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Bevacizumab in EGFR-Mutant NSCLC

Panelists: Mary Jo Fidler, MD, Rush; Roy S. Herbst, MD, PhD, Yale ; Geoffrey R. Oxnard, MD, Harvard; Naiyer Rizvi, MD, Columbia; Mark A. Socinski, MD,
Published: Thursday, Oct 15, 2015


Transcript:

Mark A. Socinski, MD
: Probably the most interesting data we saw with bevacizumab (Avastin) recently has been the use in EGFR mutant NSCLC. The Japanese data showed a huge benefit in PFS; I’ve not seen any overall survival data on that trial at this point. We have an ongoing trial in the US. I think there’s also a second trial. I’m not quite sure.

Roy S. Herbst, MD, PhD: Your former colleague is doing that.

Mark A. Socinski, MD: Dr. Stinchcombe is heading it up with Dr. Jänne. I think the accrual is slowly getting done.

Geoffrey R. Oxnard, MD: It’s picking up based on those results.

Mark A. Socinski, MD: Has that influenced your practice with bevacizumab in the EGFR-mutant setting?

Roy S. Herbst, MD, PhD: It certainly has with mine.

Geoffrey R. Oxnard, MD: Not mine.

Mark A. Socinski, MD: That’s why we had you two apart.

Roy S. Herbst, MD, PhD: Point/counterpoint. Keep it fair. Alan Sandler and I, many years ago, did the initial phase I study of bevacizumab/erlotinib (Tarceva), the BeTa trials. Remember those? Actually, the phase I data looked quite good. Back then we didn’t know about the EGFR mutants, so probably some of the patients who did very well had mutations. Then the phase II trial comparison to paclitaxel plus bevacizumab looked pretty good.

Later, we had the phase III study, bevacizumab/erlotinib versus erlotinib, in which the PFS result was extraordinary. The hazard ratio was in the 0.6 range, but there wasn’t much of a difference in overall survival. There was some crossover, but when you looked at those never-smokers or the mutant patients, there clearly was a benefit.

I was thrilled a few years ago at ASCO when I saw the Japanese group with these data. Clearly, again, the big problem with EGFR inhibitors is the resistance. Is this a way of doubling down on the whole pathway; the relationship between EGFR and VEGF? It might be. Waiting for the survival data is important. Could one use this in someone who’s resistant? I think it’s something to think about. But, I agree, we need a little more data.

Geoffrey R. Oxnard, MD: I just saw a patient who I started on erlotinib back in April for newly recurrent disease after prior surgery. We got him on the right dose of 100 mg, it took about a month. After, I said, “See you in three months.” He went to Italy, had a great summer, and came back in three months; he feels fine. I just saw him yesterday and I said, “See you in three months.”

Being on erlotinib for a responding, low burden EGFR-mutant patient is living the dream. If I’m adding bevacizumab intravenous therapy every three weeks—I want some compelling data. I agree with you that the PFS data was impressive. That was a non-brain metastasis population and I felt that the control arm didn’t do quite as well. Really, early on it seemed that the experimental arm did awesome and a ton of people dropped out of the control arm. I worry about some kind of bias. I was unsure.

I want to see it validated. I want it to be true, but it has not changed my practice just yet.

Mark A. Socinski, MD: But it would certainly change how we care for this patient population. Taking a pill once a day is a huge benefit for these people rather than being committed to chair time every three weeks. It’s not without toxicity, although, I think the EGFR-mutant population would probably be one of the safest populations to use it in for the most part. But it’s not without its downside. Naiyer, you?

Naiyer Rizvi, MD: No, I never use it.

Mark A. Socinski, MD: Mary Jo?

Mary Jo Fidler, MD: I’m not using it currently together.

Mark A. Socinski, MD: All right, Roy, you’re a lone wolf.
 
Transcript Edited for Clarity
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Transcript:

Mark A. Socinski, MD
: Probably the most interesting data we saw with bevacizumab (Avastin) recently has been the use in EGFR mutant NSCLC. The Japanese data showed a huge benefit in PFS; I’ve not seen any overall survival data on that trial at this point. We have an ongoing trial in the US. I think there’s also a second trial. I’m not quite sure.

Roy S. Herbst, MD, PhD: Your former colleague is doing that.

Mark A. Socinski, MD: Dr. Stinchcombe is heading it up with Dr. Jänne. I think the accrual is slowly getting done.

Geoffrey R. Oxnard, MD: It’s picking up based on those results.

Mark A. Socinski, MD: Has that influenced your practice with bevacizumab in the EGFR-mutant setting?

Roy S. Herbst, MD, PhD: It certainly has with mine.

Geoffrey R. Oxnard, MD: Not mine.

Mark A. Socinski, MD: That’s why we had you two apart.

Roy S. Herbst, MD, PhD: Point/counterpoint. Keep it fair. Alan Sandler and I, many years ago, did the initial phase I study of bevacizumab/erlotinib (Tarceva), the BeTa trials. Remember those? Actually, the phase I data looked quite good. Back then we didn’t know about the EGFR mutants, so probably some of the patients who did very well had mutations. Then the phase II trial comparison to paclitaxel plus bevacizumab looked pretty good.

Later, we had the phase III study, bevacizumab/erlotinib versus erlotinib, in which the PFS result was extraordinary. The hazard ratio was in the 0.6 range, but there wasn’t much of a difference in overall survival. There was some crossover, but when you looked at those never-smokers or the mutant patients, there clearly was a benefit.

I was thrilled a few years ago at ASCO when I saw the Japanese group with these data. Clearly, again, the big problem with EGFR inhibitors is the resistance. Is this a way of doubling down on the whole pathway; the relationship between EGFR and VEGF? It might be. Waiting for the survival data is important. Could one use this in someone who’s resistant? I think it’s something to think about. But, I agree, we need a little more data.

Geoffrey R. Oxnard, MD: I just saw a patient who I started on erlotinib back in April for newly recurrent disease after prior surgery. We got him on the right dose of 100 mg, it took about a month. After, I said, “See you in three months.” He went to Italy, had a great summer, and came back in three months; he feels fine. I just saw him yesterday and I said, “See you in three months.”

Being on erlotinib for a responding, low burden EGFR-mutant patient is living the dream. If I’m adding bevacizumab intravenous therapy every three weeks—I want some compelling data. I agree with you that the PFS data was impressive. That was a non-brain metastasis population and I felt that the control arm didn’t do quite as well. Really, early on it seemed that the experimental arm did awesome and a ton of people dropped out of the control arm. I worry about some kind of bias. I was unsure.

I want to see it validated. I want it to be true, but it has not changed my practice just yet.

Mark A. Socinski, MD: But it would certainly change how we care for this patient population. Taking a pill once a day is a huge benefit for these people rather than being committed to chair time every three weeks. It’s not without toxicity, although, I think the EGFR-mutant population would probably be one of the safest populations to use it in for the most part. But it’s not without its downside. Naiyer, you?

Naiyer Rizvi, MD: No, I never use it.

Mark A. Socinski, MD: Mary Jo?

Mary Jo Fidler, MD: I’m not using it currently together.

Mark A. Socinski, MD: All right, Roy, you’re a lone wolf.
 
Transcript Edited for Clarity
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