Tamoxifen doesn't work well for some ILCs?

My doc was part of the TEAM study that concluded that AIs are more effective than tamox for ILC. He was in favor of yanking my ovaries so I could go straight on an AI, instead of taking tamox while I waited for my ovaries to shut down on their own. At the time the results of the study had not been published yet, but he must have been aware of where it was going.

This is truly disturbing. 

Clearly what they don't know, they cannot share with patients and science learns more and more every year.

That study stated that a SUB-SET of lobular does not benefit from tamoxifen.  The problem is, no tests to determine if you are or are not part of that sub-set.  Since standard of care is/was tamoxifen, that is what we got fed...never knowing if we benefited or not.

It is one of the reasons my onco is not jumping on the 10 year protocol for all her patients (be it tamoxifen or ai ).

30-40 years ago, no one knew that IDC had subsets or that hormone status should be checked or that triple negative tended to be more aggressive; even Her2 info is, in the scheme of things, fairly recent and life saving.

We just all want "them" to hurry!

Hlya, yes, by "yanking" I mean removing them surgically. I was 47 when I got my DX, and turned 48 during treatment. I was not in menopause, although my periods stopped during chemo. After chemo, BMX, more chemo and then rads, I had a hysterectomy (but they left in the cervix) to put me into menopause for good. At first we were just going to remove the ovaries, but I had some huge fibroids in the uterus and some other problems that made the hyster a better choice.

JohnSmith, the alternative drug is an AI. However, I have no idea if that applies to men.

JohnSmith, ok. Your fiancee is in the same situation I was in. That is why I had my ovaries out as part of my treatment. It is not always the right way to go, but in my case we decided it was warranted. The reasons were that my cancer was stage 3, locally advanced, that I was close to menopause anyway and that we have no family history of heart disease.

hyla and others

I am very interested in this research.I was diagnosed with ILC in March. Since then I have had surgery and tried Femara / letrozole and fail to tolerate it. My oncotypee score is just OK at 23and I'm trying to decide whether to go ahead and try tamoxifen next. I am only 51 so my ovaries could still be an issue although I am technically in menopause since it's been one year. Basically I'm trying to figure out if I should bother with the tamoxifen as it possibly won't give me much benefit. my doctor originally chose letrozole because he believes tamoxifen too toxic.Have you found other research to lead you to believe that tamoxifen may not be appropriate for ILC?

John Smith - I have the exact same diagnose as your wife - altså at 45 year old - it's now 2.5 years since diagnose- Living in Denmark we are all considered "high risk" if we are less than 60 years at diagnose and if the lump is more than 1 cm. So I did chemo.

I have thought a lot about the tamoxifen question- I think I read somewhere that you don't benefit that much from tamoxifen if your have lobular with high ki67.Can anyone of you confirm that ? On the other hand - if you have stage 1 lobular with low ki67 you may not even need anti hormon according to the following research:

http://www.springerplus.com/content/pdf/2193-1801-3-70.pdf

Lena-Lou, I forgot to mention that my mom had ovarian cancer (which she survived) and my mom's sister had uterine cancer. We are also BRCA-, but I figured I was better off being rid of those particular parts. 

rivercaralee, I am not sure where the idea that lobular does not "respond" to chemo comes from. As far as I know, the only difference between IDC and ILC in chemo response is that ILC more rarely has a complete pathological response to chemo. The thing is that it is not common with ductal either, just a bit more common than with lobular.

What do you mean by this:

"At 51 I too am in that grey area where I am too old to have my ovaries out, but too young really for the AI's...but at any rate the side effects of letrozole were not tolerable."

AIs are not for a certain age, they are just for women who have passed into menopause. If you were put on femara, it means that you were already in menopause. In that case, there would be no reason to remove your ovaries.

Also this, Momine.  This is not my question posed to Johns Hopkins, but quite similar:

needed  more research!

Yes Momine, one could extrapolate from the neo to the adjuvant setting and definitely an  area for more research!

From this article:

http://jco.ascopubs.org/content/23/27/6796.1.full

More importantly,
frequently used guidelines such as NCI,⁸ NCCN⁹ and the St. Gallen Consensus Conference,¹⁰ as well as prognostic tools such as Adjuvant!¹¹
still do not consider the potential differences in the natural history
and treatment effectiveness between this ILC and invasive
ductal carcinomas, potentially exposing ILC
patients to ineffective treatment. Based on the results presented, it
would seem
that lobular carcinomas of the classic type and
invasive ductal carcinomas are two very different pathologic entities,
which
should be studied and managed as such.

River, no, you can not extrapolate that way. That is my whole point. When they look at "clinical benefit" from doing the chemo before or after, they measure the usefulness of neo-adjuvant by whether it leads to fewer mastectomies, better surgical margins etc. than adjuvant. 

My own case is a good example. The neo-adjuvant chemo definitely worked. My very large tumor halved after each infusion, and after 4 chemos it could not be felt, although some of it was still left. Because of it's placement and shape, however, a mastectomy was still necessary.

So, although the chemo I did definitely worked, I gained no particular advantage from doing it before surgery rather than after, clinically speaking.

"From October 1982 through March 1990 we randomised 1445 patients and 969 (67%) were eligible for the biomarker analysis. At 10-years 936 women had suffered a disease-free survival (DFS) event (tamoxifen, 495 events in 686 patients; CMFT, 441 events in 642 patients). The addition of CMF to tamoxifen significantly improved DFS (adjusted hazard ratio 0.82; 95% confidence interval (CI) 0.71–0.93; P = 0.003) but not overall survival (adjusted hazard ratio 0.95; 95% CI 0.85–1.08; P = 0.44). DFS was superior in Luminal A tumours (ER or PgR positive, HER2 negative and Ki67 ⩽14%) when compared to Luminal B or non-luminal (ER and PgR negative) tumours. There was no statistical evidence of heterogeneity by subtype in the benefit from CMF (P_interaction = 0.45). http://www.sciencedirect.com/science/article/pii/...

"Subtype" means lobular vs ductal.