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Myeloma Voices

DurieBlog_China2014.pngThe IMF Asia Pacific team members just returned from China, where we participated in the annual activities of the IMF's Chinese Myeloma Working Group (CMWG). The team that was in China for the April 9-13th educational events included Dan Navid (Senior Vice President, Global Affairs); Lisa Paik (Senior Vice President, Clinical Education & Research Initiatives); Susie Novis (President) and myself.

The annual the patient seminar this year was held at Zhejiang University 1
st Affiliated Hospital in Hangzhou, about one hour by train south of Shanghai. As in previous years, it was an amazing, heartwarming and heart-wrenching program. The meeting was hosted by Prof. Zhen Cai, a member of the CMWG, and approximately 200 patients and family members participated.

It was wonderful to have a chance to meet the "myeloma doctor team" taking care of patients at Zhejiang Hospital, including graduates of the IMF's Myeloma Master Class.

The meeting began with formal presentations by Prof. Cai, along with the head of nursing services for this 3,000-bed hospital! Ne
xt, the Q&A session began, and with the help of a translator, I launched into a couple of prepared questions. A few hesitant patients began asking questions. That opened the door, and then they really got rolling--it turned into a very lively session! Patients and caregivers were waving their hands, anxious to have their questions answered. It was an avalanche of questions from the audience that went on for more than an hour, until time was called. Off-stage "sidebar" questions continued until I left the hospital about an hour later.

The experience reinforced something I've emphasized many times in the past - "patients are patients" no matter where they li
ve--in China, the US, Europe, or even in Outer Mongolia (where I've actually received questions). In essence from everywhere. Patients want to know: How do I know the treatment is working? Should I switch treatment or continue maintenance? Should I have a stem-cell transplant? Will there be trials for some of the new treatments? Is my father going to be okay or should he fly to the US right away?

The basic treatment available in China is remarkably good. Typical first therapy is CyBord (cyclophosphamide, bortezomib and dexamethasone), followed by a single auto-transplant and thalidomide maintenance. As evidenced in
our recent database report from Asia and discussed in our Asia Myeloma Guidelines, overall outcomes are remarkably good. The major concerns and challenges occur when standard treatments fail. However, the back-up options are limited. Access to trials and the novel agents is definitely limited - as is unfortunately the case globally outside the US. Thus, the IMF is committed to work through the CMWG and our AMN colleagues to enhance trials and access as much as possible.

After a break for lunch we headed to further meetings, the most notable of which was our annual CMWG "summit" meeting. We discussed ongoing activities, presented this year by Prof. Jian Hou from Shanghai, and then I reviewed the opportunities for t
he implementation of the Black Swan Research Initiative in China. There is great interest and enthusiasm about BSRI. A key point is that the new flow cytometry test for myeloma (which I wrote about here) will be feasible in China, since several centers have flow cytometry available. We discussed the rollout and testing plans to incorporate the new flow cytometry method. A meeting will be held in China, similar to the one we recently held in Salamanca, Spain. This will provide a full education in China about the new cytometry method for assessing disease. Similar meetings will be held later this year in the US and Europe.

It was exciting to see how, once again, the same ideas, hopes and expectations are similar in China as elsewhere. Susie is right - we are "
One Myeloma Nation"! The solutions will come from global efforts by the IMF, CMWG, IMWG and colleagues and friends around the world - whether they be in Hangzhou, Heidelberg, Los Angeles, Nantes or who knows where! Networking with local experts is essential. Progress, thankfully, is inevitable and happening every day.

Stay tuned as we keep you abreast of exciting updates as they occur.





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A significant event in the evolution of the IMF's Black Swan Research Initiative occurred this past weekend in Salamanca, Spain. On March 21-22, the IMF-EuroFlow Workshop - co-organized by Lisa Paik (Senior Vice President of Clinical Education and Research Initiatives at the IMF) and the Salamanca-based flow cytometry team - focused on a breakthrough in the standardized detection of minimal residual disease (MRD) in myeloma. 

This new technique is an automated and highly sensitive flow cytometry for the standardized detection of minimal residual disease (MRD) in multiple myeloma. Excited to learn about the latest advance in this method, approximately 70 participants from 13 different countries attended the workshop. There, they learned in a "hands-on" fashion the full details of the new myeloma detection antibody panel and the computer software, which provides results in a standardized automated fashion: identifying each single cell (myeloma or not) in the bone marrow and/or blood samples.  

I am thrilled to report that the workshop was a success! Attendees left ready and enthusiastic to introduce the new methods in their home laboratories.  Professor Alberto Orfao (Head of the Flow Team in Salamanca) and Professor Jacques van Dongen (his colleague from the EuroFlow team at Erasmus in Amsterdam) did a fantastic job in constructing and implementing an intense and detailed program that more than fulfilled the educational needs of the attendees.

From there, Dr. Bruno Paiva (a key Black Swan investigator from Pamplona in Spain and expert at analyzing patient outcomes) and I traveled directly to the FDA in Silver Spring, Maryland to participate in the FDA-NCI Roundtable: "Symposium on Flow Cytometry Based on the Detection of Minimal Residual Disease in Multiple Myeloma." The bottom line for this roundtable was also tremendously helpful and important for the Black Swan Research Initiative. There is a strong consensus evolving that MRD assessment is both required and recommended for response assessment in clinical trials, and that the new flow methodology is the most promising current approach.

Thus, MRD testing is becoming mainstream and flow is the method of choice. So the Black Swan Research Initiative is definitely "going with flow" right now and we have high expectations that new trials including MRD assessment will lead to better outcomes for all myeloma patients.

Dr. Durie sincerely appreciates and reads all comments left here. However, he cannot answer specific medical questions and encourages readers to contact the trained IMF Hotline staff instead. Specific medical questions posted here will be forwarded to the IMF Hotline. Questions sent to the Hotline are answered with input from Dr. Durie and/or other scientific advisors and IMWG members as appropriate, but will not be posted here. To contact the IMF Hotline, call 800-452-CURE, toll-free in the US and Canada, or send an email to hotline@myeloma.org. Hotline hours are 9 am to 4 pm PST. Thank you.


after the Flow Cytometry test how does one know if the myeloma is hiding somewhere else in the body besides where it was tested. Is it a complete test or only a really really good guess?

Will this flow test need to be approved by the FDA before it can be used on a wide spread basis by all myeloma specialists?
How soon could patients expect to see this in everyday use?

Could the Flow Test Cytometry test be a viable method to track those with Non-secretory Multiple Myeloma?

Is this the same as the MULTI parametric FLOW CYTOMETRY (MFC) used at Mayo Clinic?

The Mayo team is introducing the new method now.

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A recent editorial in Leukemia authored by doctors Shaji Kumar and Vincent Rajkumar of the Mayo Clinic in Rochester, MN, provides a thoughtful overview of the current status of minimal residual disease (MRD) assessment in myeloma. In it, the authors raise three questions: What are the implications of MRD negative status? What is the best method to measure it? And what do the results mean for treatment?

In introducing answers to these questions, the authors identify key aspects of the IMF's Black Swan Research Initiative, including how to interpret MRD test information; which tests to use; and most importantly, how to use MRD test results to improve outcomes and achieve true cure for myeloma patients.

From the patient perspective, it is important to realize that a negative result (MRD-Zero) does not automatically mean a patient is cured. We are learning that sustained MRD-Zero combined with other test results such as stringent CR (sCR) plus negative imaging and/or scan results can indeed translate into cure for a subset of patients. But there is more work to be done.

A Promising MRD Testing Method

The first project of the Black Swan Research investigators team was to identify the most useful MRD method. Flow cytometry was identified as a promising technique, and a collaboration was established with EuroFlow and the University of Salamanca (now also Pamplona) to develop a very sensitive, reproducible method with a computer software readout to truly standardize the method. 

Within the last year this research project has been highly successful and the results will be presented to the myeloma scientific community at a workshop in Salamanca, Spain March 20-21. Groups from the US, Europe and the Asia-Pacific region will participate in this IMF-co-sponsored meeting to reach consensus on this new flow cytometry method for MRD testing. It is strongly anticipated that this can become the new standard test which be both widely available and affordable (approximately $100 per test). The full educational rollout of this test will occur in the coming months.

Development of this test is not the end of the story, but it provides an immediate benchmark for ongoing trials and comparisons with other methods. In the short term, MRD testing is complementary to other methods of response assessment and trial endpoints.

MRD Testing and Treatment Strategies

The important third point is how to change treatment strategies based upon MRD test results? Should treatment be stopped if sustained MRD-Zero is achieved? Is it more prudent to consider some consolidation and/or maintenance therapy? Obviously trials are needed and are in development now. If MRD is positive in the setting of high-risk disease can specific back-up therapy be recommended?

Again, a key area within the BSRI is to determine the sensitivity/resistant patterns of residual clones and initiate appropriate clinical trials. Another scenario is if the residual MRD has an "MGUS signature" pattern. Interestingly, this is probably the most secure situation right now in which we can recommend careful follow-up "off therapy" to see if the residual MGUS is sustained--indicating a functional cure state.

So it is obvious that much exciting work needs to be done--BUT having a reliable test and interpretation strategies are key steps in moving the search for a cure forward!

Stay tuned on this...there is definitely much more to come soon.

Dr. Durie sincerely appreciates and reads all comments left here. However, he cannot answer specific medical questions and encourages readers to contact the trained IMF Hotline staff instead. Specific medical questions posted here will be forwarded to the IMF Hotline. Questions sent to the Hotline are answered with input from Dr. Durie and/or other scientific advisors and IMWG members as appropriate, but will not be posted here. To contact the IMF Hotline, call 800-452-CURE, toll-free in the US and Canada, or send an email to hotline@myeloma.org. Hotline hours are 9 am to 4 pm PST. Thank you.
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MRD is interesting but to the layman what is the definition ? I can guess that there is an indication that Multiple Myeloma, which my wife has, no longer shows as a cancer in a treated patient. But there somehow lies the cancer in a somewhat dormant state. So, though the there is no apparent indication of MM Cancer, there lies some residual low level cancer which can be detected through a special test.
Please let me know if this is correct and how MRD is detected in a patient.

Thank You

Is it possible for anyone (aka me) to read the full Kumar-Rajkumar editorial?

I want to share with all myeloma patients that my father is cancer free of myeloma
After taking Alpha lipoic acid. This natural antioxidant is cheap and effective.
He was very close to death. After two weeks of taking two capsules a day the
doctor couldn't find cancer cells on the blood test. We never told the doctor
because he never aloud any suggestion that we ask him. Well this time
my father felt that he had to take a chance. It never interfere with the doctor therapy .
You can't go wrong to try it. Best wishes to all.

Hi Omar,

Good to know about your dad. Can you tell me what stage of Myeloma was your dad in and what treatment he was undergoing? Is it okay to still take Alpha lipoic acid if Velcade is already used for treatment?

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This week there are several interesting items in the news that help us understand how and why monoclonal gammopathy of undetermined significance (MGUS) occurs, and when it may or may not turn into active myeloma.

Matthew Drake and the Mayo Clinic bone research team worked with a group from Sheffield University in the UK to illustrate that the bones in MGUS patients are not normal. MGUS patients have weakened bones versus age and sex matched controls. There is increased porosity ("more holes") in surface bone and reduced bone strength. This is important and at the same time quite puzzling. It is important since we now need to be looking more closely at this to assess if bone treatments, such as we use in active myeloma, need to be considered also for MGUS patients. But the puzzling part is that we associated bone problems with the "B" in "CRAB," features characteristic of active myeloma. 

So we need a new level of scrutiny about the type and severity of bone damage that indicates transition to active myeloma. These indicators are: a positive PET/CT scan; definite lesions on a whole-body low-dose CT scan, and or/multiple lesions on an MRI scan. Just reduced bone density is not specific enough or sufficient. This is certainly not the end of the story in terms of understanding what is happening in MGUS versus the major change that occurs with serious bone destruction in active myeloma.

Another interesting story that caught my attention is the report of the full genetic sequencing of sharks that have cartilage, but no true bone like humans. It turns out that sharks are completely missing all the genes needed to make bone. It also turns out that they are also missing genes linked to the immune and blood system which are part of the same complex. What you may not know is that sharks rarely develop "bone" cancer (such as myeloma). It was thought that this was because cartilage blocks cancer formation. 

I carried out research years ago which revealed that there is some evidence for this idea. If you add cartilage components to myeloma cultures, growth of the myeloma is slowed - a little, but not a lot. Despite this there was a phase of great enthusiasm about "shark cartilage" treatments. And some short-term benefits were seen. But now it is clear that sharks lack hard bones and also lack the cells that can link in with myeloma cells to increase myeloma cell growth. Having hard strong bones is excellent. But these bone cells, if triggered the wrong way, can lead to bone destruction, immune defects, and ultimately myeloma in some cases.

Our old ideas have been turned upside down! It is not the presence of cartilage which makes the difference, it is the absence of bone cells.

Triggering the activity of the myeloma cells is the key aspect of myeloma and true bone destruction. A study from the Swedish team shows that increased Freelite levels are still a reliable indicator of disease progression to active myeloma. Yet another study looking at the overall cell genetics shows that many genes are involved in the activation of MGUS and the predisposition to MGUS in the first place.

So, lots of things in the news. Always many new things to learn. Every new detail allows us to understand better and guide patients with critical decisions for recommended diagnostic testing and treatment choices. 

Dr. Durie sincerely appreciates and reads all comments left here. However, he cannot answer specific medical questions and encourages readers to contact the trained IMF Hotline staff instead. Specific medical questions posted here will be forwarded to the IMF Hotline. Questions sent to the Hotline are answered with input from Dr. Durie and/or other scientific advisors and IMWG members as appropriate, but will not be posted here. To contact the IMF Hotline, call 800-452-CURE, toll-free in the US and Canada, or send an email to hotline@myeloma.org. Hotline hours are 9 am to 4 pm PST. Thank you.


Thank you for this information, since I was diagnosed a year ago with "smoldering multiple myeloma at age 83 yrs of age, I have wondered if there is any link to this diagnosis and the diagnosis of severe osteoporosis, I was diagnosed at 65 years of age and have been on continuous treatment of different brands of bisphonates?
I appreciate the learning opportunities from the web site Thank you Margaret Dennis

It might also be interesting to follow those with increased porosity in surface bone and reduced bone strength with no MGUS to see if MGUS develops in these folks more often than in those with normal bone density. Perhaps "putting the cart before the horse", but I've often wondered whether people with osteopenia/osteoporosis are inviting a nice "snack" that healthy solid bone tissue doesn't easily permit, even before abnormal cells are present...

I have M-Gus for many Years and wonder if a PET/Cat Scan Is advised of full Body? I do take Calcium/VitaminD and Magnesium Supplements...Was never told to do anything other than yearly Blood Tests Thank you LInda Lieberman

I had been diagnosed with several compression fractures of my back when I fell about two years ago. Never fell or had been sick. Very athletic. Ortho dr said it will heal although he mentioned I had osteoporosis. I am a healthy 68 year male. Well, 6 months later and no healing or diagnosis, I was admitted to hospital. And got hooked up with an oncologist who put two and two together and came up with Stage 3 Multiple Myeloma!! To our family shock, we did not know where or how this happened. Shortly after that, my sternum fractured and collapsed with much pain! After 8 months of chemo, we finally were ready for bone marrow transplant last March. All went well there and put my myeloma into very good partial remission (inactive) and was put on a follow up clinical study at Moffitt Cancer center of Velcade shots 4 weeks on 4 weeks off for one year, almost coming to an end in April 2014. Meanwhile, my lesions/bones have never really healed to the point of no pain. Still have much pain and on pain medication. Too late for cyphoplasty surgery because of late diagnosis. Getting Zomata IV once a month to strengthen bones. So if you could find some way to lessen bone pain in myeloma patients other than strong pain meds, this would help a lot of myeloma patients with bone pain. Appreciate your blog and am in a myeloma support group.

I find that very interesting as I probably had MGUS for several years before the progression to what was ultimately initially diagnosed as a single solitary plasmacytoma. However, the destruction was significant. T3 was toast, T4 was affected as well as the 3rd and 4th left rib. I guess the initial weakness made it more likely to have so much bone destroyed once the disease geared up. There was never anything alarming in my blood work to indicate disease....just that bone density indicated osteopenia. Wow....wish I'd known that years before. I have been living with myeloma for 7 years now. Hopefully, you will come up with a cure soon! I appreciate all the work you do.

Do the same density, porosity, and strength characteristics and trends prevail after identification/ classification (e.g. CRAB) of multiple myeloma?

Any studies available?
Thanks much!

Hello Dr. Durie,
I found out first hand that patients with MGUS can have bone abnormalities. When I was diagnosed with Myeloma in Feb. 2011, it was approx. 6-7 months after being diagnosed with MGUS.( I was 52 yrs. old) My blood work did not show full blown Myeloma as of yet. So, we were at a watch and wait period, with no major concerns about progression at that time. In Dec. of 2010, I was doing heavy work at my job after the big post- Christmas snowstom, when suddenly, my neck cracked at c-4. I did not know that that was what actually happened, so I continued to work for the next 10 days, until I literally could no longer move. An MRI revealed abnormalities inside my cedrvical spine, and a PET SCAN revealed several lessions. Sure enough, there was a plasmacytoma, which I had removed during surgery, in addition to having titanium rods placed in my neck. So yes, it is possible to have bone abnormalities with MGUS, AND IT IS POSSIBLE THAT SOMETHING MAY BE GOING ON WITHOUT SHOWING UP RIGHT AWAY IN THE BLOODWORK. Thank you for your column, Gary Soccorso

I was diagnosed in 1996 at the age of 36 with MGUS. At this point I am still considered smoldering or a stage 1. I had 10 years of Aredia so my bones seem to be very strong, however, I was recently diagnosed with HLA-B27 and do have some form of arthritis. I also do have osteopenia which I think many women my age have. My only concern and I do see my doctor every 6 months and still have avoided any treatment is that my freelite ratio is high ....30.82 mg/dl . It has been as high as 44.50 mg/dl. I feel good so have chosen and have really been advised by my doctor to not start any treatment. I hope I am doing the right thing.My IGG level fluctuates between 3900-4200. I would be curious as to what other people think of my situation. I have been extremely lucky all these years. Debbie


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A new study shows that regular aspirin use reduces the risk of myeloma. Researchers from Brigham and Women's Hospital and Harvard University studied 2,395,458 person-years and showed a 39% lower myeloma risk among individuals with a cumulative average of more than 5 adult strength (325 mg) aspirin tablets per week.

Many details were reviewed and assessed as part of this carefully designed study.  A "4 year lag period" was built in to exclude patients who might have been developing myeloma in the 4 years prior to the study. Length of aspirin use was considered. Greater than 11 years of use gave the most benefit. Men appeared to derive more benefit than women.

But, as they say, "the devil is in the details." Researchers are always worried that something unforeseen may have skewed the results. Some previous studies have shown no impact from regular aspirin use. However, more recently, there are several reports of reduced risk of solid cancers (such as colon cancer) and lymphomas with regular aspirin use.

There is also a need to understand why the aspirin is working. In research lingo, the results have to be "plausible." There are indeed good reasons why aspirin can provide benefit. The anti-inflammatory and anti-oxidant effects involve key pathways such as NF-kB, COX-2, IL-6, and cyclin D1--all known to be important in myeloma progression. Chronic inflammation produces "free radicals" in the tissues, which among other things can damage DNA. Obviously, reducing or preventing chromosome damage is a very good thing.

This is a carefully designed study, but appropriately the authors advise "caution in the interpretation of our findings." Nonetheless, with something as simple as an aspirin a day, which provides many potential health benefits, the added value is worth considering. A key question is: "Can aspirin use reduce or prevent the activation of MGUS or smoldering myeloma into full blown myeloma?" A tantalizing question indeed!  Carefully designed prospective studies are definitely warranted.

It is not clear if a baby aspirin (as used to reduce cardiovascular risks) is sufficient or whether in the case of cancer, a full adult dose (325 mg) provides any additional benefit. Stay tuned for further details. I'm sure new research results will be coming soon.

In the meantime, check with your doctor and unless aspirin use is not possible or not recommended in your situation, "an aspirin a day to keep the doctor away" is perhaps an idea whose time has come while we await definitive long-term results!

Dr. Durie sincerely appreciates and reads all comments left here. However, he cannot answer specific medical questions and encourages readers to contact the trained IMF Hotline staff instead. Specific medical questions posted here will be forwarded to the IMF Hotline. Questions sent to the Hotline are answered with input from Dr. Durie and/or other scientific advisors and IMWG members as appropriate, but will not be posted here. To contact the IMF Hotline, call 800-452-CURE, toll-free in the US and Canada, or send an email to hotline@myeloma.org. Hotline hours are 9 am to 4 pm PST. Thank you.


Thanks to the many of you who wrote in about Dr. Durie's blog on the reported effects of daily aspirin on prevention of myeloma.  Rather than answer each of you individually, as we normally do, we thought it best to add this addendum to the blog.

The medical article about daily aspirin use and the incidence of myeloma was certainly good food for thought and further research, but really raises more questions than it answers.  This is incidental data mined from a large study of male doctors over a long period of time. It was not designed to test any specific hypothesis about the long-term effects of aspirin at a given dose.
Here are some of the things we still don't know:
  • We don't know if aspirin merely lowers the risk of the incidence of myeloma, or if it actually has any anti-myeloma effect once a patient has been diagnosed.
  • We don't know whether the dose of aspirin is significant: in the study, the men taking the pill were using it for pain relief and were taking at least 325 mg (full-strength) daily.  Would 81 mg also be effective?  We have no data.
  • We don't know how much aspirin a person needs to take over what period of time to have an effect. Is the length of time of aspirin consumption--that is, the total cumulative dose--significant?  The benefits of aspirin only became apparent after many years of regular use in the reported study.  How much is enough?
Many times Dr. Durie blogs about interesting medical articles relating to myeloma or cancer research because they are good food for thought and for discussion with one's treating physician, and because they provide a new insight or a new theory that will lead to further research.  

Our present knowledge of daily aspirin use in the myeloma patient community relates only to its use as prophylaxis (prevention) of "venous thromboembolic events," or VTEs (ie blood clots) in a subset of patients who are receiving therapy with an immunomodulatory agent (IMiD, that is, Thalomid, Revlimid, or Pomalyst) AND dexamethasone.  All patients taking a combination IMiD and dex must be assessed for risk of blood clots by the treating physician, and treated according to published guidelines depending upon risk.  

Here is a link to the International Myeloma Working Group guidelines on prevention of thalidomide- and lenalidomide-associated thrombosis in myeloma: http://myeloma.org/pdfs/DVTGuidelinesDec2007.pdf

Please note:
  • Aspirin in an NSAID (non-steroidal anti-inflammatory agent). Those who are not supposed to take NSAIDS, usually because of kidney issues, should not consider daily aspirin use. 
  • Use of aspirin or any other drug specifically to prevent blood clots during therapy with an IMiD alone (for example, during Revmilid maintenance therapy) is NOT recommended by the IMWG. 


I really don't know we should take 81-mg or 320-mg aspirin?

I am a 5+ year survivor of MM and am completely confused about taking aspirin. I have spoken to many specialists in the field and some say take only 81 mg of baby aspirin; some say take full strength (325 mg and others say they do not recommend aspirin at all while on maintenance Revlimid therapy.

I'm totally confused as to the right answer!!! It sounds like this is trial and error and no one has the absolute right answer!

Please comment!

Henry, you may wish to call the hotline, but from my own experience, it is very important that you talk with the specialist that is treating your myeloma and your primary care physician and make sure that they are talking to each other!

I was on 81 mg aspirin when I was on Revlimid because Revlimid can cause blood clots. But if you take another blood thinning medication while on Revlimid, it is very possible that you do not want to be on aspirin as well.

Aspirin can also upset and cause damage to the stomach and esophagus. So you may want to avoid it if you have those issues. This is why you want to make sure that your doctors are talking with each other as your myeloma specialist may not be aware of other medical issues that you that your primary care physician does (and vice versa).

Aspirin is an outstanding drug, but is not a benign one for those with GI and/or bleeding problems. Talk with the right doctors.

You are right, though, a lot of this does seem indeed like trial-and-error, because in a sense, it is. The report above was based on a study. If I recall these studies correctly, the participants self-selected whether or not they take aspirin rather than being randomized to it. People who self-select may be more health conscious to begin with which may also lower the risk of myeloma (healthier eating, less exposure to toxins, etc.). These are some initial (and promising) findings, but there isn't absolute certainty yet.

All the best to you!

I am also a 5+ year survivor of MM diagnosed March of 2008 and also confused about taking aspirin. I have been on 81mg aspirin throughout my treatment and continue on it after my Rev/Dex/Velcade maintenance therapy has ended.

How should I discuss this with my Doctors?

If I'm in remission with MM can adult aspirin help
Prevent it from progressing? I have been taking it
For almost 2 yrs now one adult aspirin a day?
Thanks for your help

reducing inflammation, NF-KB, IL6 ... this sounds really familiar to those of us who take curcumin... studies have shown that curcumin works this way as well.

Are there or have there been any studies using aspirin to prevent progression from smoldering myeloma to active myeloma?

Dr. Durie,

I am Smoldering MM and have been told not to use NSAIDS in order to preserve kidney function (my kidney values have always been WNL); I will use acetaminophen for pain relief/inflammation.

Since aspirin is an NSAID, how do we assess this new study info ? Is the thought the potential benefit might outweigh the potential risk of kidney damage?

Hope to hear a response from the IMF team ! Thanks so much.

I hope to see you at the Boca Seminar this month.
lazy year in the breakout session you told me some very good news. I am smoldering since 2008 there is no and you said that the chance of becoming full blown lessens myeloma lessens with each additional year.
There are studies that the possibility of treating "early MM "
is being studied . The ASH 2013 has some info on that.
I am wondering your feelings on that thought.
Thank you,
Katherine Morgan

Six years cancer free following diagnosis MM treated with chemo and stem cell(own cells)transplant .Clinical trial thalidomide/prednisone 5 yrs. current drugs Coversyl 8mg,Rosuvastatin 10 mg , Aspirin 81 mg all once daily. Exercise three times weekly. blood pressure ok ,lower pulse rate. mental health good. Age 70 years 20 pounds over ideal weight. Wondering if anyone has thoughts or experience regarding Viagra or Cialis to share. Some say "caution " Thanks in advance of your response.

Dr. Durie:
Have you read Dr. Perlmutter's "Grain Brain"? He recommends a lot of the items you have suggested: aspirin or anything that reduces inflammation, reduce your blood sugar. Sleep enough. Exercise. as well as NO GLUTEN. I have been following most of his advice since November (hard to keep down the carbs! but I have been eating 85% chocolate...oh my)
--am on Pomalidomide (ok, Pomalyst) and my oncologist admitted to a "75% miracle" on my last visit.
I'm Kappa, double stem cell transplant (chemo/radiation at COH, Duarte), diagnosed 2007 (back collapsed--lost 3 inches-- hiked to the top of mt Hoffman 10,000 plus elevation2013 summer...) relapsed 2012 and had flavor of the month for the last 2 years...
Try his diet! Helped improve my recall and brain function after all the drugs.

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A recent article in the medical journal Cancer Cell documents the widespread chromosomal abnormalities present in myeloma cells. The sobering data from this study, the largest of its kind, also demonstrate why the promise of individual therapies targeted against individual genes is fading--and why the Black Swan Research Initiative approach offers a smarter plan of attack against myeloma.

We've known for several decades that myeloma cells have many chromosomal abnormalities. This is, in fact, the characteristic feature of myeloma at the molecular level. It has also been known and well documented that clonal evolution occurs and multiple subclones exist. Despite that, there has been a strong interest in developing personalized targeted therapies against individual gene mutations. (See my blog, "The Promises and Challenges of 'Personalized Medicine' for Myeloma," April 3, 2012.)

What is new and sobering, as emphasized by the authors, is the total amount of clonal heterogeneity, an amount which is even much, much greater than suspected from prior studies. Many genes are abnormal, and even within the same patient, there are multiple clones with different genetic mutations. As had been noted in the authors' earlier study of 38 patients, there are some recurring patterns of chromosomal abnormalities, including, for example, the BRAF gene. This is important because researchers have developed a cancer therapy targeting BRAF.

However, this idea of targeting individual genes is now seen to be taking us in the wrong direction. For example, not only does anti-BRAF therapy target a small fraction of a patient's myeloma cells but, more importantly, these same myeloma cells have many, many additional mutations. So while it is very interesting to identify mutations in different pathways, such as EGRI, BCL2, NFkB, and D153 and FAM46C (collectively this pair of mutations occurred in 21% of patients), the question of how to proceed in search of appropriate therapy remains unanswered. An especially important point is that an average individual patient sample has at least five subclones, each with multiple genetic mutations.

With awareness of these data, the Black Swan Research Initiative was developed in 2012.  There are several aspects to the BSRI initiative, but key points relevant to clonal heterogeneity are:

  • Best results can be expected by starting therapy before major clonal heterogeneity emerges.
  • After therapy, a much more limited number of clones remain (resistant subclones). This process is called clonal contraction (or restriction), following induction treatment. Fewer clones means many fewer mutations to deal with. 
  • Studies of these residual subclones at the molecular and drug sensitivity level are essential.
  • Using new reproducible tests for assessment of minimal residual disease (MRD), these residual clones can be detected, studied, and treated appropriately. This is the strategy for success: monitor and treat to achieve MRD-Zero.
  • It is assumed that combinations of agents and modalities and multifunctional therapies will be required to produce the best results, overcoming complex chromosomal abnormalities.
Genetic heterogeneity is a challenge, but "forewarned is forearmed." With knowledge of myeloma's widespread genetic heterogeneity, BSRI was designed to implement the best plan of attack against myeloma in 2014 and beyond.

Dr. Durie sincerely appreciates and reads all comments left here. However, he cannot answer specific medical questions and encourages readers to contact the trained IMF Hotline staff instead. Specific medical questions posted here will be forwarded to the IMF Hotline. Questions sent to the Hotline are answered with input from Dr. Durie and/or other scientific advisors and IMWG members as appropriate, but will not be posted here. To contact the IMF Hotline, call 800-452-CURE, toll-free in the US and Canada, or send an email to hotline@myeloma.org. Hotline hours are 9 am to 4 pm PST. Thank you.


Reading this article seems to imply that treatment should begin as soon as possible. What is the implication for early myeloma, I.e., what the medical profession calls smoldering?

I encourage all who read this to support the BSRI. It is an exciting approach that could yield fantastic results. Think outside the box and help fund this project!! God Bless

Are you referring to daratumumab and T-cell therapy clinical trials as leading us astray?

The genetics discussed here are abberations caused by myeloma, not the genes you were born with. There may be some hereditary susceptibility, but it is not implied in the genome sequencing referred to here. I think. I'm not an expert.

My Mother passed away with Multiple Myeloma. Are these new studies showing that her children could be at a greater risk genetically ?

Just wanted to thank you, Dr. Durie for your dedication to find a cure and inform us all about MM!!

Could you please comment on the recent
trials from Abramson Cancer Center
HUP on genetically modifying stem cells
prior to transplant?
Thank you

this article in a way confirms Dr. Bart Barlgie approach of kitchen sink (i.e. hit them so hard!)

at any rate, it's crapshoot all over.

Should we begin treatment as soon as possible for smoldering myeloma? What is the most reliable indicator?

Are there any other cases involving a young (37)patient with 1 lesion, 2 weeks into treatment dying from a heart attack? We recently lost a relative this way.
Thank you

I find it very depressing that you say that the hope of finding specific individual genetic triggers is fading. My husband (who has a Ph.D. in biology) and I still hold out hope that this approach will lead to new drugs that can target the chromosomal (and genetic) abnormalities that lead to this disease.

Interestingly enough the data provided continues to talk about early treatment for MM, however the standard testing during any physical exam does not call for this M protein screen or any other specific tests to be done to try and isolate a person having this disease until bone pain is exhibited, renal failure or other symptoms of advanced disease. In today's world being fatigued is part of the day to day to an extend and while someone may show as anemic the normal treatment is to prescribe iron and dietary changes rather than look for additional markers for myeloma. This would be especially true in younger patients that don't meet the "standard" criteria for at-risk individuals

What is being done to include MM screening as part of normal CBC style testing we would have on an annual basis.

My wife was recently diagnosed with MM only after experiencing severe back pain due to a compression fracture of her T12 vert. She had just had a surgery for a hysterectomy that entails a "complete" blood work up 6 months prior which would have caught this before we are at this point.

It screams of more action early!

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The International Myeloma Foundation (IMF) Black Swan Research Initiative (BSRI)  is moving into high gear in the new year.

Building on remarkable progress made by the BSRI team during the last months of 2013, our game-changing approach to finding a cure for myeloma has hit key scientific goals ahead of schedule. Additionally, the work is attracting significant financial support from both industry  and private partners.

BSRI is the IMF's signature research project - a multinational consortium of leading myeloma experts who are studying and harnessing new technologies and myeloma treatments. The linchpin to these studies is the quest for determining when zero Minimal Residual Disease (MRD-Zero) has been achieved and sustained.  This is where the most thrilling breakthroughs have occurred.

Professors Alberto Orfao and Bruno Paiva from Spain presented results of an automated, ultra-sensitive technique for MRD testing at an investigator meeting held in New Jersey in October. The "multiple" in multiple myeloma refers to the frequency of myeloma occurring in different patches or areas of bone. Based on this, they came up with a cocktail of eight antigens that identify myeloma regardless of its state or location in the body.

To eliminate another common variable - the human observer - a computer software program was developed to analyze the read-out from the new test. The sensitivity of the test is one part in 100,000, and probably even lower.

We Can Analyze Hundreds of Thousands of Events

At a follow-up BSRI meeting held before last December's annual meeting of the American Society of Hematology (ASH) in New Orleans, excitement about the new test was palpable. With this new test, "we can analyze hundreds of thousands of events, maybe millions," said Vincent Rajkumar of the Mayo Clinic. "No one person can do that." 

In early 2014, BSRI investigators will host a workshop in Spain to train others to run the Multicolor Flow Cytometry test, as the new technique is called. Once trained, those researchers will return to their own countries to teach others. The next step is achieving consensus on the test, then incorporating the flow cytometry testing into clinical trials so that the testing may be validated prospectively in a standardized fashion. 

Dr. Rajkumar predicted that within two to three years the software will be able to be run anywhere globally. "It's why the Black Swan Research Initiative can change the world." 

To some of the investigators on the team, it already has changed. Jesus San-Miguel asked a provocative question during the discussion of this new testing protocol at the meeting in New Orleans: "My question is--how many patients are already cured?" He was referencing the concept espoused by BSRI that finding the pathway to a cure requires systematic evaluation and validation every step of the way. 

The new cytometry test may soon identify patients who have indeed been cured - which in turn would pave the way for successfully replicating their particular portfolio of treatments. Cross correlations will prove very important in establishing a more finalized MRD testing panel. A key aspect of MRD testing and validation is to compare the flow and molecular methods, such as the Sequenta DNA method. Imaging and molecular testing will round out BSRI's testing protocol.

Five Major Objectives to Achieve Our Goals

There are five major objectives to achieve our goals: 1) Establish a standardized definition for MRD-Zero accepted by the International Myeloma Working Group (IMWG); 2) Standardize the new MRD tests themselves; 3) Validate MRD-Zero in retrospective datasets; 4) Integrate standardized/automated/validated MRD-Zero testing into trials at different disease stages; and 5) Use MRD-Zero for treatment decisions to achieve cure.

Our timeline to accomplish all of this is approximately three years. But progress may be swifter than we imagine. Leading up to the next BSRI investigator meeting in spring 2014 the team is working to establish a chain of publications that will introduce the new definition of myeloma, including ultra-high risk. 

We must also better understand the nature of resistant sub-clones to achieve MRD-Zero.

And, of course, alongside our scientific efforts we are cultivating the financial support for the costly clinical trials and labor-intensive research required to find answers to our questions. This is crucial if we are to accelerate BSRI's efforts to find a cure for myeloma.

Fortunately, support has been forthcoming--a sign we are on the right path.

Multi-Year Collaboration with Onyx Pharmaceuticals

Last December, the IMF was thrilled to announce the start of a multi-year collaboration with Onyx Pharmaceuticals, Inc., an Amgen subsidiary  Onyx is BSRI's inaugural industry partner and we are grateful for their early and enthusiastic support. 

The IMF is equally appreciative of the support given by generous individuals such as IMF Board of Directors member John O'Dwyer and his wife Dorothy. The couple are BSRI Founding Donors and, taking his commitment a step further, John has kindly agreed to serve in the important role of Chairman of the BSRI donor campaign. The O'Dwyers are also joined by Andrew and Laurie Kuzneski in the BSRI campaign.  

We are indebted to Loraine Boyle, whose Peter Boyle Research Fund--named in honor of her late husband--turned its focus this year to Black Swan at the 2013 IMF 7th Annual Comedy Celebration. Private donors have committed more than $625,000 to the initiative so far.  And local member fundraisers have begun earmarking their contributions for BSRI. The proceeds from October 2013's Miracles for Myeloma 5K run in New Jersey, for example, will fund Bruno Paiva's study of Minimal Residual Disease in myeloma.  

This is all great. We want as many members of the myeloma community as possible to participate--researchers, patients, caregivers and friends. Anyone who can contribute whatever they can, be it research, financial support, or raising awareness of our work, is welcome. By pulling together, collaborating, and expanding our minds to consider possibilities never thought of before, I am certain we will find a pathway to achieving a cure. 

Dr. Durie sincerely appreciates and reads all comments left here. However, he cannot answer specific medical questions and encourages readers to contact the trained IMF Hotline staff instead. Specific medical questions posted here will be forwarded to the IMF Hotline. Questions sent to the Hotline are answered with input from Dr. Durie and/or other scientific advisors and IMWG members as appropriate, but will not be posted here. To contact the IMF Hotline, call 800-452-CURE, toll-free in the US and Canada, or send an email to hotline@myeloma.org. Hotline hours are 9 am to 4 pm PST. Thank you.


Where can I have a Multicolor Flow Cytometry test performed? I have had no M-spike since 12/2009 but my doctor insists that I am not cured. I need to know if there is any residual disease for my piece of mind as well as discussing further treatment.
Thank you.

Thanks for all you are doing. I am a new lay diagnosed patient. Your research gives me hope and encourages me to stay positive at all times.

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In the current issue of the journal Science there is a special section called "Single-Cell Biology" (cells go solo). It is now technically feasible to study individual cells in great detail at the molecular, metabolic and functional levels. What is being discovered is that a reading of the "average" from 100, 1,000 or a million cells as has previously been done disguises the great diversity at the individual cell level. 

This raises the question: Are there high-risk genetic features in myeloma cells? 

The answer turns out to be yes and no! Some do and some don't have really abnormal genetic profiles. Discovering the ones that do can guide us to the next phase of therapy for myeloma patients. 

This is significant for the International Myeloma Foundation's signature project, the Black Swan Research Initiative, which is directed towards finding a cure for myeloma. If a myeloma patient's treatment produces an excellent result, with achievement of Minimal Residual Disease (MRD) Zero (no detectable myeloma), follow-up monitoring is required. Although it is hoped and assumed that many patients will have sustained MRD-Zero and may be cured, some will not be cured with the first attempt. These patients will start to have single cells of myeloma detectable by flow cytometry on MRD testing. 

Studies of these single residual myeloma cells will provide the clues needed to eradicate the cells with new alternate and/or higher dose therapy. Checking cells one by one, as BSRI team members Dr. Alberto Orfao and Dr. Ola Landgren are now able to do, will illustrate the diversity and need most likely for a combination approach  to eradicate all these residual myeloma cells. This new technology for single-cell analyses can be key in coming up with the answers to achieving cure! And it is just another piece of the puzzle that is the BSRI, a multifaceted approach to cure myeloma. 

To learn more, stay tuned as we update with blogs, teleconferences, and reports in 2014. 

Dr. Durie sincerely appreciates and reads all comments left here. However, he cannot answer specific medical questions and encourages readers to contact the trained IMF Hotline staff instead. Questions are answered with input from Dr. Durie and/or other scientific advisors and IMWG members as appropriate. To contact the IMF Hotline, call  800-452-CURE, toll-free in the US and Canada, or send an email to hotline@myeloma.org. Hotline hours are 9 am to 4 pm PST. Thank you.


Does anybody have any data on a Dr. Rubio and the Dr. Rubio Cancer Clinic in Tijuana, Mexico?

I have visited his clinic for a day in October 2013, had an interview with him while there and was somewhat impressed by his research and his treatment. He has been doing this for almost 25 years, with improvements in his "vaccines" over the years.
His " vaccines" are individually blended for the patient depending upon blood test results. They presumably "crack" the protein wall protecting the cancer cell from invasion by white blood cells, who just can't penetrate the protein shell.

Any rational answers would be appreciated, as I am seriously considering signing up for a 4 week stay at his clinic in early 2014.

I currently am diagnosed with Smoldering Myeloma, after being downgraded from Stage 1 initially. It's been 4 years since my diagnosis, and 3 years since my downgrade to Smoldering. I've began taking a product called Poly MVA and various supplements, from D3 , Curcumin 95,COQ10, probiotics, No table sugar , minimize red meat, etc. No treatment from my doctor, except for "watchful waiting", which I interpret as " you'll get worse, so we'll watch and hit you with drugs when you're worse". My personality is opposite that .

I began taking Revlimid last month and have just completed my first 21 days. I'm doing this based upon the recent NEMJ publication in July 2013, which published the results of a Spanish clinical trial for "high" risk Smoldering patients. My Oncologist says The decision is mine to start. The results looks statistically significant to me, so we started.

Dr. Rubio says the Revlimid should help his "vaccines" get rid of the cancer, though he doesn't normally include Revlimid in treatment.

Please advise

Thank you and Merry Christmas,

Jim Swelgin

I was diagnosed in March of 1993 with stage III-b Multiple Myeloma, type lambda, with 90% plasma cells. I achieved a three-year remission through intermittent high-dose dexamethasone until early 1996, when a small amount of Bence-Jones protein was detected. I was enrolled in a clinical trial at The Toronto General Hospital entitled ''Intensification of Stem Cell Transplantation,'' with Dr. Keith Stewart as the site PI. My SCT took pace on November 15, 1996. Since that time, I have been monitored first at 3-month intervals, and for the pasvera yers at 6-month intervals, using a protocol developed by Dr. K. Imrie, then on staff at the Sunnybrook Regional Cancer Centre, who was my oncologist.

My latest monitoring series of blood and urine tests showed no detectable markers for myeloma, a result that has been consistent since my transplant.

It has been over 20 years since my diagnosis in a late stage of MM, and over 17 years since my SCT. I do not think that this kind of result is being recorded as I have, over the pat several years, twice contacted the University Health Network in Toronto in order to report my survival to someone who reports to the cancer registry. I was told I should volunteer with a hospital network to make use of y survival story,l but I have moved from the area and am not necessarily interested in a volunteer position.

My question for Dr. Durie is this: Is there a role for a long-term survivor who is possibly cured of Multiple Myeloma in the Black Swan Research Initiative? I have previously been a patient representative on the Research Advisory Committee of Cancer Care Ontario (CCO), as well as on the Terry Fox New Initiatives grants review panel for the National Cancer Institute of Canada (NCIC). I am at least able to provide my story and my statistics to add to the life history of Multiple Myeloma, which I think might modify the stats and provide a more reality-based element of hope for those newly diagnosed.

This story further emphasis the need for 'Single cell research' in understanding cancer cell behavior for a particular patient with myeloma which is still considered to be an incurable disease despite tremendous achievements in its management in recent years.

This is good news for people suffering from Myeloma, More research is needed

I've been reading a lot of conflicting information about asparagus. Should people with myeloma avoid eating asparagus the same as people with certain kinds of leukemia?

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This year's annual meeting of the American Hematological Society (ASH) was truly exhausting, but especially exciting. So many abstracts, so little time!  One had to be a magician to cover major sessions running in parallel. Add to that the cold weather in New Orleans, travel delays, a vast, maze-like, conference center, and you end up with multiple 18-hour days.

But there was much to learn and the IMF's goal is to see the research results through the language and lens of science and point the way forward for patients towards better outcomes and a cure.

On the final evening, the IMF's Conference Series debate, "Making Sense of Treatment" went a long way to capturing the key outcomes from this year's ASH. Four topics were covered: Best Frontline Options; the Role of Maintenance; Minimal Residual Disease: Is This Important?; and New Drugs: Which Will Make an Impact?  The panel from our Stockholm Conference Series --- Doctors Antonio Palumbo, Ola Landgren, Joseph Mikhael and myself--returned to do battle again!

Best Frontline Options

The impact of novel therapies is clearly evident in the improved outcomes in the frontline setting. The panelists grappled with two main questions: How many drugs should be used in an ideal combination? And is carfilzomib (Kyprolis) now preferred over bortezomib (Velcade)? An important ancillary question  was whether or not treatment should change based upon the age or "fitness" of the patient, which is an important research interest for Antonio Palumbo.

Two drugs (Revlimid/low dose dexamethasone (Rd)) prevailed in the MM-020 trial presented at the plenary session. Rd as continuous therapy was superior for patients over age 65 years versus Rd for 18 months and MPT (Melphalan, prednisone, thalidomide) for 12 cycles- which is the standard, approved MPT protocol. So there was a clear vote for 2 drugs (Rd) in this elderly setting. But what about transplant eligible patients? 

Results with both Velcade and Kyprolis combinations as 3 drug combinations are really good. It was generally agreed that 3 drugs are enough (versus 4 or even 5 drug combinations) unless possibly one of the new monoclonal antibodies adds an important new mechanism of action.

Results incorporating either Revlimid (VRd or CRd) or Cytoxan (VCd [Cybord] or CRd) into the combinations are really excellent. But even higher percentage and deeper responses are clearly occurring with the Kyprolis combinations. 

So what did our experts have to say about all this? 

Joseph Mikhael felt that the longer term results with Cybord (Velcade/Cytoxan/dex), with, for example, 81% survival at 5 years in standard risk patients, justifies use of this regimen as a first step, especially since it is cost effective and well tolerated. Conversely, Ola Landgren indicated that CRd (carfilzomib/Revlimid/dex) gives higher and deeper responses, is well-tolerated even in the elderly and works well for both standard and higher risk patients. His perspective is that CRd can be an option across the board for all frontline patients. 

Antonio Palumbo is very much focused upon the need to assess the "fitness" of patients at diagnosis including the presence or absence of so called "co-morbidities"--other medical problems and other needed medications. Antonio's protocol results also support the value of multi-drug combinations and even high dose therapy for "fit" elderly patients. So there was a sense that the Rd two drug combos is a simple excellent option, but in fit patients it is certainly reasonable to explore the value of more aggressive combination therapies.

The Role of Maintenance

The greatest controversy emerged over the role of maintenance. The controversy at ASH this year was triggered by the presentation by Michel Attal from the IFM team, who presented the longer-term results of Revlimid maintenance following autologous stem cell transplant. As had been expected, the presentation showed improved length of remission with Revlimid maintenance, but no overall survival benefit. There have been many speculations about reasons for the lack of survival benefit, including use of 2 months of Revlimid consolidation after transplant given to all patients (including those with no maintenance). 

But what brought a flood of myeloma experts to the microphone for questions at ASH was an analysis which showed dramatically better outcomes for patients on placebo (no Revlimid maintenance) at the point of first relapse. As pointed out by Dr. Shaji Kumar from the Mayo Clinic, this was a flawed analysis in an already flawed study. But many issues were left unresolved at the time of the presentation. Other abstracts strongly affirmed the value of Revlimid maintenance (in addition to continuous or extended use in the frontline setting) using meta analyses of available trial results. 

Joseph Mikhael said he does not routinely recommend maintenance because of the confusion surrounding the data. Conversely, Antonio Palumbo, Ola Landgren, and I said we feel that the preponderance of data supports the use of maintenance, which we feel comfortable recommending, certainly from the standpoint of efficacy. 

Minimal Residual Disease -- Is It Important?

There was unanimity on the subject of the importance of Minimal Residual Disease.  MRD is important. We need to now measure MRD in a standardized fashion and use the information to compare results in randomized trials and to direct treatment to achieve MRD-Zero in trials designed to seek a cure.

Thus the central concepts of the Black Swan Research Initiative® are being enthusiastically endorsed by the myeloma expert community. 2014 is indeed going to be exciting as we see the research results and the rapid process to achieving a cure.

New Drugs -- Which Will Make an Impact?

I listed 8 drugs which are most promising from the 2013 ASH presentations: anti-CD38 monoclonal antibodies (daratumumab and SAR650984); MLN 9708; ARRY 520; ACY 1215; Selinexor; anti-CD138; panobinostat; and bendamustine. There were interesting discussion points about all 8 compounds. However, everyone agreed that the anti-CD38 compounds are both the most exciting and most likely to add a new mechanism of action to our current combination approaches.

Joe, for the first time, presented the more detailed results with SAR antibody as a single agent. About half of the patients responded, some with very deep responses (greater than VGPR).

Follow-up results with the daratumumab antibody were also presented showing substantial benefit. There is great anticipation that even more promising results are to come with anti-CD38 trials moving forward rapidly in 2014.

The IMWG Conference Series at ASH closed with a follow-up from Joseph Mikhael about the new acronym, "Lobster" that he proposed at our last debate. He now suggests that the new acronym will be "CRAB-LEGS" to identify patients with early active myeloma who do not yet have "CRAB" features. So stay tuned to hear more details about this. 

And finally, it was realized that if progress in treatment continues at the current pace, myeloma experts are in danger of putting themselves out of a job. It was agreed that if both doctors and patients end up on permanent vacation in Hawaii, it will be fine!

So here is to further improved outcomes in 2014 and an improving future for all myeloma patients everywhere!

A more comprehensive overview will be provided on the "Post-ASH" teleconference scheduled for January 16, 2014. Register here: http://bestofash2013.myeloma.org/ 

To view the archived video of the IMWG Conference Series: Making Sense of Treatment click here: http://bit.ly/1bHvql7

Dr. Durie sincerely appreciates and reads all comments left here. However, he cannot answer specific medical questions and encourages readers to contact the trained IMF Hotline staff instead. Specific medical questions posted here will be forwarded to the IMF Hotline. Questions sent to the Hotline are answered with input from Dr. Durie and/or other scientific advisors and IMWG members as appropriate. To contact the IMF Hotline, call  800-452-CURE, toll-free in the US and Canada, or send an email to hotline@myeloma.org. Hotline hours are 9 am to 4 pm PST. Thank you.


Thank you yet again for all you do for the MM community and patients in particular.

I didn't see any indication that the use of multiple antibodies targeting both CD38 and CD138 might be an option. These therapies appear to be well tolerated on their own or in combination with Revlimid. Might they also be tolerated in combination with each other?

It is my understanding that it is common for MM to express a few antibodies and often they are both CD38 & CD138 (a potential population which might show significant synergistic efficacy from such a combination).

Being a bit of math geek I see that with all the drugs currently available there is no way to find the best combination via clinical trials. There are just too many potential combinations. I am sure you are also aware that the only statistic that really matters pertains to the patient in question.

Has there been any significant movement on patient specific therapy guidance?

Thanks again!

I was diagnosed with MM in 2008; I never had any fractures. I had an autogolus stem cell transplant. For 6 months prior to transplant, I was on Rev and Dex. I am still in remission. I have never been on any maintenance drugs. I have CBC and M-protein blood tests every 6 months. I have had one bone marrow draw/biopsy since 2008 transplant. I am age 70 now.

I take Vit D and Calcium and B-12.

Do you have any recommendations for further post-transplant maintenance and/or diagnosis?

I still work part time (at desk job). I snow ski and play tennis and do lite weights 3 times a week.

Phone 360 773 5199

Great news on the research .
I was diagnosed 4 years ago with Stage 1. Didn't like the sound of watchful waiting, or some such phrase.
Began taking PolyMVA along with Curcumin,COQ10, Omega 3, 10,000 IU D3, liver pills, cut out sugar in my diet ( as much as you can in today's food) and others. After 9 months my diagnosis was changed to Smoldering.
When I learned about the results of the Spanish trial for High Risk Smoldering myeloma presented in July 2013 in the NEMJ, I talked to my Oncologist, and have started the regimen of 25 MG Rev for 21 days, and Dex 20 MG, once a week. No side effects for either drug.
Am now looking into Immune system treatments.
I'm a 71 year old male of normal height and weight for my size.
I believe it is important to be proactive, since, after all, it's my life.

Thanks for reading,

Jim Swelgin
Fallbrook, CA.

any news on pomalyst?...s theoly drug that has helped me and it is relly helping!

Thanks for the excellent review of ASH. I had some questions with regard to frontline therapy. Dr. Mikhael made the point that CyBorD had less side effects than PI/IMID/DEX and no one seemed to challenge him. I have seen early studies that around 10% of patients had a Grade 3 or 4 heart failure with Kyprolis. I also saw the the rate of PN is about 30-40% with Kyprolis/REV/DEX. Also taking into account the short overall survival of patients that are resistant and not responding to IMIDs and PI's I think CyBorD sounds like the better choice. Kyprolis/REV/DEX induction is not a cure and using it early starts building resistance to PI's and IMIDs. IMO myeloma therapy should be viewed as a marathon and not a sprint. Starting to make a patient resistant to IMIDs and PI's as soon as therapy starts seems like a major disadvantage to using a PI/IMID/DEX combo upfront. I would be most interested what your thoughts are on that subject?

I have recently gone out remission and my protein has started to climb to the point that I will start on revlimid and dex this tuesday. I have 4;14 iga myeloma and wonder if any of the new drugs mentioned have better results for intermediate risk patients

I am a multiple myeloma survivor (7 1/2 years) who has not been able to find a drug that I could stay on for any length of time. I have had two stem cell transplants (tandem) which brought me a remission of two years and nine months. I have also been on Velcade, Revlimid, Carfilmazib, and a variety of different medications. Both Velcade and Revlimid worked but I was not able to tolerate them. Most recently I have participated in a clinical trial of the new monoclonal antibody, SAR650984 which worked for seven and a half months and then stopped working. I have stopped even hoping for a cure and would just like to find a medicine that would bring me into remission and keep me there on a long-term basis. For me, Minimum Residual Disease is a concept with very little meaning, as is the whole notion of cure. I have donated to the IMF in the past and would like to do so again, but I want to know that my money is going to find new drugs that will help people like me who are less interested in knowing if they are "cured" than in just surviving on a day-by-day basis.

Australian university (UNSW)have recently found a way of collapsing the structure of cancer cells without killing the heart. Killing the heart and therefore the patient apparently caused this line of research to be abandoned around 25 years ago. 5 compounds are now being tested in the US for toxicity. A drug may be available as early as 2015. See article http://www.news.com.au/lifestyle/health/breakthrough-cancer-cell-treatment-from-the-university-of-nsw-offers-new-hope/story-fneuzlbd-1226697364320 Is there any potential relevance of this approach to mm? Are any researchers in the mm area starting to look at this avenue? If so, who?

Keep up the good work - Guy

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Last week, in Part I of my overview of abstracts released by the American Society of Hematology (ASH) in advance of the group's annual meeting in New Orleans, I focused on combinations using the approved novel agents. Hearing more details and follow-up about these novel combinations at the ASH meeting, Dec. 7-10, will be very important.

In this segment, I start by summarizing where we are with new agents in earlier trials at the Phase I-II or preclinical stages. There are eight agents which are of interest. 

  • anti-CD 38 monoclonal antibodies (MAb) daratumumab (abstracts #227 and #1986) and SAR 650984 (#284) 
  • MLN 9708 (ixazomib citrate: abstracts #535, 1944, and 1983)
  • ARRY 520 (abstracts #285 and #1982) 
  • ACY-1215 (abstracts #759 and #3190)
  • selinexor (also known as KPT-330, abstract #279)
  • anti-CD 138 monoclonal antibody (BT062, abstract #758) 
  • panobinostat (abstract #1970)
  • bendamustine (abstract #1971)

As was the case last year at ASH, the most promising single-agent activity against a new target is with anti-CD 38 monoclonal antibodies. The single-agent activity of the Sanofi compound (SAR 650984; abstract #284) is illustrated in a dose escalation study involving 32 patients which produced several greater than or equal partial responses. With daratumumab in combination with Revlimid/dexamethasone (anti-CD 38 MAb; abstract #1986) all 6 patients had greater than or equal partial responses with 3 having greater than or equal VGPR. Laboratory studies using a human-mouse hybrid model  (abstract #277) have shown strong synergy with lenalidomide (Revlimid). 

With ARRY 520 (a kinesin spindle protein [KSP] inhibitor), a 16% partial response rate was noted in a study of 32 patients incorporating weekly dexamethasone (#285). Combined with carfilzomib, a small study showed a 58% response rate (#1982). There were again several reports about MLN 9708, the new oral proteasome inhibitor. Results in the newly diagnosed (#535), relapse (#1944), and maintenance settings (#1983) all showed promise and good tolerability. 

Results with ACY- 1215 and selinexor are still early. ACY-1215 (selective HDAC 6 inhibitor) is an oral agent being evaluated in combination with Velcade (#759) and Revlimid/dexamethasone (#3190). Although the combinations are well tolerated, only a few higher-level responses have been seen thus far.

The preclinical results with the XPO 1/CRM 1-dependent inhibitor (selinexor) are reported and show good synergy with carfilzomib (abstract #279). Results with panobinostat (abstract #1970) again show some promise in combinations with Velcade and dexamethasone. Rather surprisingly, the combination of bendamustine with Velcade plus dexamethasone shows really excellent results in the relapsed/refractory setting, with PFS median results of 10.8 months and overall survival median of 23 months (abstract #1971).

And there you have it!  Not a lot dramatically new to add, but it is quite encouraging that several agents are continuing to move strongly forward in clinical trials.

As we move towards 2014, the ASH abstracts that will have the biggest impact are those which provide a better understanding of underlying biology and how to test for minimal residual disease (MRD) and risk factors, and those which provide insight into trigger factors and disease subtypes such as extramedullary disease and plasma cell leukemia.

Testing for Minimal Residual Disease (MRD) and MRD-Zero

Over 25 abstracts deal with minimal residual disease testing, monitoring, and risk assessment. Abstract #402 from the Salamanca/Pamplona team with Bruno Paiva as the lead author characterizes minimal residual disease at the immune and molecular level. In abstract #531, Paiva extends these observations by identifying and characterizing subclones which emerge during the course of treatment. This understanding of subclones which persist or emerge despite current novel therapy is key to developing more successful treatment and achieving MRD-Zero--the primary goal of the Black Swan Research Initiative (BSRI)

Quite a number of abstracts touch on the comparison of various methods to most accurately assess MRD-Zero. Another key abstract from Spain on this topic (#1848) compares flow and molecular techniques. Different aspects of risk and response assessment are covered in abstracts #762, #1841, #1842, #1868, #1878, #1902, #1936, #3126, #3152, #3223, #4290, #4647. Although DNA methods may be slightly more sensitive, a new flow technique may prove to be equally, if not, more sensitive, and has the advantage of allowing identification and molecular study of any residual clones. Hearing all the details at ASH will be very important. So much more to learn!

An important report (abstract #1936) from the Bologna team shows that 29% of patients who appear to be in complete response by other methods of assessment have positive PET/CT scans. Thus, follow-up imaging is essential to confirm the residual disease status. Another abstract (#762) shows that early improvement in the serum heavy/light chain ratio (HLCR, Hevylite) predicts for a high likelihood of subsequent development of MRD-Zero.

Understanding the Biology of Myeloma

In the category of understanding the biology of myeloma better, I draw your attention to a few abstracts. A collaboration between Washington University and Mayo Clinic researchers (abstract #397) has revealed that in mice predisposed to myeloma, one particular gene (Samsn 1) is missing in all cells (called a germline mutation), which results in both B cells (precursors of myeloma cells) and microenvironmental cells such as macrophages and osteoclasts being primed for activation. Another abstract (#3116) also suggests that we take a closer look at predisposing and triggering factors for MGUS and myeloma. 

The team of French researchers from Nantes shows that in 22.7% of patients with MGUS and myeloma, the monoclonal protein reacts against infection: specifically hepatitis C, Epstein-Barr Virus (EBV), and the stomach infection H. Pylori. This raises the possibility that infection can trigger initial disease and possibly relapsing disease. Clearly further studies are required. Another aspect is obesity, which is known to be linked to the onset of both MGUS and myeloma. A large epidemiologic study (abstract #1872) shows a strong association between increasing body mass index (BMI) at age 20 years and a younger age at diagnosis in African-Americans with multiple myeloma. Definitely food for thought!

Subtypes and Categories of Patients

Considering different subtypes and categories of patients with myeloma and related diseases, there are several abstracts: young patients (< 40 years: abstract #3226); older patients (abstract #687); IgD myeloma (#s 1880 and 1935); IgM myeloma (#1881); plasma cell leukemia (#761); extramedullary disease (EMP; #s 1896, 3141, and 3188); central nervous system involvement (abstract #3118); patients susceptible to very early death in ≤ 2 months (#3195) and those patients in remission for ≥ 6 years (abstract #3366). A small, but important point in abstract #3195 is that patients at risk of death within the first 2 months of the myeloma diagnosis are those with unrelated serious health issues. With the advent of novel therapies, it is only months to years later that the impact of high-risk myeloma features is seen as a challenge in controlling progressive or relapsing disease: a reassuring point.

As far as molecular risk features, there are fewer than the usual number of abstracts dealing with this topic at ASH 2013: abstract numbers 399, 529, 530, 1846, 1855, 1856, 1992, 3092, 3108, 3111, 3114, 3121, and 3147. There are two key practical points. In abstract #529, it is noted that poor risk features (such as FISH t(4;14) or -17p) will prevail even if there is hyperdiploidy (extra chromosomes: normally considered to be a good-risk feature). Thus the presence of hyperdiploidy does not counterbalance poor-risk features. A related, and somewhat frustrating point (in abstract #1992), is that the 1q21 FISH abnormality does confer poorer risk, but is not part of the standard FISH testing panel!  So, back to the drawing board again to have a new recommended FISH testing panel.

And there you have it for now: many interesting abstracts, some which I predict will prove to be very important, and others where we are waiting to hear more at the time of the ASH meeting in New Orleans in December.

Please remember the IMF's various educational programs at and from ASH: live-streaming of the Satellite Symposium on Friday, December 6th, and the Conference Series on Monday, December 9th, blogs/Twitter ongoing, interviews with lead investigators immediately after ASH, and post-ASH highlights in January 2014!

Dr. Durie sincerely appreciates and reads all comments left here. However, he cannot answer specific medical questions and encourages readers to contact the trained IMF Hotline staff instead. Specific medical questions posted here will be forwarded to the IMF Hotline. Questions sent to the Hotline are answered with input from Dr. Durie and/or other scientific advisors and IMWG members as appropriate. To contact the IMF Hotline, call  800-452-CURE, toll-free in the US and Canada, or send an email to hotline@myeloma.org. Hotline hours are 9 am to 4 pm PST. Thank you.


Hello, Dr. Durie
My mother died from myeloma years ago. I am very worried if it's inherited cancer.So, according mo the abstract with SAMSN1 in somatic mice it has to be strongly inherited. But, how many other children of myeloma sufferers did not become sick. I was told by my GP that it's not inherited, not like breast cancer and so on. Please, clarify, I have kids and tremendously worried about.
Thank you, Kira

Hello Dr. Durie,

I was wondering. Since there are a few drugs available right now to use as a first line of defense in treating multiple myeloma patients, are researchers now creating (or attempting to create) drugs specifically for the second line or perhaps even the third line of defense? Please let me know.

Thank you,

Elisa Smith

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