DR FUCHS: I do think that there’s confusion and conflict about the issue of response vis-à-vis the biologics — namely, there’s a notion that maybe the EGFR inhibitors, cetuximab and panitumumab, confer a better response and that perhaps bevacizumab doesn’t appreciably increase response rates exclusively. I don’t know that we really know that.
But, in particular, in a patient like this, often times I would consider a regimen like FOLFOX/bevacizumab with the idea, of course, that bevacizumab should be held at least 4 weeks prior to resection.
DR GOLDBERG: So there’s interesting data from our Italian colleagues who brought us FOLFOXIRI. And you remember, in the FOLFOXIRI study there was a 66% response rate, and 3 times as many patients with liver-limited disease who were resected had R0 resections. They’ve now gone on to FOLFOXIRI plus bev and reported, just some preliminary data on this, but the response rate was 77%, which is amazing and makes you wonder if that is going to be a good strategy to try and bring patients to resection.
DR LOVE: So, in spite of the encouraging data, bottom line, right now, if a patient comes to you what are you likely to recommend?
DR GOLDBERG: So I would consider a FOLFOXIRI regimen in this case. And the addition of bev would be on my mind.
DR O'NEIL: I have, off study, used FOLFOXIRI. And I think with FOLFIRINOX in pancreatic cancer, that kind of reminds us that that combination is an extremely active combination for a patient who we think can tolerate it. It’s really something we should think about. I suspect the response rates are better than 2 chemo drugs plus a biologic for that triplet.
DR LOVE: With or without a biologic?
DR O'NEIL: When I’ve used it I’ve only used it without a biologic.
DR GROTHEY: It’s interesting. I’m listening to my colleagues, and I was actually surprised that there is so much prevalence of bevacizumab in this K-ras wild-type cancer, where we have data, very consistent data across the board, except for 1 study, the Nordic trial, that EGF receptor inhibitors increase anatomical response rates in patients with K-ras wild-type tumors. So I actually would have thought there are various different options. And I’ve used cetuximab in exactly this patient population here, trying to induce anatomical shrinkage of metastases.
And I think this is one of the most intriguing results that can come out of RTOG-8405, for practical management. Is this a perceived difference in response rate difference? Or is it something real? I think this is an answer that 8405 can give and will give. The question is, let’s say, if there was a stronger anatomical response for cetuximab. Does this really translate into more liver surgery, more curative approaches for patients? We do know that.