New Criteria For The Diagnosis Of Multiple Myeloma And Related Disorders
The International Myeloma Working Group (IMWG) has issued updated criteria for the diagnosis of multiple myeloma.
The criteria have been published in The Lancet Oncology and are accompanied by recommendations for monitoring and updated criteria for other related plasma cell disorders.
The new diagnostic criteria represent a paradigm shift in the approach to multiple myeloma and will have considerable impact on the management of the disease.
For decades, the diagnosis of multiple myeloma required the presence of “end-organ” damage that could be attributed to the underlying plasma cell disorder. Thus, in order to be diagnosed with multiple myeloma and start treatment, patients needed to have one or more of the following “CRAB” features: increased calcium level, kidney (renal) failure, anemia, and destructive bone lesions.
One of the problems with this requirement – especially in the case of smoldering multiple myeloma – was that therapy could be started for patients only after damage to the body had already been done. In many cases, such damage can be serious and potentially irreversible. While a ”watch-and-wait” approach is appropriate and reasonable for low-risk smoldering myeloma patients, some patients diagnosed with smoldering multiple myeloma are at such a high risk of progressing to symptomatic myeloma that it did not make sense to wait for the near-inevitable to happen.
With the availability of several new treatment options for multiple myeloma, we needed to urgently identify patients who can benefit from therapy before serious organ damage occurred. There is also the potential that early therapy can prolong life. The new IMWG criteria allow the use of early indicators to diagnose myeloma before CRAB symptoms happen, and also allow the use of modern imaging methods to make an early diagnosis.
The most important changes to the diagnostic criteria for myeloma, as well as other major changes, are listed below.
Updated Definition of Multiple Myeloma
The revised IMWG criteria will allow, in addition to the classic CRAB features, the following three markers as “myeloma defining events” (MDEs).
- Sixty percent or greater clonal plasma cells on bone marrow examination
- Serum involved / uninvolved free light chain ratio of 100 or greater, provided the absolute level of the involved free light chain is at least 100 mg/L (a patient’s “involved” free light chain – either kappa or lambda – is the one that is above the normal reference range; the uninvolved light chain is the one that typically is in, or below, the normal range)
- More than one focal lesion on MRI that is at least 5 mm or greater in size.
The presence of at least one of these markers will be considered sufficient for a diagnosis of multiple myeloma, regardless of the presence or absence of symptoms or CRAB features. Each of these markers has been shown in two or more independent studies to be associated with an approximately 80 percent or higher risk of developing myeloma-related organ damage within two years.
In addition, the IMWG criteria allow the use of CT and PET-CT for detecting osteolytic bone lesions in order to make the diagnosis of myeloma. In patients with equivocal findings on MRI, CT, and/or PET-CT, the IMWG recommends follow-up imaging. The use of modern imaging methods at diagnosis and follow-up will enable the diagnosis of myeloma to be made before serious bone damage, such as pathologic fractures, can develop.
Updated Definition of Smoldering Multiple Myeloma
The revised criteria for multiple myeloma automatically affect what we call “smoldering multiple myeloma.” Thus, the diagnosis of smoldering myeloma will now have an upper limit of 60 percent for the percentage of clonal plasma cells in the marrow. Patients considered to have smoldering myeloma should not have any myeloma defining events or amyloidosis.
A new kind of smoldering multiple myeloma, termed light chain smoldering multiple myeloma, has been recently described in a study conducted at the Mayo Clinic, and the specific monoclonal protein level required for this diagnosis has also been added.
Updated Definition and Classification of Plasmacytoma
Sometimes patients present with just a single plasma cell tumor in their body. This is called a solitary plasmacytoma. When the tumor presents as a single bone lesion, it is called a solitary bone plasmacytoma. When it occurs as a single tumor outside the bone, it is a solitary extramedullary plasmacytoma.
True solitary plasmacytoma without any clonal plasma cells in the bone marrow has an excellent chance of cure, and needs to be differentiated from more advanced stages of the disease as well as myeloma.
The IMWG recommends the term “solitary plasmacytoma with minimal marrow involvement” if bone marrow clonal cells are present but less than 10 percent. Patients with a single bone lesion or extramedullary plasmacytoma who have 10 percent or more clonal bone marrow plasma cells, on the other hand, will be considered as having multiple myeloma.
Imaging recommendations
MRI, CT, or PET-CT of the whole body or spine/pelvis are needed to make a diagnosis of smoldering multiple myeloma, solitary plasmacytoma, or solitary plasmacytoma with minimal marrow involvement. If imaging studies show changes that are not clear cut, a repeat examination in three to six months is recommended.
Monoclonal Gammopathy of Undetermined Significance (MGUS)
The definition of MGUS has not changed. However, a new entity termed light chain MGUS has been defined.
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The IMWG effort to update the diagnostic criteria was a major undertaking that took years of work, including the research and publication of key papers to support the major changes. Researchers from around the world worked hard on this project and provided detailed input. These criteria will evolve as new data emerge, and many groups are continuing to investigate new biomarkers.
However, the biggest hurdle – which is a philosophical shift in what is called a malignancy – has been cleared, and this will make future changes that help patients easier to accomplish.
Finally, no written criteria can substitute clinical judgment. In many cases, physicians will need to continue to use judgment in making decisions on which patients need immediate therapy, and in deciding when continued observation will be in the patients’ best interests.
Dr. S. Vincent Rajkumar is a professor of medicine and chair of the Myeloma Amyloidosis Dysproteinemia Group at the Mayo Clinic in Rochester, Minnesota. His research focuses on clinical, epidemiological, and laboratory research for myeloma and related disorders.
"Patients considered to have smoldering myeloma should not have any myeloma defining events or amyloidosis."
So, since I do have Amyloidosis, what do I have? This sentence left me hanging, or I completely missed something. I had 40% plasma cells on my first BMB. No CRAB criteria, with the exception of the fact I have kidney involvement of the Amyloid, normal function so far.
No mention of protein count in this article
Once again, no mention of primary plasma cell leukemia. How can pPCL patients even hope for new research when even the IMWG overlooks this rare member of the MM family??
I am in exactly the same position as Kim T. 20-30% plasma cells on first BMB. No CRAB involvement other than kidney amyloid - normal renal function with proteinuria. My condition has been referred to at different times, by different doctors, as frank myeloma and amyloisosis, myeloma and amyloidosis, amyloidosis caused by an underlying plasma cell dyscrasia, and Amyloidosis and "borderline" myeloma!!
Light chain (AL) amyloidosis and multiple myeloma are both clonal plasma cell disorders but they are different diseases altogether. AL amyloidosis simply means that light chains secreted by plasma cells are forming misfolded protein and causing organ damage; it is a unique disease unto itself and the bone marrow involvement varies in this disease from patient to patient. The plasma cells that are the culprit in AL amyloidosis may or may not be malignant.
Myeloma, on the other hand, is a true malignancy. In order for a patient with AL amyloidosis to be considered as having multiple myeloma (a malignancy) on top of the amyloidosis, they need to meet the criteria for multiple myeloma (just like other patients). The reason is that we do not want to add the label of a cancer / malignancy on patients who do not have it. Based on the new criteria, patients with AL amyloidosis and no CRAB features and no other myeloma defining events will simply be considered as having AL amyloidosis.
Primary plasma cell leukemia is of major concern, and we are working on a disease definition update separately. As with myeloma, we need to publish the primary data first, and this should happen within a few months. The update to the criteria will follow. The criteria need to change because right now they are too restrictive.
Since patients with myeloma can have complete absence of monoclonal protein, there is no requirement for the presence (or a certain level) of M protein in the revised diagnostic criteria. Proof of a clonal plasma cell process on bone marrow or other tissue biopsy is sufficient. The presence or absence of M protein is simply used to divide myeloma into secretory and nonsecretory types. Most (97%) of myeloma are secretory, and about 3% are non-secretory.
Thank you very much, Dr Rajkumar, for the clarification on myeloma / AL amyloidosis.
From what you are saying, I don't think that I have CRAB features (please see my posting above). However. I am confused with the myeloma defining events. The event relevant to me concerns the light chain ratio of 100, provided the absolute level of the involved light chain is at least 100 mg/l. On diagnosis, my lambda light chain was 152 mg/l and kappa was 8.2 mg/l, giving a ratio of 0.05. Is this considered to be a myeloma defining event, defining my disease as myeloma with AL amyloidosis and not simply AL amyloidosis?
Sorry, I am confused by this definition.
Alice
Thanks Dr. Rajkumar!
If these are the new guidelines from the IMWG, what then are the next steps and approximate timing for insurance companies to accept these new definitions? I imagine that there could be a disconnect with insurance coverage for treatment of a NDMM patient if a doctor thinks a patient is symptomatic based on these new guidelines, but the insurance companies think otherwise.
On the criteria for the FLC involved level, shouldn't it be 100 mg/dL, not 100 mg/L?
The FLC ratio for this purpose is calculated by dividing the involved (clonal) light chain by the uninvolved (non clonal) light chain level.
Alice North: Your FLC ratio is 152/8.2=18.5. So it is much lower than the threshold of 100 or more that is called a myeloma defining event.
Multibilly: There will be no problems with insurance companies that I foresee. I have been recommending and treating patients based on these criteria for two years. The diagnosis of myeloma has always been a judgment call, with physicians stating that whatever end organ damage is from the plasma cell process and not something else. There is no separate ICD code for smoldering myeloma versus myeloma. What prevented us from treating smoldering myeloma is not the insurance companies. We needed data to be convinced that therapy can save lives, and the specific patient population who can benefit. We have that data now.
Rick R: No. The involved level needs to be 100 mg/L or more (10mg/dL or more). This is the threshold at which the FLC level is considered measurable. Raising the threshold for involved FLC higher will drop sensitivity without gaining much in terms of specificity.
Thank you Dr. Rajkumar. I wonder if some of us with unusual presentations fall through the cracks of any set of definitions. I presented with impaired kidney function, light chain deposition in kidneys (by biopsy), anemia, 40mg/dL kappa light chains, no monoclonal proteins, no bone involvement, negative for amyloidosis, 7% plasma cell involvement, and t(11:14). My Mayo doctor classified me as light chain deposition disease but from what I have read of LCDD that is not quite accurate. Another myeloma specialist said that I might be classified as monoclonal gammopathy of renal significance but that seems to ignore the anemia. My treatment has been identical to treatment to multiple myeloma but for some purposes (e.g., Veterans Administration assistance) I clearly don't have MM.
Dr. Rajkumar,
I have a current K/L ratio of over 200, (K=0.64, L=134 and most recent previous test previous test was k=1.09 and L=173.19.), immunoparesis and 95% of the plasma cells are cancerous in the BM test. I have also been stable for the last 4 1/2 years with no change in the M-spike and no treatment. No frequent infections. No focal lesions.
Looking back on standard blood tests, I can see that there was a point about 8 years ago where my WBC dropped and never returned to normal so I have assumed that some of this was beginning a while back. The new recommendations I believe would place me in a treatment group - but are these current recommendations primarily for people who have been recently diagnosed?
Thank you for your contributions to the Myeloma Beacon and to the myeloma community.
Dr. Vincent Rajkumar,
You said that amyloidosis is a disease in it's own right (would not have to be in connection with MM) and it causes the strange shapes of the proteins that cause organ damage. The cells that produce these light chains do not have to be malignant but in some cases they are. I have heard that is true with light chain deposition disease (LCDD). I have both LCDD and MM.
Could you tell me what the difference is between LCDD and AL?
I had an annual blood test for many years and in 2010 my kidney numbers started getting off normal - but my GP just thought I was dehydrated. That spring I also had hyperthyroidism and then hypothyroidism and I started taking 50 mcg levothyroxin. I also lost some of my hearing and got hearing aids at the same time. I was diagnosed with LCDD and MM in May of 2012. My blood cancer specialist says that those early test results from before I was diagnosed show that 2010 is when I actually developed MM & LCDD. Do you think the hearing loss and thyroid problems might have been connected to the LCDD?
Thank you.
These are all excellent questions, and important to clarify because the terminology and the concepts are not easy. However, it is difficult to provide a specific opinion on an individual patient, and so my answers will focus on broad concepts.
Light chain deposition disease is analogous to AL amyloidosis in that it is a clonal plasma cell disorder in which light chains secreted by plasma cells cause organ damage. In amyloidosis, there is misfolded protein of a specific structure, size, and staining characteristics that is deposited, whereas in light chain deposition disease there is no misfolding, and no positive staining for Congo Red.
Similar to AL amyloidosis, myeloma may occur in some patients with light chain deposition disease. However, a patient with light chain deposition disease who does not have CRAB or any of the other new myeloma defining events is not considered to have myeloma for the same reasons I discussed in the case of amyloidosis; it will then be considered as just light chain deposition disease. However, as with amyloidosis, we may use similar therapies as are used in myeloma.
It is also important to note that, as far as renal damage goes, only light chain cast nephropathy is considered as a myeloma defining event. Although light chain deposition disease and light chain cast nephropathy sound similar, they represent totally different types of kidney injury. Light chain deposition disease is not a myeloma defining event because it can be seen without the need for malignant transformation of plasma cells, and in most of those situations only affects the kidney.
Monoclonal gammopathy of renal significance (MGRS) is not a disease, but a term used to lump several unique disease together under one heading for purposes of classification.
Regarding patients who have previously been diagnosed with smoldering myeloma and have an involved / uninvolved FLC ratio of 100 or more: We know that approximately 20% of patients with an FLC ratio of 100 or more will not progress within 2 years or even much longer. The new IMWG criteria are mainly meant for newly diagnosed patients, and judgment is needed in patients who have had high levels for many years and have not progressed. Such patients are a selected group and usually we will continue observation unless the numbers continue to rise.
Dear Dr. Rajkumar,
Thanks again for this article.
I was curious if you think that there will be a unique class of treatment approaches for those patients that only exhibit these new "high risk of progression" criteria, but not any CRAB end-organ damage? Put another way, do you think the Mayo's mSMART criteria will be further refined to uniquely handle this new class of patients or will this class of patients simply be included in the current mSMART guidelines for NDMM patients?
No. These patients have multiple myeloma, and should be treated as such. They are and will be included as newly diagnosed myeloma patients in mSMART and in other classification/stratification systems.
There may be unique ways of approaching patients with high risk smoldering multiple myeloma, which is a different patient population. Here the risk of progression is about 25% per year; median time to progression of 2 years. How we diagnose these patients, which factors we use to risk stratify, and the suggested recommendations for management and trials are the subject of another paper that will be published very shortly.
Dear Dr. Rajkumar,
Thank you so much for providing the excellent paper. The article shows extramedullary plasmacytoma on end of organs without CRAB, and these organs rapidly growing tumor with abnormal genetic mutations of plasma cells will not be a malicious cancer.
Will the plasmacytoma have much different treatments to MMs?
Will it have have much better progresses then MMs?
Would you tell us what kind of medicines will be?
Do these patients have to perform SCT?
Would tell us what shall we do prepare?
Thank you so much
Thank you for both of your very timely responses Dr. Rajkumar!
I have a few questions for Dr Rajkumar concerning FLCs.
I live in the UK and was diagnosed with 'asymptomatic" myeloma in April 2008 after a random blood test revealed IgA paraprotein level of 8 g/L (0.8 g/dL). The work-up tests showed no skeletal damage, normal MRI and 12% plasma cells in the BMB. Subsequently, my FLCs were measured and showed a kappa level of 360 mg/L with a ratio of about 360 (lambda ~1). Over the intervening years (now nearly 7) all the functional indices have remained absolutely stable and normal, the paraprotein rose to 12 g/L within the first few months, but hasn't really shifted thereafter, and the kappa FLC has jumped around but nearly always in an upward direction, such that it is now about 1200 mg/L. Curiously, however, I have never shown BJP in a 24 hour urine collection.
My training is in cardio-renal physiology and I have puzzled over the possible reasons why such an apparently high level of FLC doesn't show in the urine - it's way beyond the renal threshold. One explanation that I have come across is that the FLC reading is spuriously high because of polymerisation. Indeed, I see in some earlier documents from the IMWG that such a problem with FLC measurements is referred to.
Clearly, I am alarmed by the recent redefinitions which put me fairly and squarely in the treatment category. Yet, I have had a FLC level well over 100 for nearly 7 years with no ill effects whatsoever.
So, my questions are as follows:-
1. Did the IMWG consider the caveats associated with FLC measurements whilst making their recommendations, to allow for polymerisation 'artefacts'?
2. Do you think there is a difference between a patient with high FLC who is excreting BJP compared to one who shows no BJP in the urine?
3. If a patient like myself with no symptoms is destined for treatment, what sort of treatment would be advocated? To my knowledge all that's on offer are current myeloma therapies. The problem then being that options for future treatment are being used up, with the worry that, when the disease returns, it will come back in a more 'angry' form.
I know at least one other person with a similar clinical picture to me, and he was diagnosed 14 years ago. I'm somewhat surprised that such a strong recommendation has come with regard to the prognostic significance of high FLCs when it is based almost entirely on a single study with 90 patients in the high FLC category.
I'm sorry this is rather lengthy but I would be very interested in your comments.
Thank you
Thanks to Aramis for raising some good questions. First let me answer the 3 questions raised, and then make some general comments.
1. Yes, we did. Personally, I have agonized over the pros and cons of every decision and every sentence in that paper. And so have other members of the IMWG. A lot of it requires a judgment call. A vast majority of myeloma patients in the world will not be seen by myeloma "experts," so recommendations have to be made on what is applicable to the vast majority of patients, recognizing there will be exceptions.
The occurrence of elevated FLCs without secretion in the urine can occur, but is very rare. It is most likely due to polymerization of the FLCs. In such patients, there is probably no risk to the kidney.
However, in the studies that looked at FLC ratio of 100 or more, only 25 to 30 percent of the progression events were related to acute renal failure as the presenting myeloma defining event. A high FLC ratio, therefore, is not just a marker of risk to the kidney (due to high FLC excretion in the urine), but is also a marker of the biology and quantity of plasma cells. So the fact that FLC is not excreted in the urine does not fully assure us that a high risk of progression does not exist.
2. Yes, as noted in the answer to the previous question. Patients with high FLC without Bence Jones protein in the urine (i.e., urine M protein) are likely different. If there is no Bence Jones protein in the urine, there should be no risk of light chain cast nephropathy. However, I cannot be sure that a risk of progression in bone or bone marrow does not exist.
3. We believe there is no significant difference between patients meeting the new myeloma defining events and those meeting CRAB criteria biologically. So the treatment will be the same. The risk you talk about, though, of “using up all treatments” is real, but it also is applicable to all newly diagnosed myeloma patients even prior to the new criteria. That is why for years I have argued that we need good studies to show whether our treatments really prolong life (or quality of life) and not just merely show improvements in surrogate markers. And that is why I advocate a risk adapted treatment approach to myeloma, where we do not use up all treatments in standard risk myeloma.
Now for some general comments which I think are helpful.
First, the criteria apply mainly to newly diagnosed patients. We clearly state in the paper, and as I wrote in this column, these criteria are not meant to be a substitute for clinical judgment. The FLC criteria (and the other new myeloma defining events) are based on 2 or more independent studies showing approximately 80 percent risk of progression within 2 years in newly diagnosed SMM patients. Thus, we know 20 percent of patients will not progress within 2 years. Patients who have had high levels of biomarkers for years and are stable have already declared that they are in the 20 percent who do not progress group. We are not recommending that such patients be labeled as "myeloma" and started on therapy. In fact, the risk of progression henceforth in that group is likely to be lower than when they were first diagnosed. Hope this helps.
Second, as with everything in medicine, there are exceptions to every rule. When we first see a patient, we do not have the benefit of knowing for sure what will happen in the future, 2 or 3 years later. The criteria are written with the goal (and the supporting data) that when we make a call we are right 8 out of 10 times, or more.
Third, note that just like 20 percent of patients with high FLC ratio (100 or more) do not progress in 2 years, there are also patients with anemia or even small lytic lesions (who would be considered as having CRAB features) who also do not progress within 2 years without any therapy. We do not withhold therapy in all patients to prevent overtreatment of 20 percent of patients because we will be wrong 80 percent of the time.
Dr Rajkumar, many many thanks for such a speedy and helpful response. It is greatly appreciated by me and, I'm sure, will be by others in the '20% club'!
Thanx Dr Rajkumar, one of the best pages I've read on myeloma. What are best options recommended to study clonality of plasma cells?
Thanks. The best method to study clonality at present is multiparametric flow cytometry. In flow, many of us use the kappa/lambda ratio to determine if the cells are clonal or not. The Spanish use a more complex immunophenotypic method using certain markers like CD19, CD56 etc to determine clonality; their method is probably more sensitive. Immunohistochemistry or immunofluorescence can also be used to determine clonality, and similar to flow is based on detecting an abnormal kappa/lambda ratio. Similarly, molecular methods can also be used, but the standard in most clinical laboratories in the US is flow.
Thanks Dr Rajkumar. These are the best pages I have read on multiple myeloma. Looking forward to your next paper eagerly.
Dr Rajkumar, thanks again for your reply. One of the myeloma defining events requires a ratio of > 100 for serum involved to uninvolved free light chains. Is there any similar cutoff ratio for k/l by flow?
What gives me hope for additional time in this life is the dedication of Dr. Rajkumar and others like him. Though immersed in mm research and patient care, he makes time to explain new developments and to respond to questions in this forum.
Like others above, I'm grateful, Dr. Rajkumar.
Hello,
I too am very grateful for Dr. Rajkumar time in explaining the new IMWG criteria here in the Beacon. I've just reviewed his explanation of the criteria again and, while I understand the insight leading to the changes and the crux of the changes themselves, I'm still not clear on what constitutes high risk smoldering multiple myeloma. I have seen literature describing a mix of various criteria, but I can't find anything recent or from a reliable source and since Dr. Rajkumar and other multiple myeloma specialists clearly differentiate between high risk and not high risk when discussing criteria and treatment options for SMM, I was hoping someone could clarify this?
High Beta 2 Microglobulin
High percentage of BM filtration - More than 60%?
Circulating Plasma Cells
Microvascular Density
Osteopenia
Immunoparesis
Cytogenetics
Abnormal FLC ratio
High LDH
Does the new criteria for SMM define high risk with risk criteria or is this a clinical judgement based on all of the above? Or is this still being worked on by the IMF?
Thanks for all the kind comments.
There is no flow cutoff for k/l equivalent to the FLC ratio cut off of 100. They mean and imply totally different things.
What constitutes high risk smoldering myeloma? Prior to the revision of the IMWG diagnostic criteria, one could look at smoldering multiple myeloma (SMM) as consisting of 3 groups of patients : ultra-high risk (~80% risk of progression in 2 years); high risk (~50% risk of progression in 2 years); and low risk (<10-20% risk of progression in 2 years). What the new IMWG criteria did is to rename the ultra-high risk smoldering group as "multiple myeloma" (i.e., symptomatic myeloma requiring therapy, but note that the ultra-high risk group represented only ~10-15% of SMM. The high risk and low risk SMM groups still exist, and need to be differentiated from each other because management approaches are different.
There are specific criteria that are used to classify SMM as high risk SMM. This includes FLC ratio of 8 or more (but less than 100), cytogenetic abnormalities such as t(4;14), del(17p), and 1q amp, etc. We have a paper that will come out soon that provides a specific definition on what constitutes high risk smoldering myeloma, and provides guidance on how such patients should be managed. It is in press so I am not able to provide more details.
This is very helpful information but hard to obtain when locked behind paywalls that non-medical people like myself cannot afford to access. I have enough medical background to know that I must be discerning in what I read, though.
I was diagnosed just a year ago with smoldering myeloma based on a bone marrow involvement of 15-20%; one small lytic lesion (less than 5 mm and the HMO I was part of only did a skeletal study, no follow-up MRI scan); M protein present but less than 3% and the most significant finding was a very high FLC that has continued to remain high and is progressing, albeit slowly. Most recent lab values were kappa free 3080 mg/L, lambda free 10.97 mg/L; ratio 280.77. Watchful waiting has been the norm and I have tried to find more info on light chain myeloma, without much success.
Am I interpreting this information correctly when I deduce that I do, indeed, have at least one myeloma-defining criterion as described in the summary above? If so, what is best way to proceed when approaching a new physician, as I am about to relocate to another state and may not have ideal access (rural area) to a specialist?
My current hematologist/oncologist has not spoken with me about this newest info and now that I am leaving his care I am concerned. I fully understand your statement that this new criteria must be coupled with clinical judgment, etc., but I have this nagging voice that has worried about the abnormally high FLC all along.
Any comments appreciated. Thank you!
This is the first major revision of the myeloma diagnostic criteria, and it will take some time for everyone to become familiar with it. How the criteria apply to individual patients, especially those who have had some of the features for a while, requires judgment and a careful evaluation of the patient. In many instances, I would recommend getting an opinion from a myeloma specialist.
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