Luminal A vs. Luminal B stage 1 BC

Hopeful82014

As always, you've made some excellent points, Kayb. Thanks for sharing that perspective.

farmerjo

You can see my stats below - I was told I'm Luminal A. Seriously.

farmerjo

Just rec'd Mammoprint result - high-risk, Luminal B. BS said "you should have had chemo all along". HE IS THE ONE THAT SAID NO CHEMO BASED ON ONCOTYPE of 19 and negative SNB 18 months ago. A negative SNB that really wasn't - Showed up in lymph node a few weeks ago. I was also initially told Luminal A. Lymph node bx and original IDC bx results identical.

I feel absolutely cheated.

QuinnCat

farmerjo - are they going to give you chemo now? Ki67 of 29.1% and PR 5% is not low risk! Sorry you are having to deal with this, probably when you thought you were done, and how what do you think happened to get a false negative on your SNB?

What is an ATM gene mutation?

ChiSandy

JuniperCat sent me a link to a study showing that in ER+ tumors, PR status is much more important than previously thought, because progesterone plays a huge role in blocking estrogen's access to estrogen receptors; and that though tumors in mice initially shrank when treated with tamoxifen alone, by 60 days they had grown to at least their original size; but when an experimental progesterone-antagonist was added to the mix, the tumors had shrunk to less than 1/4 their original size by day 60. However, progesterone-suppression alone was ultimately as ineffective as tamoxifen alone. Several caveats, though: the study was in mice, who were sacrificed after 60 days (hard to say how that extrapolates to human life expectancy, cancer notwithstanding); the estrogen-inhibitor tested was tamoxifen (a SERM) and the study did not address aromatase inhibitors (perhaps because first rendering the mice postmenopausal was too exacting and time-consuming); and the study was unclear as to whether progesterone itself (rather than the progesterone antagonist) can inhibit estrogen and tumor growth in estrogen-suppressed mice. The statement that progesterone enhances estrogen-suppression contradicts the methodology of using a progesterone-antagonist.

http://www.eurekalert.org/pub_releases/2016-06/uoc...

It certainly does explain how Luminal A cancers are less aggressive than Luminal B, and strongly PR+ Luminal A tumors less aggressive still than weakly PR+ ones.

Lisey

The thing I do not understand is why doctors do not seem to understand that obviously a low PR score would have a huge effect on treatment. I'm so upset I'm only 5%PR+ and that was from the initial biopsy. They didn't redo the testing on the actual tumor during the Mastectomy.

I'm 41 years old, premenopausal,, what would you ladies suggest I push for when I meet with this Kaiser Oncologist next week? I did push for a ki67 test, and an Oncotype, - they said I'll get the results hopefully next week. Should I pay for on my own another DNA test to determine my rate for tamoxifen? I had InformedDNA do a BRCA and full 21 screening, but their numbers don't make sense to me at all. Could any of you help decipher them? I'm just so upset because none of the facebook groups I belong to even know what Luminal B is. None of them seem to want to educate themselves. I'm kind of alone in this process, and frankly, don't trust the medical establishment to just treat me like they would any ordinary ER+/HR+/ stage 1.

P.S. I had Melanoma 6 years ago, so this is whole experience is really triggering me. I just am locking myself away sobbing right now.

Meow13

holy cow my pr was less than 1%. Am I doomed because I didn't do chemo?

QuinnCat

Lisey - what is "InformedDNA?" Is that like "23andMe?" I know when I signed up for 23andMe, it was about the same time I was dx'd with BC and had the real BRCA test. I remember 23andMe only tests for the 3 founder variants of BRCA1 and BRCA2. There are thousands. I was positive for BRCA2 and my brother asked to be tested at Kaiser. He had to fight them tooth and nail because he was a male. There is no reason a male should not be tested and this was with a sister who was positive. He eventually got the test.

If you have had melanoma and BC and 41, you more than qualify.

Lisey

Informed DNA is the company Kaiser partners with to test for BRCA1 and 2 and the others. they say I tested negative for all of their DNA testing, but none of that included anything the Oncotype would test for since it was just a blood draw.
I did request a Familial Melanoma DNA test, since every cousin has had it, but it was declined saying it wouldn't change my treatment for BC either way.

QuinnCat

Lisey - Can I ask you how old that test is? A friend of mine lost his <50 year old brother and father the same year to melanoma. That was about 4 years ago and he never mentioned a test.

Every cousin...that is quite amazing. So glad you survived it.

jojo9999

Lisey, FYI: when you get your onco score, it will have a ER, PR and Her2 score - different scales (not in %) but they include a graph so you can see how strong/weak ER and PR are. I recall that mine numbers agreed with the pathology from my biopsy - which relieved me, because the hospital did not test the tumor for ER/PR/HER2 from the mastectomy, just relied on the biopsy path (but the onco test is done on the mastectomy-tumor).

marijen

Half of cancers could be slowed with common hormone (progesterone)

http://www.medicalnewstoday.com/articles/296525.ph...

gerrib

Meow I didn't have chemo either. I am Pr neg (PILC). I had IDC 5 years ago. I'm very confused .

Just out of interest - in the case of BC tumours what does "Luminal" mean? Cells have lumen??

Lisey

marijen, from the article it was saying 75% of BC's are ER+ and of those 75% are PR+ = so 50% total could benefit. Is this article intended for ER+/PR+ folks then? I think if one is PR- (which is where I'm at borderline at 5%).. then adding progesterone would not be helpful.

Gerri, I'm ask confused as everyone else. Luminal means light... why that type of designation? I just wish more research would focus on the B vs. A because from what I'm gathering, just this year they are starting to realize they need completely different treatments.

QuinnCat, they told me Famiial Melanoma is a Gene that can be tested. Unfortunately, they refused to do so at this time for me since this was supposed to be for breast cancer genes.. even though all my cousins have had melanoma. We are all fair and lived in the 80s at the beach with no sunscreen, so maybe it's just environmental.

Lastly, I also read that some Melanomas are ER+ receptors - whiich is a whole nother thing I'm trying to dig into.

I went on the stage IV boards (Glutton for punishment) and I'm seeing a lot of ER+ / PR- that were cleared initially... I bet those were undetected Luminal B's that were treated just like a normal ER+ patient would be treated.

Lisey

JoJo, knowing I'll get another opinion on the status of my PR level from the oncotype gives me hope. I really can't believe they wouldn't test the actual tumor and simply rely on a small core biopsy. Those can completely miss areas. I do know they upgraded my grade level from the mastectomy biopsy. I went from a grade 1 to a grade 2.. so that was a bit concerning as well

SpecialK

The term "luminal" in breast cancer subtyping is in reference to luminal epithelial cells in the breast tissue.

QuinnCat

LIsey - "they told me Famiial Melanoma is a Gene that can be tested. Unfortunately, they refused to do so at this time for me since this was supposed to be for breast cancer genes.."

I'm a bit confused by this statement. Is the Melanoma gene a stand alone gene or part of a newer component of the brca test? Sorry...sometimes my brain goes to zero and have become very literal minded.

Lisey

Quinn, It's a completely non-related type of genetic testing they offer, but Kaiser refused to pay for or do. I had a 1 hour history session going over all the various family members and illnesses and the doc said you know, you probably should be tested for FMM, but since this has nothing to do with breast cancer, it may not be approved.

Which it wasn't... so I don't know if I have it. On the bright side I tested negative for all the DNA testing that did relate to BC. Now onto that oncotype and ki67 score next week.

QuinnCat

As I said, my brother had to fight very hard for BRCA testing at Kaiser, and he was an employee at Kaiser who designed their whole electronic medical record system (years of work) and knew most of the doctors...in other words, he had an "in." Because they don't do testing in-house, it's just one of those expenses their business model does not like. If you want, I can ask him how he eventually prevailed.

farmerjo

I am seeing the MO today...will check in later with her thoughts.

My Oncotype done at original diagnosis January 2015 was based on negative sentinel node - score of 19 and told no chemo.

I discovered large node (2cm) a few weeks ago and had ALND June 17th. Node pathology same as original BC (ER>90%, PR 5%). So I had a cancerous node all along.

Tissue from January 2015 sent for MammaPrint - showed high risk Luminal B.

Of note, medical errors are now the third leading cause of death in the US.

farmerjo

Lisey -

Saw MO today. Mammaprint/BluePrint says Luminal B and that is why hormonal therapy is not treating my cancer appropriately...it's only "half working", hence the recurrence. Fortunately, my scans are clean. TG

I saw here in the forum many months ago where someone said any amount of PR positivity is PR positive...apparently not.

Aggressive chemo starting soon.

Risk of BC with ATM mutation is up to 60%. We were testing for other mutations - not expecting Lynch Syndrome and ATM mutation.

QuinnCat

farnerjo - you have the exact same percentages of ER and PR I did on initial biopsy (ER, PR). Have always been told I was luminal B (with 60% Ki67 Onco 39). I am so glad your scans are clear, but a huge bummer you will now get chemo a year later. Luminal B is low to no PR - that is what I have read and been told. I have never heard of the ATM mutation? What chemo will you be getting?

farmerjo

QuinnCat -

Crazy I was told Luminal A at initial dx. Oncotype was 19.

Was told AC every 2 weeks times 2 months followed by Taxol weekly for 3 months? Lot of reading to do.

QuinnCat

I had a version of that, I guess. Dose dense AC (4x every 2 weeks) then dose dense Taxol (4x every 2 weeks). I wonder how the oncoscoring failed you but MammoPrint got it right. I forgot to mention to you, while my IHC initial biopsy was exactly the same as yours on ER/PR 90/5, the Oncoscoring showed the ER just mediocre. I have a suspicion my tumor was evolving to triple negative and Onco picked up a different portion, plus the time between my initial biopsy and surgery was 3.5 months (a big fiasco).

Optimist52

My hormonal stats were the same ER 90%, PR 5%, Oncotype DX 22, isolated tumour cells in 2 nodes so no chemo as advised by my MO. When I asked her what low PR meant, she said it wasn't that significant. I've had ILC so chemo not necessarily so effective on that. This whole Luminal A vs B discussion has depressed me to be honest! I thought that the ER % was a lot more important for how well hormonal therapy would work. No doctor I've seen has ever mentioned Luminal A or B. I suppose they like to keep things simple for patients.

Moondust

Optimist52, that's exactly what my MO told me - low PR is not significant. She is simply not up-to-date!! My PR% is 40% which came back as being in the negative range on the Oncotype report.

FarmerJo, I'm glad you will be getting your chemo. You need it! I had to fight to get mine. My surgery was Jan 15, my chemo started June 8. I have already finished radiation. They do classify tumors as PR+ on the pathology report if it has any PR receptors. We can only hope this simplistic way of reporting will change soon, given many new studies showing a worse prognosis for low PR. It is one of the 60% of my cells which do NOT have a PR receptor that will cause trouble down the road if my chemo doesn't do the trick. It seems like such a simple concept to me, I wonder why more MO's have not caught on.

gerrib

And I haven't even mentioned 'luminal' to my oncologist! Pleomorphic, Ki67 20%, Pr neg and weakly Er +., that was all fairly well dismissed as not a concern. Like Twincatt I have a feeling my latest tumour is more like TN.

lisey What is a good paper to read on this? One that I can acess freely

Thanks special K for explaining what luminal means in this context.

I would have to travel elsewhere to get 2nd opinion, have OS trip planned for Oct so don't know if I would have chemo anyway as I have moved on. How long after surgery can you have chemo? I had umx for 2nd primary BC in March 2016

My MO has good bed side manner but I am a bit alarmed that I am being given blanket treatment. I feel as though here in Australia we are behind US with BC treatment but maybe that's coz I live in a rural area.

Gerri

Moondust

gerrib, I had my surgery in mid-January and I started my chemo June 8, three weeks ago. I think my MO said six months after surgery is still okay. It is too bad you cannot get an Oncotype score, because that may change your MO's tune.

Tell me about your dog - is it a working sheep dog?

gerrib

He's a pet Moondust. He's a pure bred Border Collie, but bred to be family friendly. Actually I don't have a family so he is my baby. His name is Bear and he is 10 years old. I inherited him when he was 5 from a family who could not care for him anymore. He loves chasing my 2 alpacas and they retaliate by going after him. I think he has the herding instinct, but has not received proper training.

Hope you are going OK with chemo.

ChiSandy

There are many studies (I read a few abstracts today) that say oncologists are beginning to rethink their old standard of any % of staining for PR receptors as PR+, and chemo should be offered as an option to patients with as much as 5-10% of cells staining positive for PR receptors. My ODX profile was 75% ER+ and 97% PR+ (the report said that any %>50% is “positive"), though at initial core-needle biopsy my ER % was only 67%. The studies said that cells that “overexpress" a certain ER-related gene correlate to “highly ER+" and tend to respond most strongly to endocrine therapy. Yet “highly ER+" was defined (at least in Hyderabad, India, where the study took place) as >5% ER+. (Interestingly, the study's authors found that in India, PR positivity is far less common than in the west--a much higher proportion of Indian, especially S. Indian, women, have Luminal B rather than A tumors. There are also other striking ethno-genetic differences between S. Asian patients and European, African and E. Asian ancestry, chief among them high levels of lipoprotein (a)--measured as early as at birth, in cord blood, to rule out lifestyle and dietary causes--which leads to a disproportionately high rate of heart attack, stroke and Type 2 diabetes among Indians, Pakistanis and Sri Lankans, even those who are vegetarians).

Why the “Luminal" in Luminal A vs. B? The “lumen" is not just the hollow space within a blood vessel (which term you hear most often regarding coronary arteries), but the hollow space in any type of duct (analagous to the hollow space in a pipe or soda straw). Luminal A or B breast cancers involve epithelial cells that line the inner walls of the mammary ducts. The lumen is the space between those walls. The biggest difference between the two is that A is PR+ and B is PR-., though the criteria for how that's classified may be changing. Luminal tumors mostly tend to be HER2-, but some are mildly or even equivocally HER2+. The third subtype of IDC breast tumor is called HER2+ type--most commonly ER-/PR-/HER2+, but also triple-positive fits the definition. Triple-negative is sometimes called “basal-like" for its resemblance to basal epithelial cells.

What I find somewhat confusing about the articles describing progesterone's effect on estrogen receptors is that on the one hand, researchers seem to be saying that progesterone helps the tumors resist the effect of estrogen and can cause tumor-cell death and thus reduction in tumor size. But then seemingly paradoxically, the study used not progesterone but a progesterone-antagonist (sort of the difference between estrogen and either a SERM like Tamoxifen or an AI), and it was done on mice into whom ER+/PR+ tumors were introduced, and for only 60 days before the critters were “sacrificed" (my husband, who got his PhD in mouse genetics, says that's about 1/12 of a mouse's natural lifespan--so if a woman would on average be expected to live to age 84, that'd extrapolate to about 7 “human years"). After 60 days, the untreated mice's tumors grew 180%. The tamoxifen-treated mice initially had their tumors shrink but eventually rebounded for a net growth of 60%. The progesterone-antagonist-treated mice had initial tumor shrinkage but ended up exactly where they started. But the mice treated simultaneously with tamoxifen and progesterone antagonists had their tumors shrink steadily, and by day 60 the tumors had shrunk by 70%. Lest we get too excited, these were mice, we don't know whether the lucky ones would have seen further shrinkage past 60 days, how much (PCR?) or for how long; and more importantly, the progesterone-antagonist was an experimental enzyme synthesized in very small quantities. We also don't know whether AIs would have produced the same or better results than tamoxifen. So we have no idea how reproducible this is in real-world-human terms.

It is fascinating though, to posit whether giving Luminal A or even B patients on anti-estrogen therapies a shot of Depo-Provera or an Rx for inexpensive progesterone pills might be the “magic bullet" that could enhance or even replace cytotoxic chemo.