This forum thread can be used to discuss the proceedings of the International Myeloma Workshop that take place on Day 1 (Tuesday, May 3) of the conference. Feel free to use this space to highlight interesting abstracts, summarize the presentations as they happen, ask questions, and discuss any relevant topics. Everyone is encouraged to participate.
Feel free to also check out the discussions for Day 2, Day 3, and Day 4.
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Re: IMW 2011 Multiple Myeloma Discussion - Day 1
Welcome to The Myeloma Beacon's coverage of the 13th International Myeloma Workshop. The Workshop, which currently takes place very two years, is being held in Paris, France this year. The 2011 Workshop starts today and will last until late in the day this Friday. The Workshop will be a mix of oral presentations during so-called "plenary sessions"; some panel discussions; and poster presentations in the Workshop exhibition area.
Today, the first day of the Workshop, there are three plenary sessions scheduled; one in the morning on "Molecular Pathways / Genetics"; a second in the early afternoon on "Plasma Cell Biology"; and a third late in the afternoon and early evening on "Bone Disease and Animal Models". Squeezed between the second and third session is some time for visiting the poster presentations. Of course, there also is time in the schedule for lunch, a coffee break, and then some speeches and a reception this evening.
If you haven't already noticed, today's topics deal a lot with the basics of the biochemistry and molecular mechanisms related to multiple myeloma. This means two things. First, the sessions are more technical compared to many of the presentations that will be made later this week. Second, the presentations don't have as much material that will have an immediate imapct on how current multiple myeloma patients are treated. Instead, the presentations are relevant more to how treatment options for myeloma patients may expand in the intermediate to longer-term.
Therefore, if you're more interested in the latest news about current myeloma treatments or drugs that are nearing approval as new treatment options, today's sessions really aren't going to be for you.
The reporting here in the Myeloma Beacon's forum about today's sessions will focus on selected oral presentations and -- if I can swing it -- a few poster presentations. I'll typically devote a single posting to a single presentation, but don't be surprised if several postings combine a few presentations into a single report.
Don't hesitate to ask questions or make comments on whatever postings I make here. I may not be able to respond to them right away, but there may be others here at the Workshop -- or among our forum readers -- who can add to the discussion while I'm still reporting on the presentations, and I'll try to circle back in the evening (Paris time) and answer any questions that are still open.
Don't forget that The Beacon also will be publishing daily summaries of each day of the Workshop, generally within 24 hours of the close of each day's sessions.
Today, the first day of the Workshop, there are three plenary sessions scheduled; one in the morning on "Molecular Pathways / Genetics"; a second in the early afternoon on "Plasma Cell Biology"; and a third late in the afternoon and early evening on "Bone Disease and Animal Models". Squeezed between the second and third session is some time for visiting the poster presentations. Of course, there also is time in the schedule for lunch, a coffee break, and then some speeches and a reception this evening.
If you haven't already noticed, today's topics deal a lot with the basics of the biochemistry and molecular mechanisms related to multiple myeloma. This means two things. First, the sessions are more technical compared to many of the presentations that will be made later this week. Second, the presentations don't have as much material that will have an immediate imapct on how current multiple myeloma patients are treated. Instead, the presentations are relevant more to how treatment options for myeloma patients may expand in the intermediate to longer-term.
Therefore, if you're more interested in the latest news about current myeloma treatments or drugs that are nearing approval as new treatment options, today's sessions really aren't going to be for you.
The reporting here in the Myeloma Beacon's forum about today's sessions will focus on selected oral presentations and -- if I can swing it -- a few poster presentations. I'll typically devote a single posting to a single presentation, but don't be surprised if several postings combine a few presentations into a single report.
Don't hesitate to ask questions or make comments on whatever postings I make here. I may not be able to respond to them right away, but there may be others here at the Workshop -- or among our forum readers -- who can add to the discussion while I'm still reporting on the presentations, and I'll try to circle back in the evening (Paris time) and answer any questions that are still open.
Don't forget that The Beacon also will be publishing daily summaries of each day of the Workshop, generally within 24 hours of the close of each day's sessions.
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Boris Simkovich - Name: Boris Simkovich
Founder
The Myeloma Beacon
Re: IMW 2011 Multiple Myeloma Discussion - Day 1
Let's kick things off with the first plenary session of the Workshop, which was on Molecular Pathways / Genetics.
The session was introduced by Dr. Herve Avet-Louiseau of the University Hospital of Nantes, France, who gave a very useful overview of many of the topics to be discussed during the three main presentations of the session. (We'll see what we can do about getting copies of the slides.)
After Dr. Avet-Loiseau's introduction, Dr. Carol Croce of Ohio State gave a (unexpectedly) lengthy presentation titled "MicroRNAs in Myeloma." In reality, very little of the presentation was actually about multiple myeloma. Instead, Dr. Croce retraced how his thinking about microRNA and its role in cancer, in general, has evolved over more than 10 years of investigating the topic. Much of that research involved looking at the role of microRNA in various kinds of lymphoma and leukemia, before he finally switched to looking at microRNA's role in multiple myeloma.
MicroRNA is a special kind of RNA that, unlike most RNA, is not directly involved in the production of proteins in the body. Instead, microRNA is very small RNA that helps control the process of producing proteins from genes.
As its name suggest, microRNA is smaller than normal RNA. Also, there is not just one kind of microRNA. Instead, humans have about 1000 different types of microRNA.
Based on his research, Dr. Croce now feels that "microRNA is involved in all human cancer." His research also leads him to believe that microRNA plays a key role in why mutatiuons of the p53 gene are so important in multiple myeloma.
In fact, Dr. Croce feels it may one day be the case that multiple myeloma patients may be classified based on the kinds of microRNA involved in their disease, and drugs that contain microRNA, or which affect the production of microRNA, may be powerful new treatment options for the disease.
One potential drug that apparently affects microRNA production which, in turn, affects the progression of myeloma is Nutlin (including its various derivatives).
The session was introduced by Dr. Herve Avet-Louiseau of the University Hospital of Nantes, France, who gave a very useful overview of many of the topics to be discussed during the three main presentations of the session. (We'll see what we can do about getting copies of the slides.)
After Dr. Avet-Loiseau's introduction, Dr. Carol Croce of Ohio State gave a (unexpectedly) lengthy presentation titled "MicroRNAs in Myeloma." In reality, very little of the presentation was actually about multiple myeloma. Instead, Dr. Croce retraced how his thinking about microRNA and its role in cancer, in general, has evolved over more than 10 years of investigating the topic. Much of that research involved looking at the role of microRNA in various kinds of lymphoma and leukemia, before he finally switched to looking at microRNA's role in multiple myeloma.
MicroRNA is a special kind of RNA that, unlike most RNA, is not directly involved in the production of proteins in the body. Instead, microRNA is very small RNA that helps control the process of producing proteins from genes.
As its name suggest, microRNA is smaller than normal RNA. Also, there is not just one kind of microRNA. Instead, humans have about 1000 different types of microRNA.
Based on his research, Dr. Croce now feels that "microRNA is involved in all human cancer." His research also leads him to believe that microRNA plays a key role in why mutatiuons of the p53 gene are so important in multiple myeloma.
In fact, Dr. Croce feels it may one day be the case that multiple myeloma patients may be classified based on the kinds of microRNA involved in their disease, and drugs that contain microRNA, or which affect the production of microRNA, may be powerful new treatment options for the disease.
One potential drug that apparently affects microRNA production which, in turn, affects the progression of myeloma is Nutlin (including its various derivatives).
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Boris Simkovich - Name: Boris Simkovich
Founder
The Myeloma Beacon
Re: IMW 2011 Multiple Myeloma Discussion - Day 1
The second presentation during the Molecular Pathways / Genetics session was by Dr. Rafael Fonseca of The Mayo Clinic. Dr. Fonseca spoke on "The Classification of Myeloma: Subtypes of the Disease."
Dr. Fonseca said that most classifications of multiple myeloma start out by seeking to group patients in one of three ways: (1) based on similar biologic characteristics of their disease (for example, similar genetic mutations); (2) based on similar prognoses (survival likelihoods); or (3) based on similar predicted future disease paths.
That having been said, Dr. Foncesca believes that many myeloma researchers today begin by classifying patients into two broad categories based on the biology of the patients' disease. Patients either have genetic mutations that result in more than two copies of at least one chromosome ("hyperdiploidy"), or they don't have these kinds of mutations and, instead, often have chromosomal mutations that typically involve translocations, such as t(14;16). Each of these two broad categories of patients accounts for about half of all patients, but there is some overlap -- that is, patients with translocations may sometimes have hyperdiploidy.
After this relatively high level of classification, however, Dr. Fonseca believes it is very difficult to come to agreement on what basis to use to develop further subtypes of patients. What is clear, however, is that there are, indeed, *many* subtypes of myeloma patients. Indeed, Dr. Fonseca concluded his presentation by stating that he believes we should be talking about "many, many, many multiple myelomas."
Before he got to his conclusion, however, Dr. Fonseca made a number of interesting comments. He noted, for example, that one can generalize a bit and say that younger multiple myeloma patients typically have higher risk chromosomal characteristics (cytogenetics), not so much bone disease, and IgA lambda. Older patients, in contrast, are not as inclined to have high risk chromosomal characteristics, but they typically have more bone disease and are IgA kappa.
Similarly, he noted that myeloma patients typically progress from having only intramedullary disease (that is, disease that is confined to the bone), and then on to having extramedullary disease (disease that extends into other parts of the body). In addition, the p53 mutation is also typically a good measure of how far along myeloma patients are in their disease.
Near the end of his presentation, Dr. Fonseca discussed for a while the controversy surrounding the t(14,16) genetic mutation and whether it is really an indicator of poorer prognosis. He said that most myeloma researchers (himself included) believe that the mutation is, in fact, an indicator of poorer prognosis, but there have been research results that call this into question.
During his presentation, Dr. Fonseca touched briefly on the different analytical methods available to physicians for categorizing multiple myeloma patients. One method that is very common is FISH analysis. However, Dr. Fonseca believes that gene expression profiling offers an even richer data basis for classifying patients.
Dr. Fonseca said that most classifications of multiple myeloma start out by seeking to group patients in one of three ways: (1) based on similar biologic characteristics of their disease (for example, similar genetic mutations); (2) based on similar prognoses (survival likelihoods); or (3) based on similar predicted future disease paths.
That having been said, Dr. Foncesca believes that many myeloma researchers today begin by classifying patients into two broad categories based on the biology of the patients' disease. Patients either have genetic mutations that result in more than two copies of at least one chromosome ("hyperdiploidy"), or they don't have these kinds of mutations and, instead, often have chromosomal mutations that typically involve translocations, such as t(14;16). Each of these two broad categories of patients accounts for about half of all patients, but there is some overlap -- that is, patients with translocations may sometimes have hyperdiploidy.
After this relatively high level of classification, however, Dr. Fonseca believes it is very difficult to come to agreement on what basis to use to develop further subtypes of patients. What is clear, however, is that there are, indeed, *many* subtypes of myeloma patients. Indeed, Dr. Fonseca concluded his presentation by stating that he believes we should be talking about "many, many, many multiple myelomas."
Before he got to his conclusion, however, Dr. Fonseca made a number of interesting comments. He noted, for example, that one can generalize a bit and say that younger multiple myeloma patients typically have higher risk chromosomal characteristics (cytogenetics), not so much bone disease, and IgA lambda. Older patients, in contrast, are not as inclined to have high risk chromosomal characteristics, but they typically have more bone disease and are IgA kappa.
Similarly, he noted that myeloma patients typically progress from having only intramedullary disease (that is, disease that is confined to the bone), and then on to having extramedullary disease (disease that extends into other parts of the body). In addition, the p53 mutation is also typically a good measure of how far along myeloma patients are in their disease.
Near the end of his presentation, Dr. Fonseca discussed for a while the controversy surrounding the t(14,16) genetic mutation and whether it is really an indicator of poorer prognosis. He said that most myeloma researchers (himself included) believe that the mutation is, in fact, an indicator of poorer prognosis, but there have been research results that call this into question.
During his presentation, Dr. Fonseca touched briefly on the different analytical methods available to physicians for categorizing multiple myeloma patients. One method that is very common is FISH analysis. However, Dr. Fonseca believes that gene expression profiling offers an even richer data basis for classifying patients.
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Boris Simkovich - Name: Boris Simkovich
Founder
The Myeloma Beacon
Re: IMW 2011 Multiple Myeloma Discussion - Day 1
The final presentation during the Molecular Pathways / Genetics plenary session was by Dr. Stéphane Minvielle of the University of Nantes, France. He spoke on “The Genetic Progression of Multiple Myeloma.”
Much of Dr. Minvielle's presentation was quite technical, and I won't go into all the details here. However, there are a few key points worth passing along.
First, Dr. Minvielle noted that, until recently, it was very challenging to trace how a single multiple myeloma patient's cytogenetic profile evolved over time. In his opinion, the tools to do that sort of analysis just weren't sufficiently advanced.
Now, however, he believes that, especially with the availability of single nucleotide polymorphism (SNP) arrays, it is much easier to track chromsomal changes in individual patients over the course of their multiple myeloma.
As Dr. Minvielle and his colleagues have started tracking the evolution of the cytogenetics of a number of patients, however, they have learned that it is very difficult to make generalizations that are applicable across all patients. Instead, the evolution seems to be relatively unique for each patient.
Dr.. Minvielle also described some interesting results that he and his colleagues got tracking the evolution of the cytogenetics of 24 myeloma patients treated with either the VAD treatment regimen or with a Velcade-dexamethasone (Decadron) regimen. (VAD = vincristine + doxorubicin (Adriamycin) + dexamethasone.)
The researchers found that the patients treated with the Velcade-based regimen were more likely to have at least one chromosomal abnormality that persisted throughout their treatment. Many patients saw a change in their chromosomal abnormalities over time, but about a third always had at least one abnormality that was always present, and more of these patients were the ones treated with the Velcade-based regimen.
This fits with the notion that has been mentioned sometimes that, even in patients that achieve a complete response with Velcade, the disease still may be present, even if it's not readily apparent.
(On the latter point, see, for example, this article that appeared a while back in the Myeloma Beacon: https://myelomabeacon.org/news/2009/04/07/addition-of-second-drug-could-dramatically-improve-velcade-response/ .)
Much of Dr. Minvielle's presentation was quite technical, and I won't go into all the details here. However, there are a few key points worth passing along.
First, Dr. Minvielle noted that, until recently, it was very challenging to trace how a single multiple myeloma patient's cytogenetic profile evolved over time. In his opinion, the tools to do that sort of analysis just weren't sufficiently advanced.
Now, however, he believes that, especially with the availability of single nucleotide polymorphism (SNP) arrays, it is much easier to track chromsomal changes in individual patients over the course of their multiple myeloma.
As Dr. Minvielle and his colleagues have started tracking the evolution of the cytogenetics of a number of patients, however, they have learned that it is very difficult to make generalizations that are applicable across all patients. Instead, the evolution seems to be relatively unique for each patient.
Dr.. Minvielle also described some interesting results that he and his colleagues got tracking the evolution of the cytogenetics of 24 myeloma patients treated with either the VAD treatment regimen or with a Velcade-dexamethasone (Decadron) regimen. (VAD = vincristine + doxorubicin (Adriamycin) + dexamethasone.)
The researchers found that the patients treated with the Velcade-based regimen were more likely to have at least one chromosomal abnormality that persisted throughout their treatment. Many patients saw a change in their chromosomal abnormalities over time, but about a third always had at least one abnormality that was always present, and more of these patients were the ones treated with the Velcade-based regimen.
This fits with the notion that has been mentioned sometimes that, even in patients that achieve a complete response with Velcade, the disease still may be present, even if it's not readily apparent.
(On the latter point, see, for example, this article that appeared a while back in the Myeloma Beacon: https://myelomabeacon.org/news/2009/04/07/addition-of-second-drug-could-dramatically-improve-velcade-response/ .)
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Boris Simkovich - Name: Boris Simkovich
Founder
The Myeloma Beacon
Re: IMW 2011 Multiple Myeloma Discussion - Day 1
Unfortunately, technical difficulties with electricity and Internet access at the Workshop kept me from reporting on the second presentation session today. That's not too bad, however, as the session -- on "Plasma Cell Biology" -- was quite technical and very focused on potential new routes for treating myeloma that are at least 3-5 years away from becoming widely available to myeloma patients.
If you are interested in finding out more about these sessions, however, just check out the programme for the workshop, which also includes links to abstracts for most presentations. The programme is available online at this link:
http://www.myeloma-paris2011.com/content/view/15/10/
If you are interested in finding out more about these sessions, however, just check out the programme for the workshop, which also includes links to abstracts for most presentations. The programme is available online at this link:
http://www.myeloma-paris2011.com/content/view/15/10/
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Boris Simkovich - Name: Boris Simkovich
Founder
The Myeloma Beacon
Re: IMW 2011 Multiple Myeloma Discussion - Day 1
The last set of presentations today were on the topic "Bone Disease: From Physiopathology to Treatment." There were six presentations altogether, and each presentation moved along at a pretty decent clip. Still, it was a great set of presentations to really refresh your understanding of what goes on with bone disease in myeloma patients, while also providing an update on the developments taking place that could provide a number of new solutions for dealing with myeloma bone disease.
Recall that myeloma bone disease is one of the two major consequences of multiple myeloma. On the one hand, the malignant myeloma cells in the bone marrow of myeloma patients disrupt the normal production blood plasma, creating the abnormal blood protein levels that myeloma patients are all too familiar with.
On the other hand, myeloma cells also disrupt the normal cycle of bone formation and destruction that goes on in human bones. In particular, myeloma tends to suppress the formation of "osteoblasts," the cells that build up human bones, and increase the production of "osteoclasts," the cells that break down bone tissue. The net result is a general weakening of the bones seen in most myeloma patients, which is generally made worse by concentrations of myeloma cells in particular parts of the bone, creating bone lesions.
Today's Wokshop session on bone disease got started with an excellent overview presentation, "Bone Disease: From Physiopathology to Treatment," by Dr. David Roodman of the University of Pittsburgh.
The abstract accompanying Dr. Roodman's presentation contains a description of the consequences of myeloma bone disease that is worth quoting at length:
"Myeloma bone disease is responsible for some of the most devastating complications of multiple myeloma. Multiple myeloma patients experience two or more skeletal-related events per year and more than 1/3 of patients sustain a pathologic fracture within 21 months ... Even with the best current treatment, multiple myeloma patients still experience approximately one skeletal-related event every 12-18 months. These skeletal-related events can be devastating to the patients. Seventy percent of patients present with bone pain, approximately 20% will present with a pathologic fracture at diagnosis, and over the course of their disease 60% of patients sustain a pathologic fracture. Fractures in multiple myeloma patients results in a 20% increase in mortality compared to patients without fracture and an incremental cost of $63,455 for care of multiple myeloma patients with bone disease. "
Dr. Roodman's presentation also touched on the impact new myeloma treatments -- like Velcade and Revlimid -- have on myeloma bone disease, something I'll discuss at greater length in the summary of one of the later presentations during the session.
The latter part of Dr. Roodman's presentation discussed a number of new approaches that researchers are pursuing in the hopes of treating myeloma bone disease. He mentioned, for example, Amgen's Xgeva (denosumab), which offers an alternative approach to addressing myeloma bone disease than standard bisphosphonate therapy with drugs such as Zometa (zoledronic acid) and Aredia (pamidronate). He also made it clear, though, that there are further options for attacking myeloma bone disease that pharmaceutical and biotech companies can pursue (and are pursuing).
Recall that myeloma bone disease is one of the two major consequences of multiple myeloma. On the one hand, the malignant myeloma cells in the bone marrow of myeloma patients disrupt the normal production blood plasma, creating the abnormal blood protein levels that myeloma patients are all too familiar with.
On the other hand, myeloma cells also disrupt the normal cycle of bone formation and destruction that goes on in human bones. In particular, myeloma tends to suppress the formation of "osteoblasts," the cells that build up human bones, and increase the production of "osteoclasts," the cells that break down bone tissue. The net result is a general weakening of the bones seen in most myeloma patients, which is generally made worse by concentrations of myeloma cells in particular parts of the bone, creating bone lesions.
Today's Wokshop session on bone disease got started with an excellent overview presentation, "Bone Disease: From Physiopathology to Treatment," by Dr. David Roodman of the University of Pittsburgh.
The abstract accompanying Dr. Roodman's presentation contains a description of the consequences of myeloma bone disease that is worth quoting at length:
"Myeloma bone disease is responsible for some of the most devastating complications of multiple myeloma. Multiple myeloma patients experience two or more skeletal-related events per year and more than 1/3 of patients sustain a pathologic fracture within 21 months ... Even with the best current treatment, multiple myeloma patients still experience approximately one skeletal-related event every 12-18 months. These skeletal-related events can be devastating to the patients. Seventy percent of patients present with bone pain, approximately 20% will present with a pathologic fracture at diagnosis, and over the course of their disease 60% of patients sustain a pathologic fracture. Fractures in multiple myeloma patients results in a 20% increase in mortality compared to patients without fracture and an incremental cost of $63,455 for care of multiple myeloma patients with bone disease. "
Dr. Roodman's presentation also touched on the impact new myeloma treatments -- like Velcade and Revlimid -- have on myeloma bone disease, something I'll discuss at greater length in the summary of one of the later presentations during the session.
The latter part of Dr. Roodman's presentation discussed a number of new approaches that researchers are pursuing in the hopes of treating myeloma bone disease. He mentioned, for example, Amgen's Xgeva (denosumab), which offers an alternative approach to addressing myeloma bone disease than standard bisphosphonate therapy with drugs such as Zometa (zoledronic acid) and Aredia (pamidronate). He also made it clear, though, that there are further options for attacking myeloma bone disease that pharmaceutical and biotech companies can pursue (and are pursuing).
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Boris Simkovich - Name: Boris Simkovich
Founder
The Myeloma Beacon
Re: IMW 2011 Multiple Myeloma Discussion - Day 1
Dr. Roodman's presentation was followed by presentations from Dr. Shmuel Yaccoby of the University of Arkansas for Medical Sciences (UAMS) and Dr. Nicola Giuliani of the University of Parma, Italy.
Dr. Yaccoby's presentation was titled "Bone Anabolism and Tumor Growth in Myeloma." During the presentation, Dr. Yaccoby described how he and his colleagues have had success treating myeloma bone disease with daily subcutaneous injections of parathyroid hormone (PTH, presumably the drug Forteo, from Eli Lilly, but I'll check on this). The drug, which usually is prescribed for osteoporosis, appears not only to help with bone disease; it also seems to have anti-myeloma activity, as measured by changes in patients' blood protein levels.
Dr. Yaccoby also added to the list started by Dr. Goodman by describing a wide range of other options researchers believe offer the potential for treating myeloma bone disease. Several of these options may -- like PTH -- have anti-myeloma properties in addition to being effective against myeloma bone disease.
Dr. Giuliani's presentation was titled "Effect of New Anti-Myeloma Drugs on Bone Microenvironment Cells." His presentation builds on something mentioned in Dr. Roodman's presentation about the new multiple myeloma treatments such as Revlimid and Velcade.
In particular, Dr. Giuliani explained that one reason the new drugs are so effective against multiple myeloma is that they do more than just attack the malignant myeloma cells in patients' bone marrow. Instead, they also act against myeloma bone disease.
It has been known for some time, for example, that Velcade encourages bone formation by helping to increase the body's production of osteoblasts. Dr. Giuliani noted, however, that recent research he has done suggests that Velcade may also decrease the production of osteoclasts, the cells that break down bone tissue. If true, this would mean that Velcade works against myeloma bone disease in multiple ways.
Likewise, it also is generally known that thalidomide, in addition to attacking myeloma cells in patient bone marrow, tends to decrease the body's production of osteoclasts, thus helping myeloma patients retain bone tissue. New research by Dr. Giuliani and his colleagues, however, indicates that Revlimid and the potential new myeloma drug pomalidomide -- both close chemical cousins of thalidomide -- also appear to suppress the production of osteoclasts in addition to attacking myeloma cells in the marrow.
Dr. Yaccoby's presentation was titled "Bone Anabolism and Tumor Growth in Myeloma." During the presentation, Dr. Yaccoby described how he and his colleagues have had success treating myeloma bone disease with daily subcutaneous injections of parathyroid hormone (PTH, presumably the drug Forteo, from Eli Lilly, but I'll check on this). The drug, which usually is prescribed for osteoporosis, appears not only to help with bone disease; it also seems to have anti-myeloma activity, as measured by changes in patients' blood protein levels.
Dr. Yaccoby also added to the list started by Dr. Goodman by describing a wide range of other options researchers believe offer the potential for treating myeloma bone disease. Several of these options may -- like PTH -- have anti-myeloma properties in addition to being effective against myeloma bone disease.
Dr. Giuliani's presentation was titled "Effect of New Anti-Myeloma Drugs on Bone Microenvironment Cells." His presentation builds on something mentioned in Dr. Roodman's presentation about the new multiple myeloma treatments such as Revlimid and Velcade.
In particular, Dr. Giuliani explained that one reason the new drugs are so effective against multiple myeloma is that they do more than just attack the malignant myeloma cells in patients' bone marrow. Instead, they also act against myeloma bone disease.
It has been known for some time, for example, that Velcade encourages bone formation by helping to increase the body's production of osteoblasts. Dr. Giuliani noted, however, that recent research he has done suggests that Velcade may also decrease the production of osteoclasts, the cells that break down bone tissue. If true, this would mean that Velcade works against myeloma bone disease in multiple ways.
Likewise, it also is generally known that thalidomide, in addition to attacking myeloma cells in patient bone marrow, tends to decrease the body's production of osteoclasts, thus helping myeloma patients retain bone tissue. New research by Dr. Giuliani and his colleagues, however, indicates that Revlimid and the potential new myeloma drug pomalidomide -- both close chemical cousins of thalidomide -- also appear to suppress the production of osteoclasts in addition to attacking myeloma cells in the marrow.
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Boris Simkovich - Name: Boris Simkovich
Founder
The Myeloma Beacon
Re: IMW 2011 Multiple Myeloma Discussion - Day 1
The last three presentations in the bone disease session at the Workshop today were suited more for myeloma researchers.
One of them, by Dr. Bruce Ayati of the University of Iowa, concerned "Mathematical Descriptions of Bone Remodeling Dynamics in Myeloma Bone Disease." Dr. Ayati described why mathematical modeling of bone disease can be useful, and how he and his colleagues have mathematically modeled bone disease and the way myeloma treatments -- specifically Velcade -- intervene in the progression of bone disease.
The second of the three presentations, by Dr. Pierfrancesco Tassone of Magna Graecia University in Italy, described a new way to use mice to research the effect myeloma drugs have on human bone tissue. Dr. Tassone and his colleagues have developed a way to embed human bone cells in a plastic structure which can then be implanted in mice. Drugs and other forms of treatment can then be administered to the mice, giving researchers an opportunity to see how the treatments affect actual human myeloma cells.
The final presentation was by Dr. Karin Vanderkerken of the Vrije Universiteit Brussel, Belgium. It was titled "Epigenetic Changes of Myeloma Cells within the Bone Marrow Microenvironment." It summarized research by Dr. Vanderkerken and her colleagues that builds on evidence that multiple myeloma may be, at least in part, a result of "epigenetic" changes in the way the body produces proteins.
"Epigenetic" changes in a person's protein production are changes that are abnormal, but which are not due to any mutations in the patient's DNA. These changes can potentially be reversed using one or more epigenetic drugs, of which there are several already on the market and many others under development.
Dr. Vanderkerken discussed how two existing epigenetic drugs -- Vidaza (azacitidine) and Dacogen (decitabine) -- have been shown in pre-clinical studies to have anti-myeloma activity. In addition, two epigenetic drugs under development, JNJ-26481585 and panobinostat, also have been shown to be effective against myeloma cells in pre-clinical research.
Furthermore, when JNJ-26481585 is combined with Velcade in a pre-clinical setting, the combination shows greater than expected activity against both myeloma tumor cells and myeloma bone disease. Something similar also is observed when Dacogen and panobinostat are combined in pre-clinical research; together, they have a greater than expected efficacy against myeloma cells.
One of them, by Dr. Bruce Ayati of the University of Iowa, concerned "Mathematical Descriptions of Bone Remodeling Dynamics in Myeloma Bone Disease." Dr. Ayati described why mathematical modeling of bone disease can be useful, and how he and his colleagues have mathematically modeled bone disease and the way myeloma treatments -- specifically Velcade -- intervene in the progression of bone disease.
The second of the three presentations, by Dr. Pierfrancesco Tassone of Magna Graecia University in Italy, described a new way to use mice to research the effect myeloma drugs have on human bone tissue. Dr. Tassone and his colleagues have developed a way to embed human bone cells in a plastic structure which can then be implanted in mice. Drugs and other forms of treatment can then be administered to the mice, giving researchers an opportunity to see how the treatments affect actual human myeloma cells.
The final presentation was by Dr. Karin Vanderkerken of the Vrije Universiteit Brussel, Belgium. It was titled "Epigenetic Changes of Myeloma Cells within the Bone Marrow Microenvironment." It summarized research by Dr. Vanderkerken and her colleagues that builds on evidence that multiple myeloma may be, at least in part, a result of "epigenetic" changes in the way the body produces proteins.
"Epigenetic" changes in a person's protein production are changes that are abnormal, but which are not due to any mutations in the patient's DNA. These changes can potentially be reversed using one or more epigenetic drugs, of which there are several already on the market and many others under development.
Dr. Vanderkerken discussed how two existing epigenetic drugs -- Vidaza (azacitidine) and Dacogen (decitabine) -- have been shown in pre-clinical studies to have anti-myeloma activity. In addition, two epigenetic drugs under development, JNJ-26481585 and panobinostat, also have been shown to be effective against myeloma cells in pre-clinical research.
Furthermore, when JNJ-26481585 is combined with Velcade in a pre-clinical setting, the combination shows greater than expected activity against both myeloma tumor cells and myeloma bone disease. Something similar also is observed when Dacogen and panobinostat are combined in pre-clinical research; together, they have a greater than expected efficacy against myeloma cells.
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Boris Simkovich - Name: Boris Simkovich
Founder
The Myeloma Beacon
9 posts
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