Key CML research from ASH 2010

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Published: 18 Feb 2011
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Jan Geissler - Co-Founder, CML Advocates Network
Jan Geissler speaks about some of the key research into chronic myeloid leukaemia (CML) that has been presented at ASH 2010. This includes papers on the second generation tyrosine kinase inhibitors dasatinib, erlotinib and ponatinib, a poster presentation indicating that imatinib treatment does not increase the incidence of secondary cancers and research reiterating the importance of patients strictly adhering to their treatment programme.

2010 American Society of Hematology 3rd - 7th December

Interview with Jan Geissler - Co-Founder, CML Advocates Network

Key CML research from ASH 2010

IV                     Interviewer

JG                    Jan Geissler



IV         This is ecancer TV reporting live from the American Society of Hematology annual meeting right here in Orlando. Chronic myeloid leukaemia is a big topic, and Jan Geissler, you’re an expert on it because you’ve been treated for it, and you’ve scanned and looked for some of the important developments being reported right here at ASH meeting. Could I ask you, first of all, about the new data on the second-generation TK inhibitors, the imatinib replacements? What have you found about the new data, using these in frontline therapy?


JG        I think the new data is very impressive from a patient perspective. Both have been reported now for 18 months, and both have shown that the progressions are much more scarce, much more rare, than on imatinib, and I think that gives a lot of hope that people can take that as a first-line treatment and not progress into advanced disease.


IV         And new agents, of course, figure here too. There’s an agent called Ponatinib. What’s happening here?


JG        That’s quite impressive, because the first time the phase one data has been presented here, and there is a proportion of patients which are resistant against all the proved drugs in CML at the moment, so dasatinib, nilotinib and imatinib, and this drug seems to be effective on all of them, so all of the patients in that trial have responded and have had a major genetic response, and this is really reassuring; that there’s an option for those patients with that certain resistance.


IV         So what do you think is happening with the second-generation TKIs, and other drugs? Is it getting confusing? Are there too many drugs at the moment?


JG        Well, having options is always good for patients, and I think there’s a solution, or that there’s an approach for almost every patient, and I think that is very good.


IV         You found some reassuring evidence about second cancers on patients being treated with Imatinib. What was that?


JG        There’s a poster presented here at ASH, which basically shows that on imatinib there was no additional occurrence of secondary malignancies, so other tumours in those taking Imatinib, and of course there was a big worry in the patient community that taking TKIs in the long run might cause additional cancer, additional malignancies, and that is good news for us.


IV         Adherence to therapy is another issue, and there’s some news on that, isn’t there/


JG        Yes. There’s been new data coming from Hammersmith, which showed a clear correlation between those adherent on therapy and those less than 90% adherent on therapy, so taking the drugs they’ve been prescribed; there was a clear correlation that people lost their response because they were not taking the drugs. And I think we need to take it very serious in the patient community and the professional community, that this is a series issue.


IV         So adherence needs to be improved?


JG        Oh, yes. I think it’s a big issue. Because patients never had the experience of big symptoms with CML, so they might not take the treatment in long-term so serious… might not take the drugs, and I think we need to work from both perspectives: from the doctors and the patient’s community to tell about the consequences.


IV         Now, new drugs for CML is a fascinating area, of course, but we’ve got an old one here: Interferon alpha, and the word cure has been associated with it.


JG        Well, Interferon has indeed been into therapy which has been around for long, but we know about the immune stimulating effects of Interferon, and there’s a new presentation here at Ash on a poster, that had shown that despite there’s a residual number of leukaemic stem cells, people can maintain over a decade or two, in remission, and I think that’s good news because probably eradication of the disease is not that… the main goal to stop therapies.


IV         Do you feel that there is a chance of cure?


JG        I hope so. I mean we see a lot of progress on the biological side of research, as well as in clinical development, and I think there’s a chance; I really hope there is a chance in the next ten years to achieve a cure for CML.


IV         And there’s some news about new drugs in children and adolescents. They’re not a big population who… with CML, but an important one.


JG        It’s an ultra rare disease, so there’s only a very small number of cases worldwide of CML in children. But still, I think they respond very well to TKIs, but the problem is that there’s an impact on the growth of these kids before puberty, and at this Ash, again there’re presentations about that. And I think it’s very important that for such a rare disease trials are being made, and efforts are being made to help these children, because of course they should have the chance to become AD as well.


IV         So what’s your feeling about the way things are going for chronic myeloid leukaemia, based on your quick dip into the news here at the American Society of Hematology?


JG        I think I’m very positive. I mean CML, there has been major progress in CML treatment over the past ten years, which is incredible, and we are very happy about it. But still, it’s not a tick box, so there are patients that run resistance, patients that are diagnosed in already advanced disease, and so on, people getting certain type of resistance where the approved drugs don’t work. So there’s a lot of things where still research is needed, and I’m going home with a very good feeling that research is working very well on that.


IV         Well, Jan Geissler, co-founder of the CML Advocates Network, thank you very much for joining us here on ecancer TV.


JG        Thank you.