ER+, HER2+ - time to recurrence?
 

How ER+/PR+ is your friend? I think that also contributes to late recurrence rates as well as initial aggressiveness of the original tumor.

One reason (my opinion only) that highly hormone positive bc recurs later (especially if her2 negative) is that it is not so aggressive and is slow growing. In certain women, their immune systems just don't get rid of the micromets or solitary cells (and tamoxifen or an AI just keep those cells in limbo until they are off the drugs a couple of yrs). Also, one gets older as time marches on and the immune system naturally ages and gets less efficient too.

Being only ER+ and under 70%, more and more research is pointing that my tumor most likely is acting more like a hormone negative one.

I think some questions I asked of your friend's tumor can help point to how diligent she needs to be on continuing anti hormonals or not. I am just thinking out loud here. Sometimes its actually easier to do here than to say these things to your friend.

Sorry I can't help with information for your buddy, but I have the same uncertainty being triple positive also. I was an across-the-board over-achiever with strong +'s for all three markers.

I have found no research that looks specifically at triple positive recurrence rates. I find lots of data comparing er/pr- her2+ with er/pr+ Her2-.

I have always wondered if one of my positives trumps the other, or if triple positive risk of recurrence lay somewhere in the middle of the two formerly mentioned groups.

Since Her2+ is so aggressive, my hunch is recurrences would tend to happen sooner versus later. And since I just hit my three year cancersucksery, I think I am going with that for now.

I am profoundly interested in this topic, as I am one of the "oddballs," with Her2+++, 80% ER+, 50% PR+ bc. I post as many articles on this topic as I can find. It seems the "highly" hormone positive, Her2+++ cases are a small subset of all Her2+++, which are a small subset of Her2+++ in general. As such, there is not much study that reflects how we will respond to treatments that address either predominantly ER+ patients OR predominantly Her2+ patients. I posted recently a correspondence between medical authorities trying to categorize tumors based on ER and Her2:

http://her2support.org/vbulletin/sho...eferrerid=1173. One of the authors suggests that ER+ Her2+ tumors are actually hybrid tumors, that are either part "luminal A" (usually ER+/Her2- with a good prognosis) or part "luminal B" (which are generally ER+/Her2- tumors with a high proliferation gene signature, a poorer prognosis than luminal A) AND part Her2+ tumor. Unfortuately, being able to categorize the tumor like that gives absolutely no information on how to treat it or how it will behave.

For ER+ tumors in general, the findings of the Early Breast Cancer Trialists' Collaborative Group at http://www.ctc.usyd.edu.au/cochrane/...BCTCGpaper.pdf state, in pertinent part:

"Extrapolation of the 15 year results for the untreated women in the Tamoxifen trials suggests that even if they had received a treatment that persistently halved their annual breast cancer mortality rate, at least a sixth of those with node-negative disease and a third of those with node positive disease would still eventually die from breast cancer during the first, second or third decade after diagnosis (in the absence of other causes of death during those decades.)"

So, while ER+ bc is seen as "more favorable" by diagnosticians than ER- bc, that seems to be a short-term way of looking at it - the risks of relapse from ER+ bc remains higher than that for ER- bc many years after dx.

Which brings us back to the original quesiton, one I asked my onc: Would ER+/PR+ Her2+ bc be more likely to recur earlier or later? He thought earlier, but I cannot imagine there are enough patients in the data base on which to base that conclusion - I think he, like everyone else, is too freaked out by the Her2+ component of the bc to really consider how the various histiological components might work together here.

My personal opinion is that triple positives carry the same long term risks as ER+/PR+ Her2- patients do, because I don't see a way to rationalize away the conclusions I quoted above from the EBCTCG just because the tumor is also Her2+. But, again, I don't know.

Thanks for raising this discussion. I look forward to other comments.

Hopeful

Oh, gosh. Now, I am freaked out. I never thought of my being ER+ as a potentially "bad" thing. I know that I am younger, and thus have many more years for estrogen to pump through my body. I mean, I thought that since I have a "targeted" treatment it was better. Should I be worried that just when I get to the point where I am not worrying each and every hour that it will come back (after coming off Tamoxifen for good), that it will?

I have asked my ONC. at least five times if Tamoxifen "kills" it, or just keeps it at bay. I don't think he has ever given me a complete answer. Anyone? Or has that been answered up above?!?

I had to go off Tamoxifen last week, but only for two weeks. I have been having horrible joint pain and am being treated for two bulging discs. I wanted to see how much Tamoxifen was contributing to my pain, since everything started around the time I started Tamoxifen. Now, I am worried about the two weeks off. :(

Take care,

Krista,

The "good" thing about the conclusion I posted above is that more doctors and scientists are focusing on ER+ patients, and conducting tests on durations of treatment, switching between agents, etc. I am sorry that the rather stark language I quoted reads so alarmingly. I think it was intended as a challenge to researchers to try to determine which paitients require, and will respond, to extended endocrine therapy, and different types of therapy. A totally unexpected finding, reported on the Board about a month ago, was a result of giving women zolendraic acid with their endocrine therapy. Here is a link to an interview with Michael Grant from the latest issue of Breast Cancer Update with very encouraging news http://www.breastcancerupdate.com/me...08/4/gnant.asp

a portion of which is quoted below:

DR LOVE: Can you discuss the dosing schedule and results of zoledronic acid in ABCSG-12?

http://www.breastcancerupdate.com/me...llowTransp.gif DR GNANT: We administered four milligrams of zoledronic acid every six months, for a total of seven infusions over three years. Initially, we started the trial with a higher dose of eight milligrams monthly, but we were forced to change due to safety concerns. In 2000, reports surfaced that renal safety was endangered in some patients with multiple myeloma who were being treated with zoledronic acid, and at that point all the trials around the world reduced the dose to four milligrams.

We went back to what we believed would be mostly a bone-protection dose. Therefore, it’s particularly striking that we are not only protecting bone at this dose but that we are also keeping the cancer at bay (Gnant 2008; [1.3]).

Two more observations are also exciting. One is the magnitude of the effect: A 36 percent improvement in disease-free survival, translating to at least a non-significant trend toward better overall survival. That’s an accomplishment usually observed with interventions such as taxane chemotherapy. We observed that efficacy with an acceptable side-effect profile (1.4).
More importantly, we’re not only preventing bone metastases, but we’re also seeing benefit in various event subcategories, including locoregional recurrence, contralateral breast cancer and distant metastasis outside of the bone (such as liver or lung disease). That’s something most of us did not expect.

So, there is promise and hope - we just need to keep on top of our own treatments.

Hopeful

I am er, pr negative. I did not receive Herceptin in 98 and it took me 6 years to recur. I thought I was out of the woods. One can never really know the future. Try to be as healthy as possible and enjoy your break from cancer, hopefully for your life.
Hope you stay well,
Barbara H.

rephrasing the question
 

My former onc (I MISS HIM) was very forward thinking and stayed on top of HER2 research. He started me on Zometa as soon as possible because he was aware of the studies possibly indicating the benefit in terms of recurrance (this was in 06), then kept me on Lupron because of emerging info about the same benefit. In terms of AI's, he felt that by the time I had been on one for 5 years, indications would be that they should be continued indefinately.

We tried to extrapolate the numbers of triple positives in the bc population and he felt that around 5 to 8% of all BC would be triple positive.

I have also been interested in any info concerning triple positives, but have not found many others in this same subset.

Considering the small percentage of triple positives and the small number of early stage who received Herceptin during the trials, I doubt there are very many in this seven+ year category.

Also, prior to the release of the trial, most people were not tested for HER2 until metastisized, so would it not be most likely that those who were triple positive that did not recurr would not have known they were HER2+?

Does this make sense?

I don't know if this will help at all Debbie, but I am also triple positive - ER+90%, PR+50% - I was node negative. I am approaching my 2 year date of diagnosis, my 2 year cancerversary will be Dec. 18th.
Very interesting discussion. My onc.sent my tumour out for testing 3 times as the first one was inconclusive, the FISH ones were highly Her2+. He still shakes his head when he sees me, because of this very small percentage of the Her2+ population that is triple+, never mind our very small subset group in the general BC population. On top of that, my tumour was also mucinous - another very small subset (like 2%) characteristic (a favourable one, more slow growing). This mucinous aspect probably had a great deal with my tumour being a grade 2.

I am hoping that being triple+ will bode well for very, very low recurrence rates - I guess only time will tell, as we get further "out".

all the best
caya

Neither my breast surgeon nor my oncologist have ever given me statistics on my disease, and I haven't asked for them. However, I did ask my breast surgeon at my appointment 3 weeks ago when recurrences would most likely happen. She said that about 75% will occur within the first 2 years, and the other 25% could be any time out. So no, unfortunately, we can never really let our guard down.

arggg - can't find it
 

Debbie,

Being Her2+ and marginally ER+ (10% or less of cells staining) is not unusual. Being Her2+ and highly ER+ (80% or better) is. It is the highly triple positives that comprise that 5% of all bc stat Sassy quotes.

Hopeful

Hopeful said: Being Her2+ and marginally ER+ (10% or less of cells staining) is not unusual. Being Her2+ and highly ER+ (80% or better) is. It is the highly triple positives that comprise that 5% of all bc stat Sassy quotes.

That brings up issues. What IS negative ERPR? Lots of different answers to that question depending upon lab or provider. Research abstracts usually don't say what cut-off they used in assigning their subsets, although if you can get your hands on full text it's usually mentioned. Plus, there's the issue of unreliable assays, which I think is a larger issue than is thought, in non-central labs. (the EBCTCG overview that you posted, for example, used a cut-off of 10fmol of protein/mg of cytosol protein, or any evidence of immunohistochemical evidence of receptor protein" - how does that correlate with an Allred score, or a community lab report of "10%"? Lots of apples and oranges).

What about the research that seemed to suggest that Herceptin may make HER2+/ERPR+ disease more susceptible to hormone treatment?

Also, they were testing routinely for HER2 in 2001, even in my podunk community hospital. That was well before the release of the adjuvant trials data.

Sassy said: Also, prior to the release of the trial, most people were not tested for HER2 until metastisized, so would it not be most likely that those who were triple positive that did not recurr would not have known they were HER2+?
Does this make sense?

Yes, perfect sense. But I was not asking for those who have not recurred. I wanted to hear from ERPR/HER2+'s who did recur, more than 7 years out from diagnosis. Even if they didn't know their HER2 status at diagnosis, if they biopsied the mets, the HER2 status would be known (although a few do change from HER2- to +).

I have so many questions and thoughts on this topic that it's making my brain hurt.

Hopeful said: So, while ER+ bc is seen as "more favorable" by diagnosticians than ER- bc, that seems to be a short-term way of looking at it - the risks of relapse from ER+ bc remains higher than that for ER- bc many years after dx.

But even over the long term, there will be more recurrences in ER- cancers. Overall. Or there were, before Herceptin (there's that pesky issue again, of stats by definition being at least partly irrelevant to someone diagnosed at the time that the stats are released). When we start to try and break into smaller subsets, it gets hazier, especially, as you say, for the ERPR+/HER2+. But there should be some good subset data coming out of the adjuvant Herceptin trials on these details that we want.

Nothing's black and white, to put it mildly. I listened to more podcasts on my drive to/from work today, and several times it was mentioned that a fair amount of breast cancer overlaps categories, even in the huge gene array categories, like the other article that you noted, hopeful.

It's encouraging how much more we understand each year, but on the other hand, the incredible complexity becomes more apparent with each new understanding.

And OT to this - do people on this forum look at Adjuvant!? In one of the podcasts, they said that it will soon include HER2. This was in a discussion of whether Adjuvant! is as good as OncotypeDX, and the point made (Slamon, I think) was that when Peter Ravdin adds HER2 to the mix, it will be (as good). (and then he said "and it's free").

Great discussion,
Debbie Laxague

Here is a data pool of over 61,000 women with the different subsets broken down:

http://www.asco.org/ASCO/Abstracts+%...stractID=40116

triple positives accounted for just over 11% of all primary invasive breast cancers

5 year survival was much closer in % to er+pr+her2- than er-pr-her2+ (but data from 99-04)

This is a great discussion.

Debbie, I'm not sure about the widespread routine testing for HER2 prior to the study release. I was DX Feb 2005 and was not tested. It was not being done at my hospital (podunk also). It was not until I had gone to a larger research facility; heard about Herceptin on the news; pointed out that I had not been tested for this, that I was tested and, sure enough, I was HER2+.

I was mistakenly thinking of those who had not recurred, rather than those who had.

Wouldn't it be nice to discover that you are not hearing from anyone who recurred 7+ years out because they haven't recurred?!

Margerie,

Thanks for digging up that abstract; I have it in my files but could not locate it easily.

Debbie,

Here is an abstract to an interesting article (which is only available in full for a fee) concerning the eitiology of triple positive bc: http://www.ncbi.nlm.nih.gov/pubmed/1...?dopt=Abstract

Basically, it says the older you get, the more likely you are to be ER+/PR+ and the less likely you are to be Her2+, however, they found that triple positive women were dx at a younger age than women with any other ER/PR Her2 phenotype, at a median age of 52.4 years.

They say (and I must add, these are Belgian researchers writing a paper in English, which is not their first language):

"The proportion of breast cancers beint ER+Her2+ is low, representing only 6.2% of all breast cancers in our series. . . Although our findings are hypthesis generating and awaiting to be confirmed, the reason why the small group of ER+PR+Her2+ lesions appear early in life is as yet unclear. However, our findings incorporate some of the interesting biology of Her2+ breast cancers and may shed light on the carcinogenic mechanisms for early-onset of ER+Her2+ brease cancers as opposed to ER+ Her2- cases. We suggest that high estrogen levels in young women drive ER to predominantly regulate classic ER regulated genes such as PR expression independent of Her2 whereas in postmenopausal women, low estrogen levels may allow an increasing effect of growth factor signalling on ER action resulting in a different set of ER regulated genes being expressed with a lower likelihood for PR expression. Otherwise said, at young age, Her2+ breast cancers are more likely ER+ through the presence of elevated estrogen levels whereas with aging and decreasing estrogen levels, the growth of Her2+ breast cancers is less dependent of estrogens. This is also reflected in the younger age onset of PR+ compared with PR- lesions which is mainly due to the PR+ Her2+ subgroup. The biology behind this suggests that premenopausal steriods select ER+ breast cancers to appear earlier if they are PR+Her2+ than if they are PR-Her2-, PR-Her2+ or PR+ Her2-. . . . It is well known that hormonal risk factors are different by the ER expression of breast cancer, but the drive or risk factors behind the earlier appearance of ER+Her2+ cases compared with other tumour types remains to be explored."


In my reading, it also appears that two principles are emerging: tamoxifen upregulates Her2, while herceptin upregulates ER. I think the key to long survival for triple positives is extended therapy which maintains a balance in the tension between these two opposing bc pathways. Again, I am not any type of medical professional, just what I consider to be a well read patient, and these are my opinions and no more than that.

Hopeful

ER/PR + & Her2 +
 

I remember seeing a graph, a couple of years ago, that showed exactly what we are talking about.

I only remember that triple positive patients seem to do well at first, but unlike er/pr negs, the recurrences keep coming for a long time. So although they initially seem to do better, in the long run they are doing the same or even worse that er/pr negs.

Perhaps that's why my doc is leaning towards continuing AI's after 5 years?

I will try to find it later. For now I need some sleep. I spent a night at the hospital after having gone to the ER with severe stomach cramps & almost fainting. They thought it might be mets, but it turned out to be a false alarm. Its probably some pesky virus that's going round. But they didn't want to take any chances with me, so they had a look at all my internal organs. They looked wonderfully healthy. But it was a noisy night, because of a disoriented patient in the next room and I need to catch up on my sleep.

Love

Lien

Kristina, Hi just a quick note I had to prove I needed to get off Tamoxifin after three years. I was told this by a Dr at an ASCO meeting.. it took me a year to prove I was still producing hormone to get a Dr to do surgery to remove my ovaries. I than went to Aromasin which I was told was a safer med for me. I chose Aromasin from reading about side effects of all the AI's ... has you Dr not offered you any of these? going between the three AI 's might find you one that you can take with less side effects. for me it was a good choice. Are you still producing estrogen or are you post menapausal?
marily

I remember there was a discussion about how tamoxifen could interfere with Herceptin. I wondered if the recurrence of PR+ER+Her+ breast cancer has anything to do with it. Because if one can not have Tamoxifen while on Herceptin, then the ER+ part of the cancer may well be flourishing while Herceptin is stopping the Her2+ part.

Both time of my treatment I did not start Tamoxifen until finishing the Herceptin treatment (whether voluntarily or involuntarily). And I am thinking that the reason why the triples may have more problems might be because the medicines (Herceptin and Tamoxifen) can not be used simultaneously.

I have to think Ms. Budin (suddenly just can't think of her first name - Andrea?) must be ER- because she'd had more than 9 years Herceptin.

hi Debbie and everyone--
When a recurrence happens, the pathology isn't necessarily the same as the pathology we receive at the initial diagnosis. My onc and I had quite an interesting discussion about this a couple months ago when we were discussing my decision to go off Herceptin.

For example, I was Her2+++ and ER-/PR- (I don't recall the percentages negative, but that doesn't matter for purposes of this discussion). But suppose that I was 80% negative for each. That means that there were around 20% non-negative ER and PR cells in that primary tumor. So if I ever have mets down the road, the pathology may not necessarily be ER/PR negative. It depends on what cells migrated and then eventually turned into mets--if some of the minority ER/PR+ cells "got away," then the mets could display that pathology. It's also possible that the Her2 status of the mets could be different than the primary tumor.

What I find even more interesting is that the new primary case I had this year was ER+/PR- and since it was stage zero they didn't test for Her2. So I have now had cells with two distinct pathologies.

Not sure if this helps the discussion...probably clouds the issue a bit. The odds are that if someone is really strong ER/PR either way, that it will be that much more likely that the mets will match the primary. And the time to mets varies quite a bit. But the bottom line is that we can guess at the odds all day long, but each case will be different because we can't predict on what side of the odds a specific individual will end up.

That's enough of the geeky stats chat tonight :-) I'll be interested to hear what y'all have to say about this concept...I haven't seen this discussed on this board before (although I will admit my absence has been obvious the past year or so--sorry about that!!)

Val

I am not quite sure I understand this, but I thought I would post it for everyone to see. It seems to me that pathway could change, cell nature could change, everything could change...

J Mol Endocrinol. 2008 Sep 3. [Epub ahead of print</SPAN>
Improvement of Sensitivity to Tamoxifen in ER-Positive and Herceptin-Resistant Breast Cancer Cells.
B Chen, Department of Surgical Research, Beckman Research Institute of City of Hope, Duarte, United States.

Her2 overexpression in ER-positive breast cancer cells such as BT474 (BT) cells has been found to confer resistance to tamoxifen, and suppression of Her2 improves the antiproliferative effects of tamoxifen. In this study, the responsiveness to tamoxifen in BT/HerR, Herceptin-resistant BT cell lines established through constant Herceptin exposure, was evaluated. Compared with BT cells, improvement of sensitivity to tamoxifen in BT/HerR was demonstrated by ER functional analysis and cell proliferation assay. Tamoxifen in the resistant cell line was found to inhibit E2-stimulating estrogen-responsive gene pS2 expression more effectively than in BT cells in real time PCR assay. Western analysis showed cross-phosphorylation between ER and downstream components of Her2 was attenuated in BT/HerR cells. ER redistribution from cytoplasm to nucleus could be found in these cells through immunofluorescence and confocal studies and importantly, chromatin immunoprecipitation (ChIP) studies demonstrated that tamoxifen induced occupancy of the pS2 promoter by ER and nuclear receptor corepressor NCoR instead of coactivator AIB1 in these cells. Finally, combination of tamoxifen and Herceptin was found to improve the sensitivity of BT/HerR cells to Herceptin. Our results suggest that the ER genomic pathway in the ER-positive and Herceptin-resistant breast cancer cells may be reactivated, allowing tamoxifen therapy to be effective again, and a combination of tamoxifen and Herceptin can be a potential therapeutic strategy for ER-positive and Herceptin-resistant human breast cancer.
PMID: 18768663 [PubMed - as supplied by publisher]

Tamoxifen itself is a big issue for Her2+ ER+ bc, in that it has been shown in some studies to be stimulatory for this type of breast cancer. Combining Herceptin with Tamoxifen seems to ameliorate this effect, however, the duration of Herceptin treatment is one year and the duration of tamoxifen treatment is 5 years. THAT, IMO, is an issue.

Hopeful

As you can see by my stats, I was ER+, Her2+, PR+. I was told that invasive lobular BC is rarely Her2+. Proving that BC is not predictable (my thoughts!). My onc. said that "at least for me, having a drug to address the ER+ was a good thing" and in further discussion she meant that ER- has no tool to fight it. And she intends to keep me on Arimidex for more than 5 years. This is a very interesting thread!!!

I just marked 8 years on October 4. Diagnosed at age 41 with Stage 1, Grade 3 IDC. ER+(90%), PR+(80%), Her2+++. I was treated with lumpectomy, 4 A/C, 35 RADS, 3 1/2 years of Tamoxifen, and 3 years of Arimidex after my hysterectomy and oophorectomy in 2004. NO Herceptin for Stage 1 back then and NO Taxol for node negative either. So far, NED.
Recurrence crosses my mind since from what I've heard, most recurrences are within 2 years after completing treatment and, technically, I just completed treatment 11 months ago.
I have had 2 episodes of severe visual disturbances in the last 3 months; of course, everyone knows what the first thing that crossed my mind was; but, my PCP thinks it may just be something called ocular migraine but just to be sure he did order a brain MRI scheduled this Wednesday.
I will watch this discussion with much interest.
Gloria

This is a very interesting discussion and although I can't add to it I just want to thank you ladies who have posted such great info. I'm highly triple positive, I read early on tamox may interfere with herceptin and so had an ooph and began arimidex. So far so good as far as recurrance is concerned, despite the side effects.!
Thanks for great info and a great thread

This is a great discussion because my tumor was ER+(5%), PR+(2%) and HER2+++. I am young (dx age 34 should have been 33, but we won't go there). I have seen a few of you with my similar dx's and I too worry about Tamoxifen/Herceptin. I feel like there are so many opinions and different options that we all have taken, but the end result is we were diagnosed with BC and we all just want some answers about reoccurrence. My onc (and the others on her team) say no scans needed, but I have a very difficult time with this. How can anyone possibly same I am NED if they don't do any scans and see what's in there? I saw what happened with my mother (passed away on 6/17/08 of leptomeningeal brain cancer) and I know I am different because I am "early stage", but it just blows my mind. The only test I am having is a mammo in January on my left breast. Can anyone answer when I am considered NED? Is it immediately after chemo or after my herceptin tx? I haven't started Tamoxifen yet, I have the prescription, but just haven't filled it yet. I am doing the mail order thing, but I just can't send it in. Why??? I know I need to, but I am completely slacking. Thanks for listening.

second path opinion?
 

And I thought I was the only person that had happened to! I even had my original biopsy redone at Vanderbilt in late 2004 when the pathology showed as being so rare (according to that asco site earlier, only .6% of all cancers) and it came back the same. I had it re-tested (original tumor, not core biopsy) at KU Med and it came back as negative on both, and they retested it twice. Three years of hormonal therapy for nothing.

Get retested :) .

Sorry, probably getting OT. My gut is that triple positives overall will have a slower time to recurrance than her2-/er&pr+, but faster than hormone positive only, but I don't have any data to back that up wtih.

Herceptin/ Positive and Negative Hormone
 

Dear Friends:

When one first get tested you might be Hormone Receptor Positive, when and if you have a recurrence-after 5, 10, 20 years; your hormone receptors might be Negative.

I was dx in 1994, no Her2 test was available, but we knew I was Hormone Receptor Positive. Almost 91/2 years later I had a recurrence, I now am E,P,HR Negative..

Yes, my cancer- all cancers mutate.

Try not to spend a lot of time thinking about your cancer, be grateful for the now, you all are cancer-free. Enjoy Life.

Her2 status
 

Your signature indicates that you are Her2+++. I understand that once you test Her2+, your status is unlikely to change. Is it possible I misunderstood your signature?.

Just wanted to help...

Change in status vs. error in assay
 

Hi Debbie,

I know I'm in a VERY low category. But it is true. I had my surgery done in Manchester, NH an incredible surgeon (Dr. Ned Dalton) performed it. The original path came back ER+5% and the PR was neg, HER2+++. My story is complicated a bit, so I'll try and keep it short. My mother in 2004 was dx ER/PR+, Her2+, but did everything in Manchester,NH. In April '07, she was dx with a brain tumor, had a crainiotomy, 2 tx of SRS, and then on 8/10/07, it had turned into Leptomeningeal cancer. After 14 days of WBR, she went home and then in October, it had gone to her spine. She was down between BWH/DFCI and a rehab from 10/23/07 until this past February '08. Her oncologist (who I never mentioned about my "bloody nipple discharge" that I experienced in Nov '07) couldn't believe that I had just been dx'd and my mother was ultimately dying of met breast to the brain. Anyhoo, after getting a 2nd opinion at the DFCI for my surgery, I chose to stick with Dr. Dalton (same person my mother went to) because it was the exact same opinion. Ok, so now I have my mastectomy, in recovery, get my path report, call my mom's onc (Dr. Nancy Lin) and I wasn't about to stay up here to do all my tx's, so I sent all my path slides, reports etc to her. She too was a little perplexed about my results, so she had her top 3 THREE doctors take a look at it. The results (shown below) are pretty accurate in my opinion. Especially because the ER didn't change and the PR did to +. So where the heck does that put me??? In a very low category (she said approximately 8-10% of the women are dx with this low of a ER/PR). Dr. Lin also thought maybe I wasn't HER2+ because of the ER/PR results. Life is just very bizzare and you just don't know where it will take you. I am very optimistic because of the tx I have had, however I'm just looking for some advice on the scans (I saw a previous thread talking about this same subject). We are not a statistic, each of us are INDIVIDUALS. I have a very strong opinion about that one. I certainly don't sit here every day and wonder "will I reoccur", but I do wonder why I can't just get some kind of baseline for "peace of mind". I think for me, I just got done chemo, so I'm in that limbo where do I belong, what happens from here etc, etc. I'm sure ALL of you can relate to my questions and curiosity. Thanks for your support and assistance with this one.

Back to Sarah's real question
 

Hi Debbie,

Just wanted to say I love the quote you include in your signature. That sums it all up in my opinion.

That's all....Just wanted to say that.

Mary Jo

wow, Mary Jo, you made it thru to the end of that?
 

Thank you Debbie for the information as well as your opinion. I know I will do the right thing if I need to or when the time is right.