Meet The Professors: Pancreatic Cancer Edition, 2016 - Video 32Gemcitabine/capecitabine as adjuvant therapy
5:00 minutes.
TRANSCRIPTION:
DR BROOKS: So when we give adjuvant therapy, I think some patients’ expectations are not completely real. In breast cancer I go through a lot with using Adjuvant! Online. I often give them an estimate of what I think the actual benefit is. So what is the data as far as using adjuvant gemcitabine as far as actual benefit and being alive at 1 or 2 years or actually being cured, which is what the goal is? DR BEKAII-SAAB: I think the cure rate remains dismal. I mean, it’s probably 10% to 15%, maybe even less. The 5-year survival is a good landmark. And without gemcitabine, it had been less than 10%. With gemcitabine it actually doubled to a little bit more than 20%, 21%, 22%. With gemcitabine/capecitabine, when they looked at the 5-year mark, it was getting close to 40% to 45%. So we’ve already pushed a lot. Now granted that a lot of it may have to do with the fact that we have a lot of — that’s overall survival. That’s not disease-free survival, right? So that a lot of the regimens we’re using may be actually “pulling.” But it was definitely better than gemcitabine alone, which was less than 30%. So there is an incremental benefit in terms of how long we can push those patients into surviving longer with adequate and more aggressive adjuvant therapy versus single-agent or no therapy. DR BROOKS: That’s a much more impressive benefit than I would have probably explained to a patient. DR BEKAII-SAAB: It was very intriguing. The 5-year survival looked much better than the survival. DR LOVE: It’s one thing to read in papers. DR BEKAII-SAAB: The median survival. DR LOVE: Is that what you tell patients? DR BEKAII-SAAB: So for the patients, whatever I treat them with I always find the 1-year or 2-year or 5-year survival much more useful than discussing medians, because medians just don’t make sense to the patient or, frankly, to me, other than to design the next study. But using that 1-year mark, 2-year mark, 5-year mark has been much easier to discuss with patients and have them understand the value of the treatment we’re giving them. DR LOVE: I’m trying to read your facial expression. It looks dubious. DR TEMPERO: No. I tell every patient, “Look. You have a 50-50 chance here, right? You’re going to recur or you’re not going to recur. And we’re going to apply a treatment that has a chance of increasing your odds.” That’s what I tell them. DR LOVE: Let’s say we have 2 options. I’m not sure it’s 50-50. DR TEMPERO: No, no. I mean, they’re either going to recur or they’re not going to recur. Can I make a point, though? Because what happened with gemcitabine and gemcitabine and capecitabine and hopefully with gemcitabine and nab paclitaxel and other combinations is that what works a little bit in the metastatic setting has a pretty big incremental benefit in the adjuvant setting. And that’s why we are so eager when we see something that is effective in the late stage that we want to get it in the adjuvant setting. DR LOVE: What’s your theoretical explanation? Better drug penetration or — DR TEMPERO: One could argue for that, because the patients who have no evidence of disease following resection have micrometastatic disease and — DR LOVE: That was the old theory, so — DR TEMPERO: Right. Right. And you’re coming in early with hopefully something that’s going to sterilize those micrometastases. DR BEKAII-SAAB: And on that point, let me agree with that point, because we’ve actually had instances where patients presented with what appeared to be local disease. And then the surgeon goes in and removes the primary and finds multiple liver mets but still removes the primary. Those patients have done incredibly well in our practice. Those are the patients that tend to respond the best to treatment, and they tend to actually do much better. Because the primary is the one that’s, at least in the early stages that is the most stubborn, that’s just involved with this fibrous reaction, rich in stroma. And it makes it very difficult to penetrate. When you’re treating micrometastatic disease, you have less formed tumors. You are more likely to actually kill those cancer cells more effectively with effective and more aggressive chemotherapy. And so it has all to do with the volume of the disease and — using this word — with tumors that are less formed. Because, once tumor forms in pancreas cancer, they become this impenetrable fortress that becomes very difficult to break. So this is where you’re getting the advantage, at least theoretically, is in the early stages. Those cells are just roaming around or they’re just barely forming into tumors. And they’re not these solid fortresses that you can’t break. |