Hello from hot and humid NYC!
I am 10 months post stem cell transplant, achieving stringent complete remission (sCR). Currently on maintenance regimen of Velcade sub-q biweekly, 12 mg dex, also biweekly, plus 5 mg Revlimid on 21-day cycle. Maintenance began in March.
Beginning last December, I began to have oligoclonal banding, mostly IgG kappa or lambda, sometimes both. My original diagnosis was IgA kappa light chain.
A couple of months ago, the banding disappeared. My last bloodwork showed the reappearance of a faint band of IgG kappa, no M-spike. Free light chains are normal – kappa 9, lambda 12, ratio 0.75.
My question is about the reappearance of the IgG kappa. Do oligoclonal bands sometimes behave this way? My hem/onc says he is not concerned at this point. Of course, I am worried that this could be a new clone developing.
Thanks in advance for any input from the group.
Forums
Re: Oligoclonal banding post stem cell transplant
Ellen:
What, if anything, have you learned about your "banding" situation? Has anything new developed since you last wrote in August? Although I have not had a transplant, I may be experiencing something similar to you in that recently a very faint band of IgG kappa appeared on the Immunofixation test, whereas at diagnosis I was IgA kappa. I had achieved a complete response on drug therapy alone. My doctors think the appearance of the IgG kappa may just be a transient development, but we may know more after additional testing.
If others in the forum have information on this issue, I would appreciate your input, too. Perhaps you can refer me to other forum threads where the matter is discussed. I am aware of one article presented here that discusses "banding," but mostly in the context of post-transplant developments. I am having a hard time locating information on the Internet. Many thanks.
What, if anything, have you learned about your "banding" situation? Has anything new developed since you last wrote in August? Although I have not had a transplant, I may be experiencing something similar to you in that recently a very faint band of IgG kappa appeared on the Immunofixation test, whereas at diagnosis I was IgA kappa. I had achieved a complete response on drug therapy alone. My doctors think the appearance of the IgG kappa may just be a transient development, but we may know more after additional testing.
If others in the forum have information on this issue, I would appreciate your input, too. Perhaps you can refer me to other forum threads where the matter is discussed. I am aware of one article presented here that discusses "banding," but mostly in the context of post-transplant developments. I am having a hard time locating information on the Internet. Many thanks.
Re: Oligoclonal banding post stem cell transplant
Mrozdav,
It's nice to know people on the forum go back and read older postings! Here is what has happened with regard to my oligoclonal banding:
For the most part, it has disappeared. I think I may have had one more instance of it since August, but it was transient. I am still waiting for all of the blood work from my last doctor visit, which was about 10 days ago. If anything changes, I will post about it on this thread. I was still in stringent complete remission (sCR) as of March 11. I get a full myeloma panel every two weeks, which I know is a lot, but I am a very nervous nelly, so my doctor runs everything when I come in for my maintenance Velcade / dex every two weeks.
My maintenance regimen has changed since this post; I am no longer on Revlimid due to side effects, but have continued with the biweekly Velcade and IV dex (12 mg), as mentioned above. My hem/onc was not sure the side effects I was experiencing was from the Revlimid (muscle inflammation and pain, cramping, elevated CPK – which sent me to the emergency room the pain was so bad), but I feel a lot better, so it must have been the culprit. In fact, the doc took me off ALL maintenance meds, and wanted to just watch and wait, but I was not comfortable with that approach based upon my research and reading, a lot of which came from the Beacon, (thank you, Beacon!). I had addition chromosome 1 at diagnosis, which is considered high-risk by many myeloma experts.
I have also read that the oligoclonal banding CAN occur after treatment with the novel agents even without transplant, so it could be a result of that. I am interested in finding out if this has just appeared, or how long you have it, and do you have a measurable m-spike? How are your light chains? Are you currently on any treatment? Is the rest of you blood work good?
Please let us know how things go for you. I am interested in the follow up.
Ellen Harris
It's nice to know people on the forum go back and read older postings! Here is what has happened with regard to my oligoclonal banding:
For the most part, it has disappeared. I think I may have had one more instance of it since August, but it was transient. I am still waiting for all of the blood work from my last doctor visit, which was about 10 days ago. If anything changes, I will post about it on this thread. I was still in stringent complete remission (sCR) as of March 11. I get a full myeloma panel every two weeks, which I know is a lot, but I am a very nervous nelly, so my doctor runs everything when I come in for my maintenance Velcade / dex every two weeks.
My maintenance regimen has changed since this post; I am no longer on Revlimid due to side effects, but have continued with the biweekly Velcade and IV dex (12 mg), as mentioned above. My hem/onc was not sure the side effects I was experiencing was from the Revlimid (muscle inflammation and pain, cramping, elevated CPK – which sent me to the emergency room the pain was so bad), but I feel a lot better, so it must have been the culprit. In fact, the doc took me off ALL maintenance meds, and wanted to just watch and wait, but I was not comfortable with that approach based upon my research and reading, a lot of which came from the Beacon, (thank you, Beacon!). I had addition chromosome 1 at diagnosis, which is considered high-risk by many myeloma experts.
I have also read that the oligoclonal banding CAN occur after treatment with the novel agents even without transplant, so it could be a result of that. I am interested in finding out if this has just appeared, or how long you have it, and do you have a measurable m-spike? How are your light chains? Are you currently on any treatment? Is the rest of you blood work good?
Please let us know how things go for you. I am interested in the follow up.
Ellen Harris
Re: Oligoclonal banding post stem cell transplant
Hi Ellen and Mrozdav,
I don't think this is strictly correct, but I always think of "oligoclonal banding" and 'secondary MGUS" as being basically the same thing. So you my find the forum discussions on secondary MGUS to be helpful in addition to the discussions on oligoclonal banding.
Here are links that will take you to previous forum discussions on related topics. I think you will find many of the discussions helpful.
Oligoclonal banding (search for "oligoclonal" in thread title):
https://myelomabeacon.org/forum/search.php?keywords=oligoclonal&terms=all&author=&sc=1&sf=titleonly&sr=topics&sk=t&sd=d&st=0&ch=300&t=0&submit=Search
Secondary MGUS (search for "secondary mgus" in thread title):
https://myelomabeacon.org/forum/search.php?keywords=secondary+mgus&terms=all&author=&sc=1&sf=titleonly&sr=topics&sk=t&sd=d&st=0&ch=300&t=0&submit=Search
Hope this helps.
I don't think this is strictly correct, but I always think of "oligoclonal banding" and 'secondary MGUS" as being basically the same thing. So you my find the forum discussions on secondary MGUS to be helpful in addition to the discussions on oligoclonal banding.
Here are links that will take you to previous forum discussions on related topics. I think you will find many of the discussions helpful.
Oligoclonal banding (search for "oligoclonal" in thread title):
https://myelomabeacon.org/forum/search.php?keywords=oligoclonal&terms=all&author=&sc=1&sf=titleonly&sr=topics&sk=t&sd=d&st=0&ch=300&t=0&submit=Search
Secondary MGUS (search for "secondary mgus" in thread title):
https://myelomabeacon.org/forum/search.php?keywords=secondary+mgus&terms=all&author=&sc=1&sf=titleonly&sr=topics&sk=t&sd=d&st=0&ch=300&t=0&submit=Search
Hope this helps.
-

Jonah
Re: Oligoclonal banding post stem cell transplant
ME Alejandre, "Oligoclonal bands and immunoglobulin isotype switch during monitoring of patients with multiple myeloma and autologous hematopoietic cell transplantation: a 16-year experience," Clinical Chemistry and Laboratory Medicine, May, 2010 (full text of article)
Abstract:
Background: Over the last 20 years, high dose therapy followed by hemopoietic stem cell transplantation has been employed in patients with multiple myeloma (multiple myeloma). During 16 years of follow-up, the degree of tumor response and survival in 238 patients with autologous stem cell transplantation (ASCT) and changes in the serum protein electrophoretic pattern were analyzed.
Methods: Agarose gel electrophoresis with densitometric analysis and immunofixation were performed to evaluate serum monoclonal protein. IgM, IgA, IgG and β2-microglobulin (β2M) were quantitated. Urine protein electrophoresis with IF was performed on cellulose acetate gel using colloidal silver staining without concentrating.
Results: After 34 months of follow-up (range 1–160 months), eight patients (3.4%) showed a distinct monoclonal protein band that was different from their original isotype switch. This was observed to be a transient phenomenon (22.2 months). Thirty-seven patients (15.5%) developed oligoclonal bands (OB) between the first and the twentieth month after ASCT (mean 4.4 months), which persisted for 7.9 months (1–36 months). The mean overall survival time was statistically different (p<0.05) between the group with OB and the group without them. Mean values of serum albumin, β2M, and non-involved immunoglobulins did not show statistical differences.
Conclusions: The occurrence of OB could be a potential favorable prognostic marker after transplantation due to the prolonged survival observed. Close follow-up of anomalous protein bands, either in serum or urine, is essential due to the additional difficulty in interpretation when the therapeutic response and evolution are evaluated.
Abstract:
Background: Over the last 20 years, high dose therapy followed by hemopoietic stem cell transplantation has been employed in patients with multiple myeloma (multiple myeloma). During 16 years of follow-up, the degree of tumor response and survival in 238 patients with autologous stem cell transplantation (ASCT) and changes in the serum protein electrophoretic pattern were analyzed.
Methods: Agarose gel electrophoresis with densitometric analysis and immunofixation were performed to evaluate serum monoclonal protein. IgM, IgA, IgG and β2-microglobulin (β2M) were quantitated. Urine protein electrophoresis with IF was performed on cellulose acetate gel using colloidal silver staining without concentrating.
Results: After 34 months of follow-up (range 1–160 months), eight patients (3.4%) showed a distinct monoclonal protein band that was different from their original isotype switch. This was observed to be a transient phenomenon (22.2 months). Thirty-seven patients (15.5%) developed oligoclonal bands (OB) between the first and the twentieth month after ASCT (mean 4.4 months), which persisted for 7.9 months (1–36 months). The mean overall survival time was statistically different (p<0.05) between the group with OB and the group without them. Mean values of serum albumin, β2M, and non-involved immunoglobulins did not show statistical differences.
Conclusions: The occurrence of OB could be a potential favorable prognostic marker after transplantation due to the prolonged survival observed. Close follow-up of anomalous protein bands, either in serum or urine, is essential due to the additional difficulty in interpretation when the therapeutic response and evolution are evaluated.
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NKH
Re: Oligoclonal banding post stem cell transplant
Thank you all for your such helpful responses. I feel a little more encouraged after reading the suggested materials. My consultation with my specialist at Hopkins is in two weeks and I will report back what I learn.
Ellen, for about ten months my IFE and SPEP results have been normal, but I do believe that there was immunosuppression because for a few months all three of my immunoglobulins were below normal. Then they normalized. For a couple of months, although my kappa light chain was fine, my lambda was below normal, but that, too, is now normal and my ratio is well within normal range.
The blood test at the end of this February resulted in all normal results except for the IFE, which reported – for the first time – a very light band of IgG kappa in the cathodal region (I still am not sure what that means exactly). No M-spike was reported on the SPEP. My original diagnosis, as I stated earlier, was IgA kappa.
Just last week I had more testing done. I am still waiting for the IFE result, but the other results are in. Blood work is generally very good. Kappa and lambda light chains are normal, as is the ratio. My three immunoglobulins are fine except for the IgA, which has dipped slightly below normal range at 78 mg/dL (82- 453 mg/dL). The SPEP states: "The gamma region contains a faint M-spike of 0.11 g/dL. (I am assuming that the M-spike refers to the IgG and not to the IgA).
I am on subq Velcade injections once every two weeks and Zometa once every three months.
Please do post more about any new developments and what you learn from your doctor about this issue. It looks like we are not alone. And I am beginning to understand a little better what my specialist meant when she used the term "transient." I am really glad for you that your banding issue seems to have disappeared. m
Ellen, for about ten months my IFE and SPEP results have been normal, but I do believe that there was immunosuppression because for a few months all three of my immunoglobulins were below normal. Then they normalized. For a couple of months, although my kappa light chain was fine, my lambda was below normal, but that, too, is now normal and my ratio is well within normal range.
The blood test at the end of this February resulted in all normal results except for the IFE, which reported – for the first time – a very light band of IgG kappa in the cathodal region (I still am not sure what that means exactly). No M-spike was reported on the SPEP. My original diagnosis, as I stated earlier, was IgA kappa.
Just last week I had more testing done. I am still waiting for the IFE result, but the other results are in. Blood work is generally very good. Kappa and lambda light chains are normal, as is the ratio. My three immunoglobulins are fine except for the IgA, which has dipped slightly below normal range at 78 mg/dL (82- 453 mg/dL). The SPEP states: "The gamma region contains a faint M-spike of 0.11 g/dL. (I am assuming that the M-spike refers to the IgG and not to the IgA).
I am on subq Velcade injections once every two weeks and Zometa once every three months.
Please do post more about any new developments and what you learn from your doctor about this issue. It looks like we are not alone. And I am beginning to understand a little better what my specialist meant when she used the term "transient." I am really glad for you that your banding issue seems to have disappeared. m
Re: Oligoclonal banding post stem cell transplant
Hi folks,
As another data point for you, I had oligoclonal banding for awhile after I went into CR.
The first report of oligoclonal banding for me was in July 2014 and the last in November 2014. So it was a temporary phenomenon for me, as for most people who have it. I had an auto stem cell transplant in May 2013 and began Revlimid maintenance in September 2013, which I'm still on. As NKH's reference says, oligoclonal banding seems to be a positive prognostic marker. And bearing that out, I am still in CR with MRD negative as of my last bone marrow biopsy in August of last year. I'm very fortunate!
One other comment - I might be off on this, but I think there is a slight difference between oligoclonal banding and secondary MGUS. The distinction is that there are multiple bands present in oligoclonal banding, but only one band (different from your original band) present in secondary MGUS.
Best wishes,
Mike
As another data point for you, I had oligoclonal banding for awhile after I went into CR.
The first report of oligoclonal banding for me was in July 2014 and the last in November 2014. So it was a temporary phenomenon for me, as for most people who have it. I had an auto stem cell transplant in May 2013 and began Revlimid maintenance in September 2013, which I'm still on. As NKH's reference says, oligoclonal banding seems to be a positive prognostic marker. And bearing that out, I am still in CR with MRD negative as of my last bone marrow biopsy in August of last year. I'm very fortunate!
One other comment - I might be off on this, but I think there is a slight difference between oligoclonal banding and secondary MGUS. The distinction is that there are multiple bands present in oligoclonal banding, but only one band (different from your original band) present in secondary MGUS.
Best wishes,
Mike
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mikeb - Name: mikeb
- Who do you know with myeloma?: self
- When were you/they diagnosed?: 2009 (MGUS at that time)
- Age at diagnosis: 55
Re: Oligoclonal banding post stem cell transplant
Mikeb,
Others have written about secondary MGUS here (I am thinking of Goldmine), but I do not think I understand what that means. Seeking clarification:
1) Is secondary MGUS another disease, a precursor to a different form of myeloma than what one initially had?
2) If you have secondary MGUS, are you faced with the possibility of it developing into smoldering myeloma and then active myeloma at a future date?
3) Does it mean that if you started out with IgA kappa myeloma, went into complete remission, and then developed secondary MGUS with IgG kappa while still in remission, at some point both types could co-exist in your blood as monoclonal proteins signifying different active myelomas?
Perhaps my questions are redundant, but I am trying to get a handle on this. I appear to have only one band resulted from my IFE test. Thanks. m
Others have written about secondary MGUS here (I am thinking of Goldmine), but I do not think I understand what that means. Seeking clarification:
1) Is secondary MGUS another disease, a precursor to a different form of myeloma than what one initially had?
2) If you have secondary MGUS, are you faced with the possibility of it developing into smoldering myeloma and then active myeloma at a future date?
3) Does it mean that if you started out with IgA kappa myeloma, went into complete remission, and then developed secondary MGUS with IgG kappa while still in remission, at some point both types could co-exist in your blood as monoclonal proteins signifying different active myelomas?
Perhaps my questions are redundant, but I am trying to get a handle on this. I appear to have only one band resulted from my IFE test. Thanks. m
Re: Oligoclonal banding post stem cell transplant
Mrozdav,
I understand your confusion since secondary MGUS is a confusing and not a well-understood phenomenon. It is also referred to as atypical serum immunofixation patterns (ASIP).
The basic idea is that for some unknown reason some patients produce a benign detectable M-spike post-transplant, or less frequently post-treatment with novel drugs such Velcade and Revlimid. It does not develop into a new cancerous myeloma isotope.
One of the difficulties is trying to distinguish between true secondary MGUS and a new cancerous myeloma clone. There are no clear answers to these questions that I have found other than to carefully monitor other signs of relapse.
If you do a Google search of secondary MGUS and ASIP you will find a number of studies that discuss this subject.
I understand your confusion since secondary MGUS is a confusing and not a well-understood phenomenon. It is also referred to as atypical serum immunofixation patterns (ASIP).
The basic idea is that for some unknown reason some patients produce a benign detectable M-spike post-transplant, or less frequently post-treatment with novel drugs such Velcade and Revlimid. It does not develop into a new cancerous myeloma isotope.
One of the difficulties is trying to distinguish between true secondary MGUS and a new cancerous myeloma clone. There are no clear answers to these questions that I have found other than to carefully monitor other signs of relapse.
If you do a Google search of secondary MGUS and ASIP you will find a number of studies that discuss this subject.
-

goldmine848 - Name: Andrew
- When were you/they diagnosed?: June 2013
- Age at diagnosis: 60
Re: Oligoclonal banding post stem cell transplant
Goldmine848:
Thank you for your response. I went back and reread your earlier postings on this issue. They have helped me a lot to understand the whole matter. Always something new to worry about.
Thank you for your response. I went back and reread your earlier postings on this issue. They have helped me a lot to understand the whole matter. Always something new to worry about.
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