The news from the LRF Conference and the consultations with my NY doctors
What’s new you ask?
The conference and the meeting with my NY doctors helped clarify my future, even if there was the usual extreme divergence of opinion. Sometimes I think that my survival depends on finding ways to mine the wisdoms of all the different CLL gurus who are often separated by huge chasms in how they approach this illness, a disease so multifaceted that it makes the Hope Diamond look like a glass trinket.
Here is one of the many overly simplistic ways to dice the tomato.
It is fair to say there are two general schools of thought in the CLL community. The futurists and the pragmatists.
The first group’s mantra is that we need to be gentle, we need to avoid risk and toxicity so we can fight again, which we surely need to do.
In the meantime, new wonder drugs are in the pipeline, many of which. like a well scrubbed debutant, had their public coming out at the LRF conference.
They include exciting targeted small molecules that with tight focus interfere with the B cell clone ability to communicate with its neighbors that nourish and protect it from attack and encourage its growth.
New molecules that interfere with its ability to proliferate or with its annoying inability to to die when it gets the signal it is time to self destruct.
New monoclonal that attack more and more specific CLL targets, refusing to say hello and goodbye to even other B cells.
New drugs, often sons and daughters of older ones that modify the immune system in ways not well understood, but that seem to shrink the tumor burden by bringing the cancer to the attention of the authorities.
New gene therapies and vaccines that are finding ways to rekindle the immune systems and getting it to recognize the danger afoot or to resensitize the cancer cells to old killers.
New combinations are being worked out that are smarter with fewer side effects and bigger kill rates.
Watch for more on Cal 101, SYK inhibitors, IMIDs, mTors and others here and at all your favorite CLL haunts.
To these CLL warrior doctors, many of whom split their time between the clinic and the research lab, a stem cell transplant is a blunt weapon, full of certain risk and collateral damage. A must to avoid in all but the most desperate cases. An end game maneuver. If we are smart upfront, we can play this out a long long way. The trick is to avoid drug toxicity and still keep the disease from escaping control.
Don’t let the disease or its treatment kill you with a single fatal blow or a thousand tiny lashes.
Go gently forward. Look at the evidence in the trials and the underlying science. Prod around and don’t always accept the conventional wisdom, but don’t ignore the evidence. Every case is unique.
The brilliant Dr. Furman is of this ilk. He questions everything. He scans the data and needs to be convinced. He is not certain that I even have ITP. Conflicting evidence. He wants to me to hold the IVIG and see what happens. If my platelets fall without the gamma globulin coating to protect them, he recommends Rituxan, but maybe steroids or even a trial of a SYK inhibitor. Works for both CLL and ITP. He is worried about a second transplant and prefers the exciting and cleaner promise of CAL 101 or a revlimid trial. He thinks good old fashion FCR would be a great choice for me with my 11q del. He is not worried about my ITP with the FCR.
The wise and experienced Dr. Rai is more a pragmatist (not that Dr. Furman isn’t practical or Rai isn’t a world class researcher). Last time I saw him he said: DON’T DO ANYTHING STUPID. This time he refused to predict the future. He said every CLL doctor would give you a different opinion. Ain’t that the truth. He said no need to change a winning course. This is definitely ITP because the IVIG is helping. No testing needed. Don’t chase the possible accessory spleens seen on my last CT scans. He says it could be helpful very long term and there are many options if the IVIG stops working. He said I will DEFINITELY need a second transplant. That was as clear as the crystal from which the Queen sips her champagne. He told me that he has had patients that have done very well with a second transplant. He leaves the timing and the path to that to my transplant doctor. That is not his area of expertise, but my tumor load is low now, so there is no urgency. He is strongly against FCR when the time comes to treat the CLL in anticipation of the transplant. He acknowledges that others feel it is safe, but his assessment is that the evidence is weak.
I like most of what Rai has to say. Rai is dealing with what is on the ground now, not what is on the come. The future always looks rosy to the researcher.
I think I will see how long I can ride out the IVIG. Maybe I can stretch the time between treatments to 3 weeks checking Dr. Furman's hypothesis that it may not be ITP by monitoring if my counts falls off a cliff in that extra week without my protein sheath on my platelets.
If it stops working all together, I would like to jump to either HDMP+R for both the CLL and the ITP, then transplant. Or maybe just R to get the ITP whipped into shape, followed by FCR with transplant redux on its heels.
Well, that’s the plan for now.
The conference and the meeting with my NY doctors helped clarify my future, even if there was the usual extreme divergence of opinion. Sometimes I think that my survival depends on finding ways to mine the wisdoms of all the different CLL gurus who are often separated by huge chasms in how they approach this illness, a disease so multifaceted that it makes the Hope Diamond look like a glass trinket.
Here is one of the many overly simplistic ways to dice the tomato.
It is fair to say there are two general schools of thought in the CLL community. The futurists and the pragmatists.
The first group’s mantra is that we need to be gentle, we need to avoid risk and toxicity so we can fight again, which we surely need to do.
In the meantime, new wonder drugs are in the pipeline, many of which. like a well scrubbed debutant, had their public coming out at the LRF conference.
They include exciting targeted small molecules that with tight focus interfere with the B cell clone ability to communicate with its neighbors that nourish and protect it from attack and encourage its growth.
New molecules that interfere with its ability to proliferate or with its annoying inability to to die when it gets the signal it is time to self destruct.
New monoclonal that attack more and more specific CLL targets, refusing to say hello and goodbye to even other B cells.
New drugs, often sons and daughters of older ones that modify the immune system in ways not well understood, but that seem to shrink the tumor burden by bringing the cancer to the attention of the authorities.
New gene therapies and vaccines that are finding ways to rekindle the immune systems and getting it to recognize the danger afoot or to resensitize the cancer cells to old killers.
New combinations are being worked out that are smarter with fewer side effects and bigger kill rates.
Watch for more on Cal 101, SYK inhibitors, IMIDs, mTors and others here and at all your favorite CLL haunts.
To these CLL warrior doctors, many of whom split their time between the clinic and the research lab, a stem cell transplant is a blunt weapon, full of certain risk and collateral damage. A must to avoid in all but the most desperate cases. An end game maneuver. If we are smart upfront, we can play this out a long long way. The trick is to avoid drug toxicity and still keep the disease from escaping control.
Don’t let the disease or its treatment kill you with a single fatal blow or a thousand tiny lashes.
Go gently forward. Look at the evidence in the trials and the underlying science. Prod around and don’t always accept the conventional wisdom, but don’t ignore the evidence. Every case is unique.
The brilliant Dr. Furman is of this ilk. He questions everything. He scans the data and needs to be convinced. He is not certain that I even have ITP. Conflicting evidence. He wants to me to hold the IVIG and see what happens. If my platelets fall without the gamma globulin coating to protect them, he recommends Rituxan, but maybe steroids or even a trial of a SYK inhibitor. Works for both CLL and ITP. He is worried about a second transplant and prefers the exciting and cleaner promise of CAL 101 or a revlimid trial. He thinks good old fashion FCR would be a great choice for me with my 11q del. He is not worried about my ITP with the FCR.
The wise and experienced Dr. Rai is more a pragmatist (not that Dr. Furman isn’t practical or Rai isn’t a world class researcher). Last time I saw him he said: DON’T DO ANYTHING STUPID. This time he refused to predict the future. He said every CLL doctor would give you a different opinion. Ain’t that the truth. He said no need to change a winning course. This is definitely ITP because the IVIG is helping. No testing needed. Don’t chase the possible accessory spleens seen on my last CT scans. He says it could be helpful very long term and there are many options if the IVIG stops working. He said I will DEFINITELY need a second transplant. That was as clear as the crystal from which the Queen sips her champagne. He told me that he has had patients that have done very well with a second transplant. He leaves the timing and the path to that to my transplant doctor. That is not his area of expertise, but my tumor load is low now, so there is no urgency. He is strongly against FCR when the time comes to treat the CLL in anticipation of the transplant. He acknowledges that others feel it is safe, but his assessment is that the evidence is weak.
I like most of what Rai has to say. Rai is dealing with what is on the ground now, not what is on the come. The future always looks rosy to the researcher.
I think I will see how long I can ride out the IVIG. Maybe I can stretch the time between treatments to 3 weeks checking Dr. Furman's hypothesis that it may not be ITP by monitoring if my counts falls off a cliff in that extra week without my protein sheath on my platelets.
If it stops working all together, I would like to jump to either HDMP+R for both the CLL and the ITP, then transplant. Or maybe just R to get the ITP whipped into shape, followed by FCR with transplant redux on its heels.
Well, that’s the plan for now.
Labels: Dr Furman, Dr Rai, LRF Conference Oct 2009
posted by Brian Koffman at
10:34 PM
6 Comments:
Brian, Thank you for a very detailed report of your consultations with two very top CLL medics.
At a transplanted patient meeting I went a few month ago, there were several people that had a second SCT and they were well the second time around.
Judging by my own personal experience if I had to do it all over again, I would not think twice about it, even with the problems I had which I thought were expected I would stiil feel my SCT experience was far easier than the treatments I had in the past, but again we are all different and one has to balance the advantages and disadvangates on an individual basis.
I wish you all the best.
Regards
Chonette
(7 months post SCT)
Certainly no one other than the CLL experts can give you meaningful advice on these decisions.
We all would love to see the discovery of the next initamib. I do believe that one day disease modulators will be found that can meaningfully down-regulate CLL into a chronic disease.
Currently, however, when I review the available data on drugs such as Syk inhibitors, mTor inhibitors, Imids, Cal 101 and BCL inhibitors the reality of the results gets in the way of the "coolness" of their mechanism of action.
Unfortunately, we're just not there yet and most of these drugs (of necessity) have been employed on patients with far advanced disease achieving (usually) little better than 50% responses which are not long lived.
I, too, face a HSCT unless some new therapeutic option evolves. Like you, I wish that I had the luxury of more time before having to pull the trigger.
Good luck,
11qRick
When I was first told of my cytogenetic test results, I asked if enough was known to link a treatment with the results. The answer then, as now, is no. Evidence for this comes from the variable response we have as your case illustrates. If I were in your situation, I would keep asking questions but be wary of any of these advanced treatments because of the unknowns: toxicity as well as mortality.
TomD
Chonette,
Thanks for the encouragement. I know everyone is different, but hearing success stories always helps remind us of what is possible
Be well
Brian
Rick,
Well said. Couldn't agree more.
As we know, studies are often designed to find a "signal" in the sickest and most desperate groups of patients.
Maybe many of these meds would do better in less heavily treated refractory patients, but that is harder to prove ( and get FDA approval ultimately) because we already have choices in those circumstances. Hence, the lower research interest. Follow the money.
Nevertheless it an exciting time to be a CLLer. Something just might break in the next few years Keating is sure a cure is 3-5 years away. From his lips to G-d's ears.
Be well
Brian
TomD
Cytogenetics can not predict an individual's disease course or the response to therapy, but there are a two exceptions.
If you are 17p del, I would avoid F based treatment or at least very closely assess response after a single cycle.
If you are 11q del (like Rick and me), I would strongly favor FCR or FR based on the recent German data.
Delayed and unexpected toxicity is always a concern with new drugs, but also with old ones (delayed CNS infections w R comes to mind)
Be well
Brian
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