This forum thread can be used to discuss the proceedings of the International Myeloma Workshop that take place on Day 4 (Friday, May 6) 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 1, Day 2, and Day 3.
Forums
8 posts
• Page 1 of 1
Re: IMW 2011 Multiple Myeloma Discussion - Day 4
Let's get to the presentations that were given on the fourth (and final) day of the Workshop. (And, yes, I know I'm a bit behind in these updates. There have been minor things to take care of like getting back to the States and preparing some of the daily updates we've been publishing. 
)
The first session on the final day included presentations summarizing consensus reports related to four topics: Vaccination and infection prevention; the management of anemia; deep vein thrombosis; and bone disease.
We'll be covering these reports in more detail in full articles at The Myeloma Beacon. So I won't discuss them further here. However, anyone interested in reading the reports can do using the attachments that I've appended to this posting.
)The first session on the final day included presentations summarizing consensus reports related to four topics: Vaccination and infection prevention; the management of anemia; deep vein thrombosis; and bone disease.
We'll be covering these reports in more detail in full articles at The Myeloma Beacon. So I won't discuss them further here. However, anyone interested in reading the reports can do using the attachments that I've appended to this posting.
- Attachments
-
VaccinationAndInfection.pdf- (214.92 KiB) Downloaded 232 times
-
- ManagementOfAnemia.pdf
- (89.64 KiB) Downloaded 174 times
-
- DVT.pdf
- (258.02 KiB) Downloaded 131 times
-
- BoneDisease.pdf
- (128.87 KiB) Downloaded 330 times
-
Boris Simkovich - Name: Boris Simkovich
Founder
The Myeloma Beacon
Re: IMW 2011 Multiple Myeloma Discussion - Day 4
The next presentation session was different than many of the sessions in that it didn't have one single unifying theme. Instead, it was an opportunity for researchers looking at a variety of different myeloma-related topics to present the latest results of their research in a "Abstract Session".
In most cases, a researcher was given about 15 minutes to summarize the results of their research, and then, after every several presentations, there also was a chance for people to ask questions about the abstracts (article summaries) that had been presented.
The first presentation during the session was a bit of an exception. It lasted about 30 minutes. It was given by Dr. P. Andrew Futreal of the Sanger Institute in Cambridge, United Kingdom. Dr. Futreal talked about the work that led to the mapping of the myeloma genome, including how it was done and some of the initial learnings from that work.
As would be expected, the presentation was relatively technical in nature. Also, since it concerned a very recent development that is still evolving, there were not really any takeaways that can be applied to the treatment of current myeloma patients.
The first true abstract presentation during the session was given by Dr. Federica Cavallo of the University of Turin, Italy. She presented the results of a clinical trial comparing the use of
Lovenox (enoxaparin) and aspirin to prevent blood clotting in patients receiving Revlimid treatment regimens for their myeloma.
Blood clots in the leg or lungs have been observed to happen relatively often in myeloma patients being treated with Revlimid and dexamethasone. Because these clots can be dangerous, it is now is common to give patients being treated with Revlimid something to reduce the chance of blood clotting. Low-dose aspirin is one option, as are warfarin and Lovenox.
(For a recent Beacon article on the issue of blood clot prevention in myeloma patients, go to this link: https://myelomabeacon.org/news/2011/04/27/more-studies-are-needed-on-medications-to-prevent-blood-clots-in-multiple-myeloma-patients/ .)
The trial carried out by Dr. Cavallo and her colleagues involved about 400 newly diagnosed myeloma patients who were randomly assigned to take either Lovenox or aspirin while being treated with Revlimid both before and after receiving a stem cell transplant.
The preventative ("prophylactic") treatment with aspirin and Lovenox was very effective in preventing blood clots. Only 2.3% and 1.2% of the patients taking aspirin and Lovenox, respectively, experienced a serious blood clot during their treatment. Although the observed rate of clotting is clearly lower among the patients who took Lovenox, the difference is not statistically significant.
Almost all the serious blood clots that occurred took place in the early stages of each patient's Revlimid treatment. The median time until a blood clot occurred was only 1.3 months after initiation of Revlimid therapy. However, there was some difference in the timing of the clotting between the aspirin-treated patients and those treated with Lovenox. Those patients who received aspirin and got blood clots tended to get them earlier than the patients taking Lovenox.
Overall, Dr. Cavallo believes the data from this trial make it clear that patients taking Revlimid definitely should take some kind of preventative medication against blood clots during the first 4-6 months of their treatment. She also said that, in her opinion, patients taking Revlimid who are particularly at risk of developing a blood clot should be given Lovenox rather than aspirin.
In most cases, a researcher was given about 15 minutes to summarize the results of their research, and then, after every several presentations, there also was a chance for people to ask questions about the abstracts (article summaries) that had been presented.
The first presentation during the session was a bit of an exception. It lasted about 30 minutes. It was given by Dr. P. Andrew Futreal of the Sanger Institute in Cambridge, United Kingdom. Dr. Futreal talked about the work that led to the mapping of the myeloma genome, including how it was done and some of the initial learnings from that work.
As would be expected, the presentation was relatively technical in nature. Also, since it concerned a very recent development that is still evolving, there were not really any takeaways that can be applied to the treatment of current myeloma patients.
The first true abstract presentation during the session was given by Dr. Federica Cavallo of the University of Turin, Italy. She presented the results of a clinical trial comparing the use of
Lovenox (enoxaparin) and aspirin to prevent blood clotting in patients receiving Revlimid treatment regimens for their myeloma.
Blood clots in the leg or lungs have been observed to happen relatively often in myeloma patients being treated with Revlimid and dexamethasone. Because these clots can be dangerous, it is now is common to give patients being treated with Revlimid something to reduce the chance of blood clotting. Low-dose aspirin is one option, as are warfarin and Lovenox.
(For a recent Beacon article on the issue of blood clot prevention in myeloma patients, go to this link: https://myelomabeacon.org/news/2011/04/27/more-studies-are-needed-on-medications-to-prevent-blood-clots-in-multiple-myeloma-patients/ .)
The trial carried out by Dr. Cavallo and her colleagues involved about 400 newly diagnosed myeloma patients who were randomly assigned to take either Lovenox or aspirin while being treated with Revlimid both before and after receiving a stem cell transplant.
The preventative ("prophylactic") treatment with aspirin and Lovenox was very effective in preventing blood clots. Only 2.3% and 1.2% of the patients taking aspirin and Lovenox, respectively, experienced a serious blood clot during their treatment. Although the observed rate of clotting is clearly lower among the patients who took Lovenox, the difference is not statistically significant.
Almost all the serious blood clots that occurred took place in the early stages of each patient's Revlimid treatment. The median time until a blood clot occurred was only 1.3 months after initiation of Revlimid therapy. However, there was some difference in the timing of the clotting between the aspirin-treated patients and those treated with Lovenox. Those patients who received aspirin and got blood clots tended to get them earlier than the patients taking Lovenox.
Overall, Dr. Cavallo believes the data from this trial make it clear that patients taking Revlimid definitely should take some kind of preventative medication against blood clots during the first 4-6 months of their treatment. She also said that, in her opinion, patients taking Revlimid who are particularly at risk of developing a blood clot should be given Lovenox rather than aspirin.
-
Boris Simkovich - Name: Boris Simkovich
Founder
The Myeloma Beacon
Re: IMW 2011 Multiple Myeloma Discussion - Day 4
The presentation that followed Dr. Cavallo's was on the topic of minimal residual disease, which is the presence of some myeloma cells in a patient even when traditional blood protein-based measures of a patient's response to treatment indicate a complete response.
The presentation on minimal residual disease (MRD) was given by Dr. Roger Owen of St. James University Hospital in Leeds, United Kingdom. Dr. Owen and his colleagues used a technique called multiparameter flow cytometry to test for residual disease in a subset of the patients participating in the large MRC Myeloma IX trial that was conducted in the United Kingdom. Of these patients, 701 were in an arm of the trial that included a stem cell transplant, and 510 were in a non-transplant arm.
The patients in the transplant arm of the trial were given one of two combination induction regimens, either cyclophosphamide-vincristine-doxorubicin-dexamethasone or cyclophosphamide-thalidomide-dexamethasone -- followed by high-dose melphalan. After their transplants, some patients also then received thalidomide maintenance therapy.
Patients in the non-transplant arm of the trial received induction therapy with either a melphalan and prednisone or cyclophosamide, thalidomide, and dexamethasone. Some of these patients then also went on to receive maintenance therapy with thalidomide.
Dr. Owen and his colleagues used flow cytometry to determine if patients had MRD after their induction therapy, after their high dose melphalan (if they received it), and during the thalidomide maintenance therapy (if they received it).
The results of the MRD testing indicate that whether or not a patient achieves no residual disease is an important predictor of both progression free survival and overall survival. For example, progression free survival was 39 months for patients in the transplant arm who had no residual disease after their high dose melphalan therapy, but only 21 months for those who had at least some residual disease. Although fewer patients in the non-transplant arm achieved no residual disease status, those that did also had longer progression free survival.
The MRD testing also demonstrated that the thalidomide-containing induction therapy was more effective at helping patients achieve no residual disease, and patients receiving thalidomide maintenance therapy also were more likely either to maintain no residual disease or achieve that status if they hadn't already.
Dr. Owen also spoke during his presentation about whether the treatment outcomes predicted by flow cytometry were similar to those predicted by the normal blood protein-based measures of response which also were done for all patients in the trial. The results apparently were similar for the two different approaches to measuring response for higher-risk myeloma patients (based on cytogenetics). However, the flow cytometry measures seemed more useful for patients in the standard risk category.
The presentation on minimal residual disease (MRD) was given by Dr. Roger Owen of St. James University Hospital in Leeds, United Kingdom. Dr. Owen and his colleagues used a technique called multiparameter flow cytometry to test for residual disease in a subset of the patients participating in the large MRC Myeloma IX trial that was conducted in the United Kingdom. Of these patients, 701 were in an arm of the trial that included a stem cell transplant, and 510 were in a non-transplant arm.
The patients in the transplant arm of the trial were given one of two combination induction regimens, either cyclophosphamide-vincristine-doxorubicin-dexamethasone or cyclophosphamide-thalidomide-dexamethasone -- followed by high-dose melphalan. After their transplants, some patients also then received thalidomide maintenance therapy.
Patients in the non-transplant arm of the trial received induction therapy with either a melphalan and prednisone or cyclophosamide, thalidomide, and dexamethasone. Some of these patients then also went on to receive maintenance therapy with thalidomide.
Dr. Owen and his colleagues used flow cytometry to determine if patients had MRD after their induction therapy, after their high dose melphalan (if they received it), and during the thalidomide maintenance therapy (if they received it).
The results of the MRD testing indicate that whether or not a patient achieves no residual disease is an important predictor of both progression free survival and overall survival. For example, progression free survival was 39 months for patients in the transplant arm who had no residual disease after their high dose melphalan therapy, but only 21 months for those who had at least some residual disease. Although fewer patients in the non-transplant arm achieved no residual disease status, those that did also had longer progression free survival.
The MRD testing also demonstrated that the thalidomide-containing induction therapy was more effective at helping patients achieve no residual disease, and patients receiving thalidomide maintenance therapy also were more likely either to maintain no residual disease or achieve that status if they hadn't already.
Dr. Owen also spoke during his presentation about whether the treatment outcomes predicted by flow cytometry were similar to those predicted by the normal blood protein-based measures of response which also were done for all patients in the trial. The results apparently were similar for the two different approaches to measuring response for higher-risk myeloma patients (based on cytogenetics). However, the flow cytometry measures seemed more useful for patients in the standard risk category.
-
Boris Simkovich - Name: Boris Simkovich
Founder
The Myeloma Beacon
Re: IMW 2011 Multiple Myeloma Discussion - Day 4
Next on the agenda was a presentation by Dr. Elena Zamagni of the University of Bologna, Italy. Her talk focused on the extent to which the results of combined PET/CT scans of myeloma patients correlate with patient progression free survival and overall survival.
The study by Dr. Zamagni and her colleagues involved a retrospective analysis of data for 192 newly diagnosed myeloma patients who underwent induction therapy followed by an autologous stem cell transplant. All patients in the study were given combined PET/CT scans at diagnosis, following induction therapy, and after their stem cell transplant. Patients were followed for a median of 42 months after diagnosed.
When analyzing the results of the PET/CT scans, Dr. Zamagni and her colleagues focused on three metrics: the number of focal lesions found during the scan; the "standardized uptake value" (SUV) calculated during the scan; and whether or not the scan found extramedullary disease. Each of these metrics was found to be correlated with patient survival.
The "standardized uptake value" is a single value calculated during PET scans that is intended to reflect how much tumor growth is detected by the scan. Extramedullary disease in myeloma patients is myeloma tumor growth outside of the bone.
Dr. Zamagni and her colleagues found that, at diagnosis, 44 percent of the newly diagnosed patients in the trial had three or more focal lesions; 46 percent had SUV values greater than 4.2; and six percent had detectable extramedullary disease.
Patients who had three or more focal lesions at diagnosis had a 77 percent chance of surviving four years versus a 90 percent chance for those with less than three focal lesions. Those with extramedullary disease had a 60 percent chance of surviving four years versus an 89 percent chance for those without extramedullary disease. Both these differences in survival were statistically significant.
During her presentation, Dr. Zamagni said that, when she and her colleagues used statistical techniques to determine what metrics independently predict survival in the patients in their trial, they found that the presence of extramedullary disease and poor cytogenetics at diagnosis were the key variables.
It's not clear whether this last statement is a somewhat updated version of the analysis that Dr. Zamagni presented in the abstract for her presentation. There, she wrote that (a) extramedullary disease, and (b) whether or not a patient's SUV stayed high even after transplantation, were the key predictive variables. Given what she said during her presentation, however, it is possible that analyses done after her abstract was submitted showed that poor cytogenetics was correlated with persistence of a high SUV after transplantation, and poor cytogenetics did a better job of predicting poor survival compared to the persistence of a high SUV.
Dr. Zamagni also noted during her presentation that the PET/CT scans done after patients received their transplants gave results that were highly correlated with standard blood protein-based measures of treatment response.
The study by Dr. Zamagni and her colleagues involved a retrospective analysis of data for 192 newly diagnosed myeloma patients who underwent induction therapy followed by an autologous stem cell transplant. All patients in the study were given combined PET/CT scans at diagnosis, following induction therapy, and after their stem cell transplant. Patients were followed for a median of 42 months after diagnosed.
When analyzing the results of the PET/CT scans, Dr. Zamagni and her colleagues focused on three metrics: the number of focal lesions found during the scan; the "standardized uptake value" (SUV) calculated during the scan; and whether or not the scan found extramedullary disease. Each of these metrics was found to be correlated with patient survival.
The "standardized uptake value" is a single value calculated during PET scans that is intended to reflect how much tumor growth is detected by the scan. Extramedullary disease in myeloma patients is myeloma tumor growth outside of the bone.
Dr. Zamagni and her colleagues found that, at diagnosis, 44 percent of the newly diagnosed patients in the trial had three or more focal lesions; 46 percent had SUV values greater than 4.2; and six percent had detectable extramedullary disease.
Patients who had three or more focal lesions at diagnosis had a 77 percent chance of surviving four years versus a 90 percent chance for those with less than three focal lesions. Those with extramedullary disease had a 60 percent chance of surviving four years versus an 89 percent chance for those without extramedullary disease. Both these differences in survival were statistically significant.
During her presentation, Dr. Zamagni said that, when she and her colleagues used statistical techniques to determine what metrics independently predict survival in the patients in their trial, they found that the presence of extramedullary disease and poor cytogenetics at diagnosis were the key variables.
It's not clear whether this last statement is a somewhat updated version of the analysis that Dr. Zamagni presented in the abstract for her presentation. There, she wrote that (a) extramedullary disease, and (b) whether or not a patient's SUV stayed high even after transplantation, were the key predictive variables. Given what she said during her presentation, however, it is possible that analyses done after her abstract was submitted showed that poor cytogenetics was correlated with persistence of a high SUV after transplantation, and poor cytogenetics did a better job of predicting poor survival compared to the persistence of a high SUV.
Dr. Zamagni also noted during her presentation that the PET/CT scans done after patients received their transplants gave results that were highly correlated with standard blood protein-based measures of treatment response.
-
Boris Simkovich - Name: Boris Simkovich
Founder
The Myeloma Beacon
Re: IMW 2011 Multiple Myeloma Discussion - Day 4
The next presentation during the morning "Abstract Session" was given by Dr. Ulf Mellqvist of the Sahlgrenska University Hospital in Gothenburg, Sweden. He presented results of a trial examining the use of Velcade as consolidation therapy after patients receive an autologous stem cell transplant.
The trial involved 370 patients. Of those patients, 188 received Velcade after a stem cell transplant preceded by high dose melphalan treatment. The other 182 patients also received a transplant after high dose melphalan therapy, but they did not receive the Velcade consolidation therapy.
All patients in the trial had not received Velcade at any time since being diagnosed with myeloma.
The patients receiving Velcade consolidation therapy started receiving the drug 3 months after their transplant. They were given infusions at the standard dose (1.3 mg/m2) twice weekly for two three-week cycles, then once weekly for four four-week cycles, for a total of 20 doses over a 21-week period. No dexamethasone or other corticosteroid was given to the patients along with the Velcade.
Patients who received the Velcade consolidation therapy achieved a higher proportion of complete or near complete responses (45 percent of the patients in the Velcade consolidation group versus 35 percent in the control/placebo group). A higher propotion of patients in the Velcade also achieved at least a very good partial response (71 percent versus 58 percent in the control group). Both these differences in patient shares were statistically significant.
There also was a statistically significant difference in progression free survival observed between the two groups. The median progression free survival is 27 months for the Velcade-treated group of patients versus 20 months for the control patients.
Overall survival, however, is not any different between the two groups. It is 87 percent for both groups after a median of 27 months of follow-up.
Dr. Mellqvist said that, in terms of side effects, there were no major issues with neutropenia (low white blood cell counts) among the Velcade-treated patients. Blood platelet counts also were acceptable in that group.
There was, on the other hand, a greater incidence of neuropathy (tingling and lack of sensation in the extremities) in the Velcade-treated patients, though Dr. Mellqvist characterized the incidence of neuropathy among those patients as not particularly large.
The trial involved 370 patients. Of those patients, 188 received Velcade after a stem cell transplant preceded by high dose melphalan treatment. The other 182 patients also received a transplant after high dose melphalan therapy, but they did not receive the Velcade consolidation therapy.
All patients in the trial had not received Velcade at any time since being diagnosed with myeloma.
The patients receiving Velcade consolidation therapy started receiving the drug 3 months after their transplant. They were given infusions at the standard dose (1.3 mg/m2) twice weekly for two three-week cycles, then once weekly for four four-week cycles, for a total of 20 doses over a 21-week period. No dexamethasone or other corticosteroid was given to the patients along with the Velcade.
Patients who received the Velcade consolidation therapy achieved a higher proportion of complete or near complete responses (45 percent of the patients in the Velcade consolidation group versus 35 percent in the control/placebo group). A higher propotion of patients in the Velcade also achieved at least a very good partial response (71 percent versus 58 percent in the control group). Both these differences in patient shares were statistically significant.
There also was a statistically significant difference in progression free survival observed between the two groups. The median progression free survival is 27 months for the Velcade-treated group of patients versus 20 months for the control patients.
Overall survival, however, is not any different between the two groups. It is 87 percent for both groups after a median of 27 months of follow-up.
Dr. Mellqvist said that, in terms of side effects, there were no major issues with neutropenia (low white blood cell counts) among the Velcade-treated patients. Blood platelet counts also were acceptable in that group.
There was, on the other hand, a greater incidence of neuropathy (tingling and lack of sensation in the extremities) in the Velcade-treated patients, though Dr. Mellqvist characterized the incidence of neuropathy among those patients as not particularly large.
-
Boris Simkovich - Name: Boris Simkovich
Founder
The Myeloma Beacon
Re: IMW 2011 Multiple Myeloma Discussion - Day 4
There were three more presentations during the morning and early afternoon Abstract Session. Two of them concerned potential new myeloma drugs -- pomalidomide and carfilzomib -- that are still under development. I will discuss those presentations in my last posting about the session.
Now, though, I'd like to focus on the last presentation, which was given by Dr. Edward Libby of the University of New Mexico Cancer Center. (Dr. Libby is also a Myeloma Beacon Medical Advisor.)
Dr. Libby's presentation summarized the results of a study that he did with several colleagues looking at what has happened to myeloma mortality rates in the United States over the past 40 years. The motivation for this study was to see if advances in the treatment of myeloma that have occurred in the past 10-20 years have had an impact on myeloma mortality rates.
By "myeloma mortality rate," we mean the number of deaths in a year from myeloma for every 100,000 people. If the myeloma mortality rate for a given year is, for example, 10, it means that in that year 10 people died from myeloma for every 100,000 people in the population.
This definition is important, because it points out that changes in the myeloma mortality rate can change for at least two reasons.
Obviously, the myeloma mortality rate will decline if treatments for myeloma get more effective. We all hope, for example, that someday soon there will be a true cure for myeloma. When that happens, the myeloma mortality rate should drop considerably, reaching close to zero.
There is a second factor, however, that also can affect mortality rates. If, for example, there is a change in the environment that causes a greater share of the population to get myeloma each year, then, all things being equal, the myeloma mortality rate will increase.
You might also think that changes in the age distribution of the population might change the myeloma mortality rate. If the population gets increasingly older over time, and myeloma is more prevalent among older people (which it is), this would increase the myeloma mortality rate.
Most of the time, however, myeloma mortality rates are "age-adjusted" so that changes in the population's age distribution have little or no affect on the reported mortality rates.
So what do the mortality data tell us?
Dr. Libby and his colleagues focused mainly on two different myeloma mortality rates. In particular, they looked at the myeloma mortality rate in the population that is less than 65 years old, and at the rate in the population older than 65.
What they found is that, in the U.S. population younger than 65 years of age, the myeloma rate increased slightly every year from 1970 to about 1995. It went from 0.85 deaths from myeloma for every 100,000 people under the age of 65 in 1970 to about 1.15 deaths per 100,000 in 1995. (See the first graph below.)
From 1995 onward, however, the myeloma mortality rate in this age group dropped almost every year, reaching about 0.75 in 2007, the last year for which there is data.
In the population 65 years of age and older, the pattern is a bit different. (See the second graph below.) There is still a noticeably increase in mortality rates from 1970 until about 1993. Rates go from 14 myeloma deaths per 100,000 people to in 1970 to about 22 deaths per 100,000 people in 1993. After 1993, however, mortality rates stay constant until about 2002, when they start to drop, reaching about 20 myeloma deaths per 100,000 in 2007.
What accounts for these patterns in the mortality rate? Dr. Libby and his colleagues find it easiest to explain the pattern for the under 65 population. Stem cell transplants started to become a common treatment option for myeloma in the 1980s and 1990s, and the first novel myeloma therapy -- thalidomide -- started seeing increasing use in the early 2000s. Together, these factors probably account for the decline in under-65 mortality starting in 1995.
The flattening of over-65 mortality between 1993 and 2002 is a bit more difficult to explain. Only a limited share of older myeloma patients typically receive stem cell transplants, so the spread of that treatment option really can't explain the flattening of mortality rates in the 1990s and early 2000s.
Perhaps, Dr. Libby and his colleagues speculate, the flattening might be due to improvements in supportive care that may have been been implemented during these years.
The improvement in mortality rates in the older population after 2002, on the other hand, is almost certainly due to the increasing use of novel myeloma therapies (thalidomide, Velcade, and eventually Revlimid) in older myeloma patients.
Now, though, I'd like to focus on the last presentation, which was given by Dr. Edward Libby of the University of New Mexico Cancer Center. (Dr. Libby is also a Myeloma Beacon Medical Advisor.)
Dr. Libby's presentation summarized the results of a study that he did with several colleagues looking at what has happened to myeloma mortality rates in the United States over the past 40 years. The motivation for this study was to see if advances in the treatment of myeloma that have occurred in the past 10-20 years have had an impact on myeloma mortality rates.
By "myeloma mortality rate," we mean the number of deaths in a year from myeloma for every 100,000 people. If the myeloma mortality rate for a given year is, for example, 10, it means that in that year 10 people died from myeloma for every 100,000 people in the population.
This definition is important, because it points out that changes in the myeloma mortality rate can change for at least two reasons.
Obviously, the myeloma mortality rate will decline if treatments for myeloma get more effective. We all hope, for example, that someday soon there will be a true cure for myeloma. When that happens, the myeloma mortality rate should drop considerably, reaching close to zero.
There is a second factor, however, that also can affect mortality rates. If, for example, there is a change in the environment that causes a greater share of the population to get myeloma each year, then, all things being equal, the myeloma mortality rate will increase.
You might also think that changes in the age distribution of the population might change the myeloma mortality rate. If the population gets increasingly older over time, and myeloma is more prevalent among older people (which it is), this would increase the myeloma mortality rate.
Most of the time, however, myeloma mortality rates are "age-adjusted" so that changes in the population's age distribution have little or no affect on the reported mortality rates.
So what do the mortality data tell us?
Dr. Libby and his colleagues focused mainly on two different myeloma mortality rates. In particular, they looked at the myeloma mortality rate in the population that is less than 65 years old, and at the rate in the population older than 65.
What they found is that, in the U.S. population younger than 65 years of age, the myeloma rate increased slightly every year from 1970 to about 1995. It went from 0.85 deaths from myeloma for every 100,000 people under the age of 65 in 1970 to about 1.15 deaths per 100,000 in 1995. (See the first graph below.)
From 1995 onward, however, the myeloma mortality rate in this age group dropped almost every year, reaching about 0.75 in 2007, the last year for which there is data.
In the population 65 years of age and older, the pattern is a bit different. (See the second graph below.) There is still a noticeably increase in mortality rates from 1970 until about 1993. Rates go from 14 myeloma deaths per 100,000 people to in 1970 to about 22 deaths per 100,000 people in 1993. After 1993, however, mortality rates stay constant until about 2002, when they start to drop, reaching about 20 myeloma deaths per 100,000 in 2007.
What accounts for these patterns in the mortality rate? Dr. Libby and his colleagues find it easiest to explain the pattern for the under 65 population. Stem cell transplants started to become a common treatment option for myeloma in the 1980s and 1990s, and the first novel myeloma therapy -- thalidomide -- started seeing increasing use in the early 2000s. Together, these factors probably account for the decline in under-65 mortality starting in 1995.
The flattening of over-65 mortality between 1993 and 2002 is a bit more difficult to explain. Only a limited share of older myeloma patients typically receive stem cell transplants, so the spread of that treatment option really can't explain the flattening of mortality rates in the 1990s and early 2000s.
Perhaps, Dr. Libby and his colleagues speculate, the flattening might be due to improvements in supportive care that may have been been implemented during these years.
The improvement in mortality rates in the older population after 2002, on the other hand, is almost certainly due to the increasing use of novel myeloma therapies (thalidomide, Velcade, and eventually Revlimid) in older myeloma patients.
- Attachments
-
- LibbyEtAl-Under65USMyelomaMortalityRateV2.png (123.63 KiB) Viewed 1499 times
-
- LibbyEtAl-65AndOverUSMyelomaMortalityRateV2.png (103.74 KiB) Viewed 1499 times
-
Boris Simkovich - Name: Boris Simkovich
Founder
The Myeloma Beacon
Re: IMW 2011 Multiple Myeloma Discussion - Day 4
I hope everyone has found these notes from the IMW 2011 conference helpful.
I know there is a lot of material in the postings, and I also know the postings are sometimes relatively technical.
However, if you can find the time to work your way through the session summaries, I think you'll find them very helpful for understanding what myeloma researchers currently think about the best ways to diagnosis and treat myeloma.
As I start to wrap up these notes, I want to thank again the Tackle Cancer Foundation,
http://www.tacklemyelomafoundation.com/
for providing some of the financial support needed to allow us to cover the Workshop in such detail. The Foundation, as many of you know, is the legacy of Elijah Alexander, an NFL linebacker who was diagnosed with myeloma in 2005 and, unfortunately, passed away as a result of the disease last year. Elijah's Foundation is still doing great work, and we appreciate the support they provided for our coverage of this year's Workshop.
I know there is a lot of material in the postings, and I also know the postings are sometimes relatively technical.
However, if you can find the time to work your way through the session summaries, I think you'll find them very helpful for understanding what myeloma researchers currently think about the best ways to diagnosis and treat myeloma.
As I start to wrap up these notes, I want to thank again the Tackle Cancer Foundation,
http://www.tacklemyelomafoundation.com/
for providing some of the financial support needed to allow us to cover the Workshop in such detail. The Foundation, as many of you know, is the legacy of Elijah Alexander, an NFL linebacker who was diagnosed with myeloma in 2005 and, unfortunately, passed away as a result of the disease last year. Elijah's Foundation is still doing great work, and we appreciate the support they provided for our coverage of this year's Workshop.
-
Boris Simkovich - Name: Boris Simkovich
Founder
The Myeloma Beacon
8 posts
• Page 1 of 1