I don't understand the a hormone receptor tests
I am ER/PR positive and HER2 negative. I was told that was a good thing. After reading more it says that the positive receptors help the cancer cells grow. So how is that a good thing? Does the % of the receptors make a difference? I'm just really confused about this.
Thanks for any help. This is all so new to me I'm just a little overwhelmed and don't know the right questions to ask.
Comments
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Hi honey, I was the same thing. I will not be of any help to your question. I still do not understand it. However, You did come too the right place for answers. I just want to say sorry for your diagnosis. Remember this, to keep Positive, Strong and keep your Faith. Were here for you. Bye now.
Kaloni
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The ER/PR positivity is good because there are treatments for it. I think of it this way, it indicates that our particular cancer cells need estrogen to grow, we are offered medication that will either block the estrogen from getting to the cancer cells (tamoxifen) or stop our estrogen production (aromatase inhibitors). the ER/PR positivity is a WEAKNESS which can be exploited. The medications are daily pills. I am not sure if there is much significance about the percentages. I know mine was 100% ER+ and 50% PR+ and I felt that made it more important to take the meds. I would think the pros/cons of taking the meds becomes questionable when the ER% is in the single digits.
HER2 is also a characteristic of some breast cancer cells for which there is a treatment, herceptin - which is administered by infusion over a period of time (about a year). HER2 positive BC is more aggressive and although there is a treatment for it, but it is just more serious.
The BCO site has much info on these topics.
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Hi Wynne --
We understand this can be confusing. According to the main Breastcancer.org site's page on Hormone Receptor Status:
"Testing for hormone receptors is important because the results help you
and your doctor decide whether the cancer is likely to respond to
hormonal therapy or other treatments. Hormonal therapy includes
medications that either (1) lower the amount of estrogen in your body or
(2) block estrogen from supporting the growth and function of breast
cells. If the breast cancer cells have hormone receptors, then these
medications could help to slow or even stop their growth. If the cancer
is hormone-receptor-negative (no receptors are
present), then hormonal therapy is unlikely to work. You and your doctor
will then choose other kinds of treatment."Read more about Hormone Receptor Status and other parts of your pathology report, including HER2 status, in the Your Diagnosis section of the main Breastcancer.org site.
We hope this helps!
--The Mods
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there are different kinds of BC and supposedly ER/PR + with HER2 - is the least aggressive form of BC. that's why it's considered good prognosis. (i could be wrong...someone pls correct me)
Her2 + means it can be aggressive, bc of some protein expression. sorry i haven't read too much about her2
from another angle, if you are ER/PR -, means your cancer grew without hormone....then it gets a lot more complicated.
it's all about the cancer growth vs treatment.
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juneping - It does not have as much to do with the aggressiveness of the cancer as the treatments available. Basically ER/PR + cancers need ER/PR to grow - you can think of ER/PR as being food to them (it's not really but it works as an analogy). So, if you can cut off the supply of 'food', the cells starve and die.
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thanks ziggy.....why would i have that notion...??
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My oncologist was ecstatic that I was strongly ER/PR + and HER2 -. In addition to meds to reduce estrogen receptors, there are lifestyle changes you can make (exercise, no alcohol, etc.) that can reduce the estrogen in your body. I've suspected I was strongly estrogen driven for years anyway (fibroids, early menstruation, was still ovulating at age 53), and knowing that it probably contributed in part to the bc, I know I have options to reduce it and give myself a "better" chance of keeping it at bay.
My MO was happy; I was happy. Taking arimidex now.
Claire
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Wynne that is a good thing. Yes it sucks for us Triple Negative girls! We have no targeted therapy for our type. After Chemo we just have to hope and pray for the best. Sorry for being a Debbie Downer. I am seven months out from treatment and my anxiety rises every week. I was on Remeron but have tapered off because it wasn't helping. I'm currently tapering off Klonopin since it's not safe to be on Benzo's long term. I worry about every little thing thinking it's back or has spread. It has just robbed me of my security.
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Juneping - it makes sense that you would think that, and it may be true (although I am not sure) that er/pr+ would be a 'worse' cancer to have were it not for the fact that there are ways of starving it. Generally speaking the grade of the cancer is related to its aggressiveness.
Luv - I am sorry; sometimes when I am writing to somebody (not here specifically) and saying 'that's a good thing', it occurs to me that somebody else is reading it who doesn't have that thing. That time after treatment from what I can tell is the worst for most of us as far as fear and anxiety is concerned. Many women have PSTD symptoms and when you think about it, that is not surprising. Can you talk to your doc about therapy? I haven't done it myself, but have heard from many women that it helped them. It's a really awful feeling when you want to really be enjoying your life (after having fought to keep it) and find yourself depressed or anxious instead. (((hugs)))
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ziggy, you don't have to apologize. My response wasn't aimed at you or anyone. I have seen a few therapists and they all just want me to read books which to me haven't been helpful. I mean I know I have anxiety and don't need a definition of it. I don't need them to tell me I need to get out and live my life. I know what I need to do. It's just hard to move on and I miss the old days soooo much! But I can't change what happened and just forget it. I get so jealous of people complaining about little things like weather, bratty kids, etc. I wish those types of things were what I had to worry about! Hugs to you too!
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Thanks everyone for contributing. This has helped me understand all the things people have posted regarding HER2, etc. I was wondering though, someone who has had a total abdominal hysterectomy (TAH) several years ago and then develops breast cancer, would this mean it is NOT hormone related? Estrogen is produced by the ovaries and if there are no ovaries.....? And, if someone develops BC after a TAH would it then be considered more difficult to treat? Trying to see if I understand all of this.
I am soooo thankful for each one of you. I am praying for health and peace for all of us!
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Renee51,
Estrogen is produced elsewhere is the body too - not just in the ovaries. Many of us are diagnosed with estrogen & progesterone positive breast cancer even years after hysterectomy & removal of ovaries. in other words, presence or absence of ovaries makes no difference in hormone receptor status of the breast cancer. And no, it doesn't make the cancer more difficult to treat. Having had a hysterectomy means there are actually more anti-hormonal agents that can be used in addition to Tamoxifen - like Arimidex, Femara and Aromasin.
You might be able to get more information on the Hormonal Therapy forum: https://community.breastcancer.org/forum/78
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No Renee, you still make estrogen, just not from the ovaries. It is primarily synthesized from body fat, so the leaner you are, the better. If you didn't still make estrogen postmenopausal women wouldn't need to take aromatase inhibitors. Here's some info:
In premenopausal women, the ovaries are the principle source of estradiol, which functions as a circulating hormone to act on distal target tissues. However, in postmenopausal women when the ovaries cease to produce estrogen, and in men, this is no longer the case, because estradiol is no longer solely an endocrine factor. Instead, it is produced in a number of extragonadal sites and acts locally at these sites as a paracrine or even intracrine factor. These sites include the mesenchymal cells of adipose tissue including that of the breast, osteoblasts and chondrocytes of bone, the vascular endothelium and aortic smooth muscle cells, and numerous sites in the brain. Thus, circulating levels of estrogens in postmenopausal women and in men are not the drivers of estrogen action, they are reactive rather than proactive. This is because in these cases circulating estrogen originates in the extragonadal sites where it acts locally, and if it escapes local metabolism then it enters the circulation. Therefore, circulating levels reflect rather than direct estrogen action in postmenopausal women and in men. Tissue-specific regulation of CYP19 expression is achieved through the use of distinct promoters, each of which is regulated by different hormonal factors and second messenger signaling pathways. Thus, in the ovary, CYP19 expression is regulated by FSH which acts through cyclic AMP via the proximal promoter II, whereas in placenta the distal promoter I.1 regulates CYP19 expression in response to retinoids. In adipose tissue and bone by contrast, another distal promoter--promoter I.4--drives CYP19 expression under the control of glucocorticoids, class 1 cytokines and TNFalpha. The importance of this unique aspect of the tissue-specific regulation of aromatase expression lies in the fact that the low circulating levels of estrogens which are observed in postmenopausal women have little bearing on the concentrations of estrogen in, for example, a breast tumor, which can reach levels at least one order of magnitude greater than those present in the circulation, due to local synthesis within the breast. Thus, the estrogen which is responsible for breast cancer development, for the maintenance of bone mineralization and for the maintenance of cognitive function is not circulating estrogen but rather that which is produced locally at these specific sites within the breast, bone and brain. In breast adipose of breast cancer patients, aromatase activity and CYP19 expression are elevated. This occurs in response to tumor-derived factors such as prostaglandin E2 produced by breast tumor fibroblasts and epithelium as well as infiltrating macrophages. This increased CYP19 expression is associated with a switch in promoter usage from the normal adipose-specific promoter I.4 to the cyclic AMP responsive promoter, promoter II. Since these two promoters are regulated by different cohorts of transcription factors and coactivators, it follows that the differential regulation of CYP19 expression via alternative promoters in disease-free and cancerous breast adipose tissue may permit the development of selective aromatase modulators (SAMs) that target the aberrant overexpression of aromatase in cancerous breast, whilst sparing estrogen synthesis in other sites such as normal adipose tissue, bone and brain.
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It is important to also make the distinction about what the percentage of ER and PR really means. These percentages are not a measure of circulating hormone in the body. Someone with ER of 90% does not have more estrogen to fuel breast cancer than someone who has an ER of 40%. These percentages represent the number of receptors present on 100 cells looked at under the microscope on your biopsy or surgical sample. So, an ER of 90% means that 90 out of 100 cells had receptors.
Her2+ breast cancer is driven by a genetic over expression that signals more rapid replication of malignant cells. This is independent of hormonal status.
Renee - I had a total just/ooph nine years prior to my breast cancer Dx, was 96% ER positive, and maintained a healthy BMI throughout that time. I had hot flashes many times a day throughout that entire time, so definitely estrogen deprived!
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This questions has been circulating through my brain as well. I'm 92% ER+ and 9% PR+, that was biopsy. I didn't get any numbers with lumpectomy, but meet with my oncologist on Monday so will ask.
So it makes no difference whether you are 92% ER+ or 14% ER positive, just that you are ER+, therefore for me being pre-menopausal tamoxifen is beneficial once I get through radiation? I don't start until around May 1.
Thanks! -
I am just trying to figure things out myself. My tumor is ER -, yet it's PR+ 1%..... HER2-.
The surgeon said that it's not hormone related.
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I got results back yesterday from steriotactic biopsy. I have DCIS. I know this is the "good" kind to have if you have to have cancer. So, I am thankful for that. I guess I will get all the ER, PR and HER numbers when I have surgery. If I understand correctly, there isn't enough tissue to make those determinations? For now, have to decide on lumpectomy with radiation or mastectomy. So overwhelming.
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Hi Renee, yes, definitley the 'good' cancer, if you have to have any (which we'd all prefer!). But still a shock and a whole lot to take in.
Mum didn't get her ER, PR, HR info until after surgery, though she only had a fine needle biospy beforehand so even less tissue.
That's such a big decision to have to make, and the research suggests the 2 are pretty similar as far as future prognosis goes (unless there's individual issues in which case you doctor would advise). So it really comes down to all those personal feelings about how you feel about keeping your breasts, about the idea of reconstruction or non-reconstruction after mastectomy, whether you'd prefer to avoid the risk of further surgeries if you have a lumpectomy then local recurrence requires a mastectomy later, more likelihood of avoiding radiation if you have a mastectomy, etc etc - there's some really detailed discussion on these issues elsewhere.
Good luck with making the right decision - which is simply the one that your heart is most ok with.
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jazygirl - is it triple negative??
Renee - i think they could give you the er/pr expression from the biopsy. May be it hasn't turned cancer yet in the ducts
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