Exploring Disease Risk and Treatment Options for CML

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Topics include: Treatment and Understanding

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Dr. Michael Deininger, chief of hematology at the Huntsman Cancer Institute at the University of Utah, explores ongoing research to fine-tune treatment for CML. Dr. Deininger discusses second-generation TKIs in frontline therapy, considerations for switching or ceasing medication, and the need to refine molecular testing into a sophisticated, reliable prognostic method.

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Please remember the opinions expressed on Patient Power are not necessarily the views of our sponsors, partners or Patient Power. Our discussions are not a substitute for seeking medical advice or care from your own doctor.  Please have this discussion with your own doctor. That’s how you’ll get care that’s most appropriate for you.

Another I think focus of the meeting is to see whether there are patients where we can stop treatment altogether, so patients in whom the response will be maintained in the absence of any active treatment.  And that’s of obviously--that’s obviously of major interest for the community and for an increasing number of patients who live long, have excellent responses but have to continue taking the drugs. 

And a third I--I think interesting development is the third-line inhibitors for resistant disease.  So in other words we are interested in improving results in the very good responders to a degree that allows us to stop treatment altogether, and on the other extreme of the spectrum there are people with very aggressive disease where we try to push the envelope towards, you know, inducing remissions in these patients who failed other inhibitors.  And I think there are some interesting drugs developing along these lines. 

What we haven’t seen yet is an impact on overall survival, so I think it needs to be balanced with each other.  We certainly see a reduction of relapse rate, and the expectation is that this will translate into an overall survival benefit at some point, but it will require more observation time. 

It should also be noted that there are differences in terms of response according to the individual patient’s risks.  So low-risk patients tend to do very well on Gleevec, or imatinib.  High-risk patients tend to do less well on imatinib and may be prime candidates for drugs like nilotinib or dasatinib. 

And obviously one approach to that is to use genome-wide scanning techniques to get at the genomic makeup of bad disease versus good risk disease.  And we’ve done some work along these lines.  Other labs [have] also worked along these lines.  So I think we are getting closer to defining high-risk disease on a molecular basis, but we need to do more work, and it needs to be done within a prospective study.  So one appeal of course to everyone in the CML community is to not, you know, start--stop thinking about clinical trials in CML because it’s a disease that is easily treated in the general practice.  If we want to make progress and really put this disease on the heap of history we’ve got to continue these studies, and enrollment in clinical trials is the very basis for that. 

So does that correlate or is that equivalent to a cure?  Well, the answer is we don’t really know.  There is no way of knowing whether in these patients there are still sleeping residual leukemia cells, or whether they--the clone has died out, has just been subject to death by attrition over time.  In reality, we’ll never be able to know that because it’s just a limitation of sensitivity, and maybe any successful cancer treatment is just like that.  We will never know whether we’ve got all the cancer cells. 

But for practical purposes these patients have been maintaining their responses now for--for long periods of time, so I think that there is something that clearly needs to be exploited.  And we need to understand who are these patients who will be able to maintain their responses and can we--can we--is there wiggle room for us.  Can we improve from therapeutic side?  So maybe the exciting thing about the new inhibitors is that they do increase the number of patients who achieve undetectable disease, which is arguably the basis to even think about stopping the drug. 

The only exception to this rule to some extent is if your blood counts drop very low.  That is a more repetitive theme, so if you have that maybe you just don’t have enough normal marrow to make up for the dying leukemia cells, and that of course is going to occur with any agent.  But just like with a number of other things where you have therapeutic choices it’s a good thing for the patient to have because, you know, you just figure out what works best for you. 

So these leukemia stem cells we need to learn better how to characterize them, how to define their survival signals that allow them to hibernate in the presence of a TKI, and I think this is a major challenge to the field.  It’s not easy to study that, but I think we’ll see incremental progress over the next few years.  And maybe at some point we’ll turn CML into a disease that, you know, you had it at some point in your life and now it’s a thing of the past. 

 

Please remember the opinions expressed on Patient Power are not necessarily the views of our sponsors, partners or Patient Power. Our discussions are not a substitute for seeking medical advice or care from your own doctor.  Please have this discussion with your own doctor. That’s how you’ll get care that’s most appropriate for you.

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