vary as well (although it is getting better)

So these are ballpark figures

They are based on IHC(immunohistochemistry using stains and monoclonal antibodies on slides of formalin preserved tissues), not molecular subtypes, which are based on gene arrays(best done on fresh frozen tissues)

By the way, a high Ki67 is not unique for triple positive-- it is characteristic for her2+er- and basal type triple negatives as well. It is just what may differentiate it from ER+ her2- (although those can also have a high Ki67 and be categorized as luminal B)

Hope this helps!

It is hard to correlate them with subtypes ie, Luminal A, Luminal B, her2 and basal subtypes as large proportion of triple negatives are not basal, a smallish percent of ER+her2-s are Luminal B--they have a high Ki67 but not because of amplification of her2 or its signalling pathway , and not all triple positives really fit into the Luminal B category.

There still is a lot to learn it seems

Six and seven years ago a lot of papers said triple positive bc was rare--that has been disproved. Was the second opinion doctor at a major cancer center or an oncologist who treated only/mainly breast cancer?

There is a lot of literature to keep up on regarding her2+ breast cancer-- it is a relatively quickly evolving field.