TRANSCRIPT
Ghassan Abou-Alfa: Thank you very much, everybody. It's so nice to see you all at a little bit of a different ASCO this year. My name is Ghassan Abou-Alfa from Memorial Sloan Kettering Cancer Center in New York.
You are all at ASCO, but you are virtually all at ASCO, so we're together and far away from each other. I hope you're having a great meeting.
Actually, it's quite exciting in regard to hepatocellular carcinoma. There's a lot of things going on. If anything, now we have subjects that we can discuss in regard to the disease.
We have seen quite interesting data in regard to some of the TKIs, among which is anolitinib and at the same time also apatinib. Quite interesting data, but if anything, there was some differentiation here in regard to etiology of the disease being hepatitis B, for example, prior exposure to chemotherapy, and many others that, again, Dr. Meyer tried to help us dissect one way or the other.
That will actually bring me to the second point I would like to discuss today, which is what we have been thinking for the last 15 -- and maybe even before years -- is the disease will differ based on etiology.
This is again, one more time that we this delineation as we have seen it before that with Dr. Abby Chang when we did the sunitineb versus sorafenib, looking at the sorafenib arm.
We have seen it with Dr. Rouge looking at the sorafenib in regard to hepatitis C versus hepatitis B. I, myself and others have spoken about it and wrote about it quite a bit of times. And, if anything, we always thought that these are different diseases.
This dimension is still being looked at, intriguing us to try to analyze it further. But I would say there is a newer dimension which we have to be very attentive to and look into it more carefully, which is after all probably hep-B versus hep-C, when the disease develops versus NASH, versus alcohol. It's really the same flavors of the same disease.
I think a more important component is what we have seen with the AC-22 analysis, which is, who are those patients that respond the best? Who are the patients who don't respond that well?
What should be the directives that they have within their tumor in regard, as we just mentioned, to the CD3, CD, the Ki67, the PD-1 expression? Which, by the way, has been looked at also in our study, and we have seen that it always shared best with the patient with more than one-percent PD-1 expression. What about Fc gamma receptors?
I think this is going to probably bring an interesting, multidimensional approach that will tell us that this specific patient with the following features in regard to the tumor will probably fair best on this specific therapy.
