Dear forum members,
I'm sure, that overcoming relapse is the way to a myeloma cure. The myeloma rollercoster is caused by the persisting fear of "it". But: What are the recent insights? Please do not think, that I'm not reading all the forum informations (eg. Dr. Tiedemann's research) and news about the topic. But I'm wondering what's scientists achieved really in 2013/14 and what that mean for therapy and drug development? Perhaps some patients are following the topic, spoke with experts and could share there insights about the cancer stem cell advances?
Thank you in advance,
Thomas
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Re: Recent research about preventing relapse?
Considering that Tiedemann's research came out in Sept 2013, at least in my mind, it would be years before any of this makes a difference, if at all. As his research points out, the role of progenitor cells is still unsettled and multiple myeloma resistance remains controversial. To quote Dr. Shain on this issue (from 2012, pre Tiedemann's study),.. "whether they are a target for treatment and/or the key to a cure are questions yet to be answered. Today, we are not equipped to directly target these cells clinically. Hopefully, with time we will find the answers and maybe these cells will be one of the keys to long term control of myeloma."
That said, if one were to take the 2013 study at face value, it becomes clear that a proteasome inhibitor would not lead to a cure. However, this is not necessarily horrible in my mind since the focus is shifting away from inhibitors to antibody immunotherapies. If I understand the 2013 study with my layman limitations, it identified CD38, CD138, and CD20 expressions in multiple myeloma progenitor cells. Well, there are presently antibodies that target those expressions. For example, daratumumab and SAR650984, two of the promising new meds, target CD38.
So, I am hopeful that some of the new meds, despite the fact that they do not target progenitors specifically, would induce a long term OS, and possibly a cure (at least for some of us). Hopefully these will keep some of us alive long enough to where the recent multiple myeloma gene mapping studies will come to fruition and have a clinical application.
As to your main question regarding the latest on this - I think the following article addresses your issue directly (March, 7 2014). "Common progenitor cells in mature B-cell malignancies: implications for therapy" (http://www.ncbi.nlm.nih.gov/pubmed/24811163).
Regrettably, I don't have access to the entire article. Maybe the Beacon can be kind enough to look into this and let us know what's the latest. Good luck.
That said, if one were to take the 2013 study at face value, it becomes clear that a proteasome inhibitor would not lead to a cure. However, this is not necessarily horrible in my mind since the focus is shifting away from inhibitors to antibody immunotherapies. If I understand the 2013 study with my layman limitations, it identified CD38, CD138, and CD20 expressions in multiple myeloma progenitor cells. Well, there are presently antibodies that target those expressions. For example, daratumumab and SAR650984, two of the promising new meds, target CD38.
So, I am hopeful that some of the new meds, despite the fact that they do not target progenitors specifically, would induce a long term OS, and possibly a cure (at least for some of us). Hopefully these will keep some of us alive long enough to where the recent multiple myeloma gene mapping studies will come to fruition and have a clinical application.
As to your main question regarding the latest on this - I think the following article addresses your issue directly (March, 7 2014). "Common progenitor cells in mature B-cell malignancies: implications for therapy" (http://www.ncbi.nlm.nih.gov/pubmed/24811163).
Regrettably, I don't have access to the entire article. Maybe the Beacon can be kind enough to look into this and let us know what's the latest. Good luck.
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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: Recent research about preventing relapse?
I came across this article while researching progenitor cells. I, too, am trying to learn as much as I can!
http://www.jhoonline.org/content/6/1/91 (full text)
Kellner et al., "Fact or fiction - identifying the elusive multiple myeloma stem cell", Journal of Hematology & Oncology 2013, 6:91
Abstract:
Multiple Myeloma (multiple myeloma) is a debilitating disease of proliferating and malignant plasma cells that is currently incurable. The ability of monoclonal recurrence of disease suggests it might arise from a stem cell-like population capable of self-renewal. The difficulty to isolate the cancer stem-like cell in multiple myeloma has introduced confusion toward this hypothesis. However, recent evidence has suggested that multiple myeloma originates from the B cell lineage with memory-B cell like features, allowing for self-renewal of the progenitor-like status and differentiation to a monoclonal plasma cell population. Furthermore, this tumor-initiating cell uses signaling pathways and microenvironment similar to the hematopoietic stem cell, though hijacking these mechanisms to create and favor a more tumorigenic environment. The bone marrow niche allows for pertinent evasion, either through avoiding immunosurveillance or through direct interaction with the stroma, inducing quiescence and thus drug resistance. Understanding the interaction of the multiple myeloma stem cell to the microenvironment and the mechanisms utilized by various stem cell-like populations to allow persistence and therapy-resistance can enable for better targeting of this cell population and potential eradication of the disease.
http://www.jhoonline.org/content/6/1/91 (full text)
Kellner et al., "Fact or fiction - identifying the elusive multiple myeloma stem cell", Journal of Hematology & Oncology 2013, 6:91
Abstract:
Multiple Myeloma (multiple myeloma) is a debilitating disease of proliferating and malignant plasma cells that is currently incurable. The ability of monoclonal recurrence of disease suggests it might arise from a stem cell-like population capable of self-renewal. The difficulty to isolate the cancer stem-like cell in multiple myeloma has introduced confusion toward this hypothesis. However, recent evidence has suggested that multiple myeloma originates from the B cell lineage with memory-B cell like features, allowing for self-renewal of the progenitor-like status and differentiation to a monoclonal plasma cell population. Furthermore, this tumor-initiating cell uses signaling pathways and microenvironment similar to the hematopoietic stem cell, though hijacking these mechanisms to create and favor a more tumorigenic environment. The bone marrow niche allows for pertinent evasion, either through avoiding immunosurveillance or through direct interaction with the stroma, inducing quiescence and thus drug resistance. Understanding the interaction of the multiple myeloma stem cell to the microenvironment and the mechanisms utilized by various stem cell-like populations to allow persistence and therapy-resistance can enable for better targeting of this cell population and potential eradication of the disease.
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gardengirl - Name: gardengirl
- Who do you know with myeloma?: Me
- When were you/they diagnosed?: Nov. 2013
- Age at diagnosis: 47
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