she called me and said luminal A... I have to wait for the reports to be sent to me from agendia. I'm assuming the mammoprint said low, and the blueprint said luminal A. I'm still in shock as to how the doc knew?. She did tell me weeks ago that ki value on healing tumor tissue (healing from the biopsy) is artificially high. And she felt my Pr from the biopsy wasn't homogenis with the rest of the tumor. I rebutted it could go the other way too. And she laughed and said she'd bet me on the mammoprint. As I mentioned earlier, her confidence made me want to trust her... but I had to know for sure. My low mitosis level on both biopsy and tumor were what she was sticking to.

Well.. From what I've read, the main difference is that Luminal B tends to have more aggressive cells and much lower PR+ (or PR-). It is ER+. It can have HER2, or not. The Ki-67 value has been used to determine aggressiveness, but like I mentioned, my doctor dismissed Ki, and said to focus on my Mitosis rate of 1. Luminal B is not treated as well with Tamoxifen, as the low PR tends to help the cell evolve to beat Tamox, but AIs do better for it. I am seriously thinking my PR+ must be higher than 5%, because that is just really low. Doc seemed to think it was higher than the biopsy found. It's just odd. Here's an overview of the options for Luminal B.

The thing is.. with my score of 30-35% Ki-67, and my low PR+, all the signs were pointing to B... BUT from what I've read (thanks to you ladies posting links), different labs cannot read ki-67 the same, so there is no standard and the same tissue can be read completely differently based on the lab. So perhaps they gave me a false high Ki?

http://www.breastcancer.org/research-news/20121217-5

Here's another one on the differences and outcome differences:

http://jnci.oxfordjournals.org/content/101/10/736/F4.expansion.html

QuinnCat, ME TOO! My doc insisted that the ki value wasn't to be trusted. Here is a study showing that Ki-value does well for grade 1 and grade 3 tumors but not for grade 2. In fact for grade 2 tumors the same specimens were label 30% or 5% depending on who was eyeballing it.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0037379

Abstract

Adjuvant chemotherapy decisions in breast cancer are increasingly based on the pathologist's assessment of tumor proliferation. The Swiss Working Group of Gyneco- and Breast Pathologists has surveyed inter- and intraobserver consistency of Ki-67-based proliferative fraction in breast carcinomas.

Methods

Five pathologists evaluated MIB-1-labeling index (LI) in ten breast carcinomas (G1, G2, G3) by counting and eyeballing. In the same way, 15 pathologists all over Switzerland then assessed MIB-1-LI on three G2 carcinomas, in self-selected or pre-defined areas of the tumors, comparing centrally immunostained slides with slides immunostained in the different laboratoires. To study intra-observer variability, the same tumors were re-examined 4 months later.

Results

The Kappa values for the first series of ten carcinomas of various degrees of differentiation showed good to very good agreement for MIB-1-LI (Kappa 0.56–0.72). However, we found very high inter-observer variabilities (Kappa 0.04–0.14) in the read-outs of the G2 carcinomas. It was not possible to explain the inconsistencies exclusively by any of the following factors: (i) pathologists' divergent definitions of what counts as a positive nucleus (ii) the mode of assessment (counting vs. eyeballing), (iii) immunostaining technique, and (iv) the selection of the tumor area in which to count. Despite intensive confrontation of all participating pathologists with the problem, inter-observer agreement did not improve when the same slides were re-examined 4 months later (Kappa 0.01–0.04) and intra-observer agreement was likewise poor (Kappa 0.00–0.35).

Conclusion

Assessment of mid-range Ki-67-LI suffers from high inter- and intra-observer variability. Oncologists should be aware of this caveat when using Ki-67-LI as a basis for treatment decisions in moderately differentiated breast carcinomas.

MIB-1-LI results were all below 8% for G1 and above 30% for G3 carcinomas. However, interobserver variability was substantial for the G2 cases, values ranging between 5 and 30% for the same cases

Warrior Woman, there are two areas to look at. 1 is that Luminal B does not do as well on Tamoxifen. Can you ask that your tumor sample be sent in? They can do testing years after it's collected. So even if you are a normal metabolizer of Tamox, it still means if you are Luminal B, an AI is better for treatment.

and 2 is that if you are Poor metabolizer (PM), and Luminal A then it still could be an issue for you. Keep in mind that even some PMs had low but still there endoxifen levels, so Tamox uses MULTIPLE pathways, the 2D6 pathway is just a primary one. The only way to know if Tamox is working for you, if you aren't having any symptoms, is to get your Endoxifen tested and not many labs test for it.

I figured there is a 75% chance I'm going to have to switch to an AI/OS within the year. Definitely if the mammoprint came back Luminal B (I figured 50% chance) and definitely if I test as a PM on the Kailos genetics test and have no symptoms on Tamox (I am currently symptomless 3 weeks in).

Here is a thread that discusses all the back and forth and rebuttals to rebuttals. It's defintiely has some merit, we just don't have work arounds yet or know enough to help change things.

https://community.breastcancer.org/forum/73/topics/798301?page=10

Warrior, have you told them you are willing to pay out of pocket for the testing? Perhaps they feel they can say no because they think you are asking them to cover it. The Mammoprint/Blueprint will end up costing me $500... which is very much worth it 'to know' and not have this nagging doubt.

FarmerJo, isn't it just like a coin toss on our stats? They are nearly identical. I wonder how it is that Mammaprint gave me a low reoccurrence score (Luminal A) and you with equal stats got a high score (I'm assuming?) I see you are likewise Grade 2, do you mind if I ask what your mitosis number was?

On the AI, I've read it's equally effective for Luminal B.. but Tamoxifen is not. Did you mean Tamox?

Welp... I'm sticking to my plan, but found this small study showing that mammoprint/blueprint/targetprint Vs. Oncotype are really not working with eachother. what I did find fascinating is that Oncotype designated more of the tumors as low risk than Mammoprint did. 52 v 49. So here I am with an Intermediate Oncotype and mammaprint designates me low risk. But mammoprint pulled 18 Low Oncotypes up to "high risk". Really interested stuff..

http://meeting.ascopubs.org/cgi/content/abstract/33/15_suppl/11017