Breast Cancer - Episode 11
Hope Rugo, MD, FASCO: One of the questions that comes up, Evita, for many of us is how important it is to be strongly versus less strongly ER [estrogen receptor]–positive. Obviously, if you have 2% ER, it’s clear that you’re not strongly ER-positive. But how secure can we be in the percentage of estrogen receptor and progesterone receptor positivity detected by IHC [immunohistochemistry]?
Evita Sadimin, MD: In our own practice, if it’s straightforward we just report it. With borderline cases or situations with a focal area that is strongly ER-positive but everything else is negative around it, then we would communicate to the clinicians the nature of the specimen and that it may just be a certain heterogeneity to the tumor.
Sometimes you can actually take a look at certain morphology and predict which area is going to be strongly positive versus the surrounding area, which is going to be different. Not in all cases, but sometimes that’s what happens, and you just communicate it. We think that probably applies to a certain portion within the tumor population.
Hope Rugo, MD, FASCO: We often have situations where a metastatic site might be ER-negative, but it possibly has to do with the amount of cells that we’ve taken out during the biopsy or when decalcifying the bone, etc. A lot of us will use the phenotype and the clinical situation to try and decide about use of endocrine therapy. But one of the things that comes up, Ian, is that patients will have progression either while on an AI [aromatase inhibitor] or less than 12 months after completion of adjuvant therapy, and they might have liver or lung metastases. Do you still use endocrine therapy first, in that setting, with fulvestrant?
Ian Krop, MD, PhD: Again, I think that’s another area where we’re starting to have to draw the line between what is visceral crisis and what patients are unlikely to benefit from hormonal therapy. Multiple factors go into that. How much lung disease do they have? How close is it to being symptomatic? I think those are the important things to weigh when you’re making that decision.
A related question is when do you use fulvestrant versus an aromatase inhibitor? Again, if they didn’t actually progress on the aromatase inhibitor… I think these are all questions that depend on the specific patient in front of you. But I still, for the vast majority of cases, tend to use hormonal therapy plus a CDK4/6 inhibitor. I think that decision is so much more clear now that we have CDK4/6 inhibitors. Back when we only had hormonal therapy as monotherapy—for which response rates are relatively low—the question was more complicated. Here, when you saw the data that Adam presented with 50% response rates, that’s as good as you’re likely to get with chemotherapy. I tend to use hormonal therapy for most cases, unless they’re fairly symptomatic and I’m worried they need a response right away.
Transcript edited for clarity.