I've been on maintenance Revlimid (10 mg daily) for 13 months now. My numbers have remained low and stable. With my history of quick relapse, I assume I will stay on this therapy until it stops working.
I want to know if it would be a good idea to change therapies before my myeloma become resistant to Revlimid. Would changing to carfilzomib (for example) for 3-4 months, and then back to maintenance Revlimid be a good idea?
Wouldn't this make Revlimid last longer as an effective maintenance drug for me?
Thanks, Stann
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Re: resistance to Revlimid
Stann,
You pose an interesting question. You titled this resistance to Rev, have you experienced resistance,? It sounds like your labs are good.
I have questions about maintenance...are you on lenalidomide alone? i.e. no steroids.
How are your labs. Are you having symptoms.
I want to hear about that, from everyone here at the forum on maintenance lenalidomide.
It would also be nice if the clinicians who treat multiple myeloma would provide commentary on what they are seeing clinically, in terms of signs/symptoms, with their patients on lenalidomide maintenance.
I too am on 10mg Rev maintenance (6months). I am experiencing significant dependent edema, i.e. ankle swelling and pitting edema. Weight gain, and what I think is steroid belly is not going away and I wonder if that is lenalidomide. I also have had aching joints. My labs continue to be exceptionally in terms of showing disease...all are zero.
Have you had any symptoms on maintenance?
What do you mean when you say quick relapse, are you what is considered 'high risk'? What therapeutic regimens were you on prior to relapse?
Personally, the results from carfilzomib therapy are so exceptionally, that if I were in your shoes, I would ask for 6 cycles of it. And yes, I would do that without relapse. I would also do all the most sensitive labs, multiparametric cytometry along with IFE.
Have you ever had a CR or sCR? Are you considered 'high risk' based on cytogenetics?
The jury, as you know, is still out on maintenance Rev. Personally, I am in a trial that includes maintenance and I have some concerns, but those are outweighed by what I perceive as the benefits. However, lenalidomide is excreted soley by the kidneys...and that is now giving rise to some concern on my part given the edema.
Just my thoughts...I truly have more questions than answers...and await your feedback.
You pose an interesting question. You titled this resistance to Rev, have you experienced resistance,? It sounds like your labs are good.
I have questions about maintenance...are you on lenalidomide alone? i.e. no steroids.
How are your labs. Are you having symptoms.
I want to hear about that, from everyone here at the forum on maintenance lenalidomide.
It would also be nice if the clinicians who treat multiple myeloma would provide commentary on what they are seeing clinically, in terms of signs/symptoms, with their patients on lenalidomide maintenance.
I too am on 10mg Rev maintenance (6months). I am experiencing significant dependent edema, i.e. ankle swelling and pitting edema. Weight gain, and what I think is steroid belly is not going away and I wonder if that is lenalidomide. I also have had aching joints. My labs continue to be exceptionally in terms of showing disease...all are zero.
Have you had any symptoms on maintenance?
What do you mean when you say quick relapse, are you what is considered 'high risk'? What therapeutic regimens were you on prior to relapse?
Personally, the results from carfilzomib therapy are so exceptionally, that if I were in your shoes, I would ask for 6 cycles of it. And yes, I would do that without relapse. I would also do all the most sensitive labs, multiparametric cytometry along with IFE.
Have you ever had a CR or sCR? Are you considered 'high risk' based on cytogenetics?
The jury, as you know, is still out on maintenance Rev. Personally, I am in a trial that includes maintenance and I have some concerns, but those are outweighed by what I perceive as the benefits. However, lenalidomide is excreted soley by the kidneys...and that is now giving rise to some concern on my part given the edema.
Just my thoughts...I truly have more questions than answers...and await your feedback.
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suzierose - Name: suzierose
- When were you/they diagnosed?: 2 sept 2011
Re: resistance to Revlimid
Hi Suzie,
I had the low risk chromosomal makeup (I forget which were or weren't deleted) and I also have primary amyloidosis (which hasn't reared its ugly head as far as I can tell).
After a round of VDPACE, my mspike dropped from 3 to 0.5. But within 3 months was back to 2.5.
My multiple myeloma specialist said even though my chromosomal makeup indicated low risk, my "relapse" was the proof in the pudding and he thought I was in the high risk group.
Another round of VDPACE yielded nothing.
2 SCTS dropped me down to .20, where I am now and have been for a year. (never achieved CR)
No more active bone lesions.
I had to drop from 15 mg to 10 mg due to neutrophil and platelet levels dropping. But now all is well. Slightly low WBC and RBC, but nothing alarming.
I am only on Revlimid 10mg--no dex. 13 months and no side effects. (Im 49 so maybe that helps?).
It sure sounds like these therapies are similar to pesticides in terms of resistance. If growers use the same pesticide over and over again, of course you get resistance in the population of whatever you're trying to control. If you rotate and use a pesticide with a different mode of action, you not only continue to control the pest, but you also wipe out any of the pests that may have been in the early stages of developing resistance to the primary pesticide.
I don't understand why that theory wouldn't also apply to myeloma therapy.
I'm glad to hear you are having a good response to carfilzomeb. Good job!
I wonder if you could drop to 5 mg of Revlimid and still maintain CR?
I had the low risk chromosomal makeup (I forget which were or weren't deleted) and I also have primary amyloidosis (which hasn't reared its ugly head as far as I can tell).
After a round of VDPACE, my mspike dropped from 3 to 0.5. But within 3 months was back to 2.5.
My multiple myeloma specialist said even though my chromosomal makeup indicated low risk, my "relapse" was the proof in the pudding and he thought I was in the high risk group.
Another round of VDPACE yielded nothing.
2 SCTS dropped me down to .20, where I am now and have been for a year. (never achieved CR)
No more active bone lesions.
I had to drop from 15 mg to 10 mg due to neutrophil and platelet levels dropping. But now all is well. Slightly low WBC and RBC, but nothing alarming.
I am only on Revlimid 10mg--no dex. 13 months and no side effects. (Im 49 so maybe that helps?).
It sure sounds like these therapies are similar to pesticides in terms of resistance. If growers use the same pesticide over and over again, of course you get resistance in the population of whatever you're trying to control. If you rotate and use a pesticide with a different mode of action, you not only continue to control the pest, but you also wipe out any of the pests that may have been in the early stages of developing resistance to the primary pesticide.
I don't understand why that theory wouldn't also apply to myeloma therapy.
I'm glad to hear you are having a good response to carfilzomeb. Good job!
I wonder if you could drop to 5 mg of Revlimid and still maintain CR?
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Stann
Re: resistance to Revlimid
The concept of switching therapies to try and minimize chemotherapy resistance has been advocated by oncologists in the past for a variety of cancers. There really does not seem to be good evidence that doing so is successful at preventing chemo resistance.
In myeloma, the closest example of this is probably in the "total therapy" regimens, although for the most part the maintenance treatments are continued until progression of disease.
There is also concern alternating therapy will generate a resistant popluation of myeloma cells that will make chemotherapy ineffective when reintroduced after a break from that drug.
My pattern of practice is to continue effective therapy until no longer effective. I think that most myeloma doctors do the same.
In myeloma, the closest example of this is probably in the "total therapy" regimens, although for the most part the maintenance treatments are continued until progression of disease.
There is also concern alternating therapy will generate a resistant popluation of myeloma cells that will make chemotherapy ineffective when reintroduced after a break from that drug.
My pattern of practice is to continue effective therapy until no longer effective. I think that most myeloma doctors do the same.
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Dr. Jason Valent - Name: Jason Valent, M.D.
Beacon Medical Advisor
Re: resistance to Revlimid
Thank you Dr. Valent for you reply.
On a related note, I found an article that was interesting regarding resistance management with cancer treatment. I wonder if there has been any research that specifically has looked at myeloma.
"An analogous situation also occurs in cancer therapy, where cell lineages within a tumor compete for access to space and nutrients. There, the argument has recently been made that less aggressive chemotherapy might sustain life better than overwhelming drug treatment, which simply removes the competitively more able susceptible cell lineages, allowing drug-resistant lineages to kill the host (94, 95). Mouse experiments support this: Conventionally treated mice died of drug-resistant tumors, but less aggressively treated mice survived.
http://www.pnas.org/content/108/suppl.2/10871.full
On a related note, I found an article that was interesting regarding resistance management with cancer treatment. I wonder if there has been any research that specifically has looked at myeloma.
"An analogous situation also occurs in cancer therapy, where cell lineages within a tumor compete for access to space and nutrients. There, the argument has recently been made that less aggressive chemotherapy might sustain life better than overwhelming drug treatment, which simply removes the competitively more able susceptible cell lineages, allowing drug-resistant lineages to kill the host (94, 95). Mouse experiments support this: Conventionally treated mice died of drug-resistant tumors, but less aggressively treated mice survived.
http://www.pnas.org/content/108/suppl.2/10871.full
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stann
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