Hi,
I was curious regarding the following. There are several T cell depleted allo transplants going on that are supplemented by some form of immunotherapy where cells are grown in the lab and immunized with a protein that is expressed in myeloma cells. The hope is to minimize graft-v-host and maximize graft v myeloma. Other trials have attempted a similar approach with auto transplants and third have relied on a similar approach through vaccinations.
From my layman understanding, the allo transplant potentially carries the highest probability of cure. What I do not understand is why.
Let's say that the modified T cells or lymphocytes that are infused in the patient do indeed successfully kill myeloma. That much I think has been proven that can be done. For there to be a cure, those cells must exhibit the immunized protein over a long period of time.
Is that even possible? Don't cell cycle through your body and continuously replenish? Wouldn't the modified cells simply disappear after several months, a year or so? What then? With the vaccine, I understand that. Also I understand it with immunomodulatory meds like daratumumab. Those you have to continuously take to maintain remission with the hope that your body does not become refractory.
With the modified cells single infusion process I see two problems. One, those cells likely disappear down the road, and two, even if they don't, why wouldn't the patient become refractory just as with all other meds?
In too many words, how the heck would you obtain a cure by doing this unless you know what protein the refractory cells exhibit and target that protein (which if I recall correctly was discovered just last year).
These are probably most suitable for my doc, but all of this popped up in my head after our last meeting and my next meeting (with God's help) is 6 months down the road. I was curious if anyone has pondered these questions.
Also, I'd be curious if anyone has experience with the T cell depleted allo with immunotherapy or lymphocyte infusion.
Thanks all.
Forums
7 posts
• Page 1 of 1
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ivanm - Name: Ivan Mitev
- Who do you know with myeloma?: self
- When were you/they diagnosed?: August, 2011
- Age at diagnosis: 37
Re: T cell depleted transplants and immunotherapy
Hi IvanM,
I will try and answer your question.
I did a partially t cell depleted allogeneic transplant with myeloablative (full) conditioning. I used ATG (antithymocyte globulin) for in vivo t cell depletion. I used a low to moderate dose of ATG and I had Grade 1 acute GVHD [graft versus host disease] and for one month I had limited chronic GVHD after I discontinued my immunosuppressive med (Prograf). It is considered a good thing to have minor GVHD like that because it is a sign that the donor cells were active.
I did not get a DLI [donor lymphocyte infusion] because I attained a molecular response after my allo so we did not feel any more therapy was required. I have not had any chronic GVHD for 2.5 years so that is no longer something I need to worry about. I had no other immunotherapy added.
Note: I had a female donor and of the matched pairs female donor to male recipient is associated with the most immunotherapy and a lower relapse rate, so my doctor did not feel I needed any more immunotherapy other than what I got from the donor immune system.
Sometimes you will hear patients say they found a "perfect match" on the donor registry or they had a sibling that was a perfect match. That is actually not true - the only possible perfect match is if a patient has an identical twin. What patients are matched on are major histocompatibility antigens. There are differences in minor histocompatibility antigens. It is those differences that allow the donor immune system to continue to recognize the cancer cells as foreign and kill them.
Take note of this article co-written by well known myeloma doctor Ken Anderson of Dana-Farber that relates to a case study of a myeloma patient that did a transplant from an identical twin:
"Targets of curative donor-derived graft-versus-myeloma (GVM) responses after allogeneic hematopoietic stem cell transplantation (HSCT) remain poorly defined, partly because immunity against minor histocompatibility Ags (mHAgs) complicates the elucidation of multiple myeloma (multiple myeloma)–specific targets. We hypothesized that syngeneic HSCT would facilitate the identification of GVM-associated Ags because donor immune responses in this setting should exclusively target unique tumor Ags in the absence of donor-host genetic disparities."
"Defining the target Ags of GVT and GVHD may provide insight into their mechanisms and suggest rational methods for their separation. Minor histocompatibility Ags (mHAgs) make up one major class of Ags against which potent donor-derived T- and B-cell immunity develops after HSCT. mHAgs with broad or nonhematopoietic cell expression are implicated in GVHD,10 whereas those with restricted hematopoietic expression play a well-accepted role in GVT responses.10–12 The extent to which nonpolymorphic tumor-associated Ags are targets is less well understood. Tumors may be distinguished from normal cells by genetic alterations, including chromosomal translocations. Tumors can also overexpress or aberrantly express genes compared with their normal counterparts.13 In support of the existence of immunogenic Ags with tumor-restricted expression, Nishida et al described T-cell immunity against leukemia cells after allogeneic HSCT that was not directed against mHAgs.14 The discovery of such naturally immunogenic tumor-associated Ags (TAAs) could lead to the development of immunotherapeutic strategies to target tumor in a selective fashion and thus avoid GVHD toxicity."
Because allogeneic HSCT can result in durable curative remission, it provides a useful clinical backdrop for identifying Ags that are naturally immunogenic to normal donor cells. However, defining TAAs in the allogeneic setting can be complicated by the presence of alloimmune responses. In the present study, we describe a context in which effective donor-derived tumor immunity occurred in the absence of alloimmunity: myeloablative syngeneic HSCT resulting in durable molecular remission in an individual with multiple myeloma (multiple myeloma)."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321874/
While cells "cycle" and die off, the donor immune system is renewing itself and therefore that immunity remains. One of the tests that they use for allo transplant recipients is donor plasma cell chimerism. Plasma cells are made by the immune system - therefore an allo transplant recipients plasma cells should convert to 100% donor and stay that way (hopefully!) for life. The donor immune system gets more mature and stronger as time goes on.
You can see this in a couple of ways. Take note of this small study.
"Molecular remissions are seen more often after allogeneic than after autologous stem cell transplantation. In patients who achieved clinical CR, 9 out of 14 were allograft patients, but only 2 out of 15 autograft patients entered molecular remission. IT IS OF INTEREST THAT MOLECULAR REMISSION AFTER ALLOGRAFTING OCCURRED IN SOME PATIENTS MORE THAN 3 YEARS AFTER TRANSPLANTATION."
http://www.nature.com/leu/journal/v21/n9/full/2404775a.html
That is a clear sign that in those patients the donor immune system is getting stronger as time goes by. The other you can see that is on PFS (progression free survival) graphs of patients that do allografts.
Take note of the graphs of the patients that did allos as part of upfront therapy. The relapses mostly occur during the first 20 months after the allo. In this study the relapse rate is very low after 20 months for the upfront group so the immunotherapy appears to be getting stronger from the donor immune system as time goes on, not weaker.
https://ash.confex.com/ash/2011/webprogram/Paper37067.html
The donor immune system are not "modified cells". They make up an entirely new immune system that can function normally.
Does that explain what you are asking?
Mark
I will try and answer your question.
I did a partially t cell depleted allogeneic transplant with myeloablative (full) conditioning. I used ATG (antithymocyte globulin) for in vivo t cell depletion. I used a low to moderate dose of ATG and I had Grade 1 acute GVHD [graft versus host disease] and for one month I had limited chronic GVHD after I discontinued my immunosuppressive med (Prograf). It is considered a good thing to have minor GVHD like that because it is a sign that the donor cells were active.
I did not get a DLI [donor lymphocyte infusion] because I attained a molecular response after my allo so we did not feel any more therapy was required. I have not had any chronic GVHD for 2.5 years so that is no longer something I need to worry about. I had no other immunotherapy added.
Note: I had a female donor and of the matched pairs female donor to male recipient is associated with the most immunotherapy and a lower relapse rate, so my doctor did not feel I needed any more immunotherapy other than what I got from the donor immune system.
Sometimes you will hear patients say they found a "perfect match" on the donor registry or they had a sibling that was a perfect match. That is actually not true - the only possible perfect match is if a patient has an identical twin. What patients are matched on are major histocompatibility antigens. There are differences in minor histocompatibility antigens. It is those differences that allow the donor immune system to continue to recognize the cancer cells as foreign and kill them.
Take note of this article co-written by well known myeloma doctor Ken Anderson of Dana-Farber that relates to a case study of a myeloma patient that did a transplant from an identical twin:
"Targets of curative donor-derived graft-versus-myeloma (GVM) responses after allogeneic hematopoietic stem cell transplantation (HSCT) remain poorly defined, partly because immunity against minor histocompatibility Ags (mHAgs) complicates the elucidation of multiple myeloma (multiple myeloma)–specific targets. We hypothesized that syngeneic HSCT would facilitate the identification of GVM-associated Ags because donor immune responses in this setting should exclusively target unique tumor Ags in the absence of donor-host genetic disparities."
"Defining the target Ags of GVT and GVHD may provide insight into their mechanisms and suggest rational methods for their separation. Minor histocompatibility Ags (mHAgs) make up one major class of Ags against which potent donor-derived T- and B-cell immunity develops after HSCT. mHAgs with broad or nonhematopoietic cell expression are implicated in GVHD,10 whereas those with restricted hematopoietic expression play a well-accepted role in GVT responses.10–12 The extent to which nonpolymorphic tumor-associated Ags are targets is less well understood. Tumors may be distinguished from normal cells by genetic alterations, including chromosomal translocations. Tumors can also overexpress or aberrantly express genes compared with their normal counterparts.13 In support of the existence of immunogenic Ags with tumor-restricted expression, Nishida et al described T-cell immunity against leukemia cells after allogeneic HSCT that was not directed against mHAgs.14 The discovery of such naturally immunogenic tumor-associated Ags (TAAs) could lead to the development of immunotherapeutic strategies to target tumor in a selective fashion and thus avoid GVHD toxicity."
Because allogeneic HSCT can result in durable curative remission, it provides a useful clinical backdrop for identifying Ags that are naturally immunogenic to normal donor cells. However, defining TAAs in the allogeneic setting can be complicated by the presence of alloimmune responses. In the present study, we describe a context in which effective donor-derived tumor immunity occurred in the absence of alloimmunity: myeloablative syngeneic HSCT resulting in durable molecular remission in an individual with multiple myeloma (multiple myeloma)."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321874/
While cells "cycle" and die off, the donor immune system is renewing itself and therefore that immunity remains. One of the tests that they use for allo transplant recipients is donor plasma cell chimerism. Plasma cells are made by the immune system - therefore an allo transplant recipients plasma cells should convert to 100% donor and stay that way (hopefully!) for life. The donor immune system gets more mature and stronger as time goes on.
You can see this in a couple of ways. Take note of this small study.
"Molecular remissions are seen more often after allogeneic than after autologous stem cell transplantation. In patients who achieved clinical CR, 9 out of 14 were allograft patients, but only 2 out of 15 autograft patients entered molecular remission. IT IS OF INTEREST THAT MOLECULAR REMISSION AFTER ALLOGRAFTING OCCURRED IN SOME PATIENTS MORE THAN 3 YEARS AFTER TRANSPLANTATION."
http://www.nature.com/leu/journal/v21/n9/full/2404775a.html
That is a clear sign that in those patients the donor immune system is getting stronger as time goes by. The other you can see that is on PFS (progression free survival) graphs of patients that do allografts.
Take note of the graphs of the patients that did allos as part of upfront therapy. The relapses mostly occur during the first 20 months after the allo. In this study the relapse rate is very low after 20 months for the upfront group so the immunotherapy appears to be getting stronger from the donor immune system as time goes on, not weaker.
https://ash.confex.com/ash/2011/webprogram/Paper37067.html
The donor immune system are not "modified cells". They make up an entirely new immune system that can function normally.
Does that explain what you are asking?
Mark
-
Mark
Re: T cell depleted transplants and immunotherapy
Mark,
Thank you so much for your reply. Posts such as yours is one of the reasons why this community is invaluable.
While I will have to read and re-read this probably several times, I think I understand the gyst of it. This explains why a depleted T cell allo would work. It makes perfect sense that the donor cells would continue to cycle through and retain their GVM properties. At least that's the hope.
What I am not sure about is whether this is the case for clinically grown cells that are conditioned to kill myeloma cells by being immunized against certain protein, let's say WT1 sensitized T cells that have been grown in the lab and are immunized against the Wilms' tumor protein. I am not sure if there is evidence that this type of cell will continue to replicate and exhibit the same immunization.
So in other words, once you mess with the donor cell, does it continue to replicate in its altered state?
Obviously the alteration and immunization is considered an improvement but it may carry additional risk for inquiring patients. I am bordering the limits of my medical knowledge here and I hope I am expressing this correctly.
Thanks again.
Thank you so much for your reply. Posts such as yours is one of the reasons why this community is invaluable.
While I will have to read and re-read this probably several times, I think I understand the gyst of it. This explains why a depleted T cell allo would work. It makes perfect sense that the donor cells would continue to cycle through and retain their GVM properties. At least that's the hope.
What I am not sure about is whether this is the case for clinically grown cells that are conditioned to kill myeloma cells by being immunized against certain protein, let's say WT1 sensitized T cells that have been grown in the lab and are immunized against the Wilms' tumor protein. I am not sure if there is evidence that this type of cell will continue to replicate and exhibit the same immunization.
So in other words, once you mess with the donor cell, does it continue to replicate in its altered state?
Obviously the alteration and immunization is considered an improvement but it may carry additional risk for inquiring patients. I am bordering the limits of my medical knowledge here and I hope I am expressing this correctly.
Thanks again.
-
ivanm - Name: Ivan Mitev
- Who do you know with myeloma?: self
- When were you/they diagnosed?: August, 2011
- Age at diagnosis: 37
Re: T cell depleted transplants and immunotherapy
Hi IvanM,
I think I understand your question.
To the best of my knowledge, in the non-allo setting no form of immunotherapy has shown long term clinical effectiveness for myeloma patients. There are many reasons for that, one of which is what you mentioned - the effect of the therapy is short lived and does not provide ongoing protection like the donor immune system can. Hopefully they will come up with a form of immunotherapy that older myeloma patients can benefit from with the knowledge they gain from these trials.
I think one of the reasons they are adding approaches like the one you mentioned in the allo setting is for the short term benefit. Take note of the PFS and OS graphs in the study I listed above. The problem with allo transplant when done sometime other than the upfront setting (first complete response at minimum - MRD negative status is ideal) is that the patients lose remission before the donor immune system can strengthen. You see that on the graphs by the fact that few patients relapse after 2 years in both the first line and not first line groups.
The problem in the non first line group is most all of the patients relapse early and are not in remission during the time the donor immune system is getting stronger. It would seem that reducing the early relapses after allo transplant would help cure a lot more patients.
Also immune systems have memory t cells. These additional therapies can help get the immune system to "learn" how to kill things it should be able to identify as "non-self"
"Memory T-cells are derived from normal T-cells that have learned how to overcome an invader by ‘remembering’ the strategy used to defeat previous infections."
"Adaptive immunity is said to have memory because the immune system learns. In this way we gain life-long immunity to infections such as mumps or chicken pox. T-cells constitute a highly evolved arm of the adaptive immune system that is able to distinguish between pathogens and is capable of evolving or adapting during the lifetime of an individual such that immunity becomes better with each successive exposure to pathogen. This is because, following infection, some of the activated T-cells become memory cells that exist in a state of readiness and have the ability to rapidly expand and fight off recurrence of the same disease. In a way, these cells learn from their experience of fighting a particular infection and so can use the most effective strategy to manage the same infection later. This ability to remember and learn is exploited during the process of vaccination."
http://www.tcells.org/scientific/memory/
A great example of using a form of immunotherapy other than allo transplant to aid allo transplant is seen in ALL (acute lymphoblastic leukemia) . You may have seen news stories discuss CAR t cell therapy targeted at CD19. Here is how the doctors at MSKCC use the therapy for relapsed ALL patients. This is from a very small pilot study (5 patients) published in 2013.
"Despite available chemotherapy and allogenic hematopotetic stem cell transplantation (allo-HSCT), adult patients with relapsed B cell acute leukemia (B-ALL) have a very poor prognosis. Long-term survival of adult patients with relapsed B-ALL is dependent upon achieving a complete remission (CR) induced through salvage chemotherapy followed by allo-HSCT (1, 2). Unfortunately, many patients never receive a potential life saving allo-HSCT due to a failure in achieving a second CR following salvage chemotherapy (1). Further, in patients undergoing an allo-HSCT, those with minimal residual disease (MRD+) by FACS or PCR have a significantly worse prognosis compared to patients with no evidence of MRD (MRD−) at the time of allo-HSCT (3). For this reason, novel therapeutic regimens for this patient population are needed."
"Of the 5 patients treated on this protocol, 4 have undergone subsequent allo-HSCT (Table 1). MSK-ALL01 died of a suspected pulmonary embolus 2 months after allo-SCT, while in CR without any evidence of disease. The other 3 patients have had no significant complications post allo-SCT and all remain in CR. MSK-ALL03 remains in a CR 18 months after allo-SCT. MSK-ALL05 is in a CR 3 months after allo-SCT. MSK-ALL06 was in a MRD− remission for 122 days post-T cell infusion before being treated with an allo-SCT. To date, this patient remains MRD− 6 weeks after allo-SCT."
"MSK-ALL04, who was ineligible for allo-HSCT due to multiple, pre-existing co-morbidities, was observed expectantly following CAR modified T cell therapy. This patient relapsed 13 weeks after T cell therapy and subsequently expired (Table 1). The relapsed tumor cells expressed the same malignant IgH rearrangement identified in the initial malignant clone and expressed the target CD19 antigen at pre-treatment levels (Fig. 5A). Further, the recurrent tumor cells retained sensitivity to lysis by autologous 19-28z+ T cells as assessed by a 51Chromium release assay (Fig. 5B). The relapse observed in this patient, despite previously having achieved MRD− status, is therefore not due to antigen escape but may be imputed, at least in part, to the abrogated persistence of the infused 19-28z+ T cells caused by the requisite need for high-dose steroid therapy to treat cytokine mediated toxicities (Fig. 2B)."
"These results demonstrate the marked anti-tumor efficacy of 19-28z CAR modified T cells in patients with relapsed/refractory B-ALL and the reliability of this novel therapy to induce profound molecular remissions, an ideal bridge to potentially curative therapy with subsequent allo-HSCT."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3742551/
In this small study the new form of immunotherapy gets the ALL patients into an MRD negative status and the allo transplant is used to maintain the remission. In my case Velcade/Doxil/dex and high dose melphalan got me to remission and the allo transplant was used to consolidate and maintain it. Allo transplant is not very effective at getting myeloma patients a durable 2nd remission after relapse even though it is often used for that purpose.
Mark
I think I understand your question.
To the best of my knowledge, in the non-allo setting no form of immunotherapy has shown long term clinical effectiveness for myeloma patients. There are many reasons for that, one of which is what you mentioned - the effect of the therapy is short lived and does not provide ongoing protection like the donor immune system can. Hopefully they will come up with a form of immunotherapy that older myeloma patients can benefit from with the knowledge they gain from these trials.
I think one of the reasons they are adding approaches like the one you mentioned in the allo setting is for the short term benefit. Take note of the PFS and OS graphs in the study I listed above. The problem with allo transplant when done sometime other than the upfront setting (first complete response at minimum - MRD negative status is ideal) is that the patients lose remission before the donor immune system can strengthen. You see that on the graphs by the fact that few patients relapse after 2 years in both the first line and not first line groups.
The problem in the non first line group is most all of the patients relapse early and are not in remission during the time the donor immune system is getting stronger. It would seem that reducing the early relapses after allo transplant would help cure a lot more patients.
Also immune systems have memory t cells. These additional therapies can help get the immune system to "learn" how to kill things it should be able to identify as "non-self"
"Memory T-cells are derived from normal T-cells that have learned how to overcome an invader by ‘remembering’ the strategy used to defeat previous infections."
"Adaptive immunity is said to have memory because the immune system learns. In this way we gain life-long immunity to infections such as mumps or chicken pox. T-cells constitute a highly evolved arm of the adaptive immune system that is able to distinguish between pathogens and is capable of evolving or adapting during the lifetime of an individual such that immunity becomes better with each successive exposure to pathogen. This is because, following infection, some of the activated T-cells become memory cells that exist in a state of readiness and have the ability to rapidly expand and fight off recurrence of the same disease. In a way, these cells learn from their experience of fighting a particular infection and so can use the most effective strategy to manage the same infection later. This ability to remember and learn is exploited during the process of vaccination."
http://www.tcells.org/scientific/memory/
A great example of using a form of immunotherapy other than allo transplant to aid allo transplant is seen in ALL (acute lymphoblastic leukemia) . You may have seen news stories discuss CAR t cell therapy targeted at CD19. Here is how the doctors at MSKCC use the therapy for relapsed ALL patients. This is from a very small pilot study (5 patients) published in 2013.
"Despite available chemotherapy and allogenic hematopotetic stem cell transplantation (allo-HSCT), adult patients with relapsed B cell acute leukemia (B-ALL) have a very poor prognosis. Long-term survival of adult patients with relapsed B-ALL is dependent upon achieving a complete remission (CR) induced through salvage chemotherapy followed by allo-HSCT (1, 2). Unfortunately, many patients never receive a potential life saving allo-HSCT due to a failure in achieving a second CR following salvage chemotherapy (1). Further, in patients undergoing an allo-HSCT, those with minimal residual disease (MRD+) by FACS or PCR have a significantly worse prognosis compared to patients with no evidence of MRD (MRD−) at the time of allo-HSCT (3). For this reason, novel therapeutic regimens for this patient population are needed."
"Of the 5 patients treated on this protocol, 4 have undergone subsequent allo-HSCT (Table 1). MSK-ALL01 died of a suspected pulmonary embolus 2 months after allo-SCT, while in CR without any evidence of disease. The other 3 patients have had no significant complications post allo-SCT and all remain in CR. MSK-ALL03 remains in a CR 18 months after allo-SCT. MSK-ALL05 is in a CR 3 months after allo-SCT. MSK-ALL06 was in a MRD− remission for 122 days post-T cell infusion before being treated with an allo-SCT. To date, this patient remains MRD− 6 weeks after allo-SCT."
"MSK-ALL04, who was ineligible for allo-HSCT due to multiple, pre-existing co-morbidities, was observed expectantly following CAR modified T cell therapy. This patient relapsed 13 weeks after T cell therapy and subsequently expired (Table 1). The relapsed tumor cells expressed the same malignant IgH rearrangement identified in the initial malignant clone and expressed the target CD19 antigen at pre-treatment levels (Fig. 5A). Further, the recurrent tumor cells retained sensitivity to lysis by autologous 19-28z+ T cells as assessed by a 51Chromium release assay (Fig. 5B). The relapse observed in this patient, despite previously having achieved MRD− status, is therefore not due to antigen escape but may be imputed, at least in part, to the abrogated persistence of the infused 19-28z+ T cells caused by the requisite need for high-dose steroid therapy to treat cytokine mediated toxicities (Fig. 2B)."
"These results demonstrate the marked anti-tumor efficacy of 19-28z CAR modified T cells in patients with relapsed/refractory B-ALL and the reliability of this novel therapy to induce profound molecular remissions, an ideal bridge to potentially curative therapy with subsequent allo-HSCT."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3742551/
In this small study the new form of immunotherapy gets the ALL patients into an MRD negative status and the allo transplant is used to maintain the remission. In my case Velcade/Doxil/dex and high dose melphalan got me to remission and the allo transplant was used to consolidate and maintain it. Allo transplant is not very effective at getting myeloma patients a durable 2nd remission after relapse even though it is often used for that purpose.
Mark
-
Mark
Re: T cell depleted transplants and immunotherapy
Thanks Mark. This is much appreciated. If I had to figure this out by myself, probably it would have taken me a week. I will talk to my doc-s about this when I meet them and confirm, but this makes sense to me. From everything I've seen, the T cell depleted allo with an immunized donor cell infusion has the most promise for a cure at this stage. This is something that is being done right now and I consider going that route when I relapse (hopefully not anytime soon).
-
ivanm - Name: Ivan Mitev
- Who do you know with myeloma?: self
- When were you/they diagnosed?: August, 2011
- Age at diagnosis: 37
Re: T cell depleted transplants and immunotherapy
Mark,
I'm very curious about your views on allo transplants as I am likely headed there myself. I have complex, high-risk genetics and a relatively young age (currently 43, diagnosis at 41). I will be seeking the opinions of specialists on either side of the allo debate. This week I am going to see a well-known specialist who does not advocate allos.
Would you be available to chat briefly so I could get your thoughts, especially on my questions for this specialist?
Thank you,
Brent
I'm very curious about your views on allo transplants as I am likely headed there myself. I have complex, high-risk genetics and a relatively young age (currently 43, diagnosis at 41). I will be seeking the opinions of specialists on either side of the allo debate. This week I am going to see a well-known specialist who does not advocate allos.
Would you be available to chat briefly so I could get your thoughts, especially on my questions for this specialist?
Thank you,
Brent
-
Brent
Re: T cell depleted transplants and immunotherapy
Hi Brent,
Most myeloma docs are not allo transplant experts. I would most likely not ask this particular myeloma expert anything about it. I would just ask him about the long-term strategy he / she is proposing. I am not sure it is an efficient use of your time to have this particular doctor discuss why his / her transplant team is not able to incorporate allo transplant / immunotherapy successfully into his / her patients therapy.
As you can see from reading Cindy's account of her allo transplant, they can be a challenging journey. Fortunately, mine went very smoothly, and I currently enjoy an excellent quality of life. But it is tough spending 29 days in the hospital like I did, staying away from crowds while the donor immune system gets up to speed, etc., and is generally very challenging in the short term. It is something you need to be really committed to doing.
I have noticed from your posts that you have had myeloma for over a year, done 2 autos, and you are going for an opinion from a doctor who you know will not recommend an allo. I may be reading this incorrectly, but it seems you would prefer to not do the allo. If that is the case, I would not do it if I were you. As many of us who have done them have mentioned, they are not for everyone.
Best of luck with your decision and keep us up to date on how things progress.
Mark
Most myeloma docs are not allo transplant experts. I would most likely not ask this particular myeloma expert anything about it. I would just ask him about the long-term strategy he / she is proposing. I am not sure it is an efficient use of your time to have this particular doctor discuss why his / her transplant team is not able to incorporate allo transplant / immunotherapy successfully into his / her patients therapy.
As you can see from reading Cindy's account of her allo transplant, they can be a challenging journey. Fortunately, mine went very smoothly, and I currently enjoy an excellent quality of life. But it is tough spending 29 days in the hospital like I did, staying away from crowds while the donor immune system gets up to speed, etc., and is generally very challenging in the short term. It is something you need to be really committed to doing.
I have noticed from your posts that you have had myeloma for over a year, done 2 autos, and you are going for an opinion from a doctor who you know will not recommend an allo. I may be reading this incorrectly, but it seems you would prefer to not do the allo. If that is the case, I would not do it if I were you. As many of us who have done them have mentioned, they are not for everyone.
Best of luck with your decision and keep us up to date on how things progress.
Mark
-
Mark11
7 posts
• Page 1 of 1