ASCO 2013: A Call for New Ways of Thinking
LIVE from ASCO 2013
It's huge.
It's crazy.
It's crowded.
But boy is there a ton of new research to share.
While ibrutinib and idelalisib have kicked open the door to explore new less toxic pathways to control not just CLL, not other B cell cancer, they did not close the door behind them.
Novel pathway inhibitors beyond PI3K and BTK and BCL-2 are being explored and being explored in novel ways with more open access.
New and potentially potent BTK and PI3K inhibitors are in trials now.
Combinations are being considered.
Dr. Wiestner said these new drugs offer us the opportunity to think in new ways.
Hence my disappointment when I hear speakers rightly celebrate the lack of bone marrow suppression with these new targeted therapies, but then got all excited about how that allows them to pile on the old school bone marrow damaging chemotherapy. Maybe we do need to go in that direction, but can't we try to leverage the low toxicity of these drugs but adding other low toxicity agents to them, offering patients like us gentler and less risky control of our disease.
I like the idea of adding together more than one TKI or adding a monoclonal antibody or an IMID.
In my book, adding in bendamustine or fludarabine or chlorambucil or their ilk should make a significant difference in outcomes to justify the additional downside risk.
I understand the temptation to revert to tried and true paths. And it might turn out to be the best call. Medicine must be both conservative and progressive.
But we have a sea change, a paradigm shift, happening in CLL. Let's try to keep innovating and exploring using the kind of thinking that got us the breakthroughs with ibrutinib and idelalisb and ABT-199.
That is the next stage of research that has me excited.
That is the future that I want for all of us.
It's huge.
It's crazy.
It's crowded.
But boy is there a ton of new research to share.
While ibrutinib and idelalisib have kicked open the door to explore new less toxic pathways to control not just CLL, not other B cell cancer, they did not close the door behind them.
Novel pathway inhibitors beyond PI3K and BTK and BCL-2 are being explored and being explored in novel ways with more open access.
New and potentially potent BTK and PI3K inhibitors are in trials now.
Combinations are being considered.
Dr. Wiestner said these new drugs offer us the opportunity to think in new ways.
Hence my disappointment when I hear speakers rightly celebrate the lack of bone marrow suppression with these new targeted therapies, but then got all excited about how that allows them to pile on the old school bone marrow damaging chemotherapy. Maybe we do need to go in that direction, but can't we try to leverage the low toxicity of these drugs but adding other low toxicity agents to them, offering patients like us gentler and less risky control of our disease.
I like the idea of adding together more than one TKI or adding a monoclonal antibody or an IMID.
In my book, adding in bendamustine or fludarabine or chlorambucil or their ilk should make a significant difference in outcomes to justify the additional downside risk.
I understand the temptation to revert to tried and true paths. And it might turn out to be the best call. Medicine must be both conservative and progressive.
But we have a sea change, a paradigm shift, happening in CLL. Let's try to keep innovating and exploring using the kind of thinking that got us the breakthroughs with ibrutinib and idelalisb and ABT-199.
That is the next stage of research that has me excited.
That is the future that I want for all of us.
Labels: ASCO 2013, chemotherapy, ibrutinib, Idelalisib, low toxicity
posted by Brian Koffman at
10:39 PM
4 Comments:
Brian,
Excellent commentary from your observations at ASCO. You write about speakers who express disappointment about the lack of bone marrow surpression from the new crop of kinase inhibitors and I'll wager they have never had CLL/SLL.
I am perhaps one of the slower patients to respond if one looks at just how fast my peripheral blood tumor burden, as reflected by ALC, is going down but I would think a slow process of tumor reduction would be considered a GOOD thing. Less shock to the system and specifically the kidneys. On top of that, all patients I have talked with including myself, have remarked at how rapidly one feels so good after getting Ibrutinib even as one gets the predicted temporary rise in lymphocyte count early in the course of the Clinical Trial.
Ibrutinib sure beats the dyspnea, chronic coughing, heart arrhythmias and near fatal kidney failure with my previous Treatments of FR and HD-RTX .
WWW
OOPS...
Trying to write too fast. I meant to emphasize your disappointment in speakers feeling it was a great idea to be able to add on marrow suppressing chemos to kinase inhibitor therapies because the kinase inhibitors alone DO NOT suppress the marrow.
That line of thinking is at least as bad as my sloppy inattention to what I was expressing in my previous post.
WWW
Thank you Brian for all your comments and especially your video interviews with CLL experts. You are an invaluable resource.
Great insights and exciting developments! Thanks for all you are doing for all of us... It is really invaluable.
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