19–20 january 2018 vienna, austria - stil_ cd · participants: michele cavo, maria-victoria...

19–20 January 2018Vienna, Austria

supported by unrestricted grants by

Chairs:Heinz Ludwig (Austria)Jesús San-Miguel (Spain)

3 European Multiple Myeloma Academy | 19 – 20 January 2018 | Vienna, Austria

WElcoME ...........................................................................4

ProgrAMMEThursday, 18 January – Dinner Meeting ........................ 6Friday, 19 January – Morning Session .......................... 6Friday, 19 January – Afternoon Session ........................ 7Saturday, 20 January – Morning Session ...................... 8

FAculTy-BiogrAPhiES & KEyPoinTShervé Avet-loiseau .......................................................10Joan Bladé .....................................................................12Michele cavo .................................................................14Paul cockwell ................................................................16Peter croucher ..............................................................18Konstantinos Dimopoulos ..............................................20hermann Einsele ...........................................................22richard JW groen .........................................................24Alessandra larocca .......................................................26heinz ludwig .................................................................28Maria-Victoria Mateos ....................................................30giampaolo Merlini .........................................................32Philippe Moreau .............................................................34Mohamad Mohty ................................................................ 36Enrique ocio ..................................................................38charlotte Pawlyn ...........................................................40noemi Puig ....................................................................42Jesús San-Miguel ..........................................................44Pieter Sonneveld ...........................................................46Evangelos Terpos ..........................................................48niels van de Donk .........................................................50Katja Weisel ...................................................................52Elena Zamagni ..............................................................54

ContACtS

Scientific Coordinator:

univ.-Prof. Dr. heinz ludwigWilhelminen cancer research institutec/o Dept. of Medicine i, centre of oncology,haematology and Palliative careWilhelminenspital, Montleartstr. 371160 Vienna, Austria+43 1 491 50 21 [email protected]

and

EMEri – Medical Education and research [email protected]

Congress & Travel Affairs:

Mondial Medica reisebuero gmbhWaehringer guertel 18-20 (AKh)1090 Vienna, Austria+43 1 402 40 61-0www.emma-vienna.org

Verena [email protected]. (Fh) Barbara [email protected]

Contents

17th European Multiple Myeloma Academy

19 – 20 January 2018Vienna, Austria

InterContinental Hotel Vienna

5 European Multiple Myeloma Academy | 19 – 20 January 2018 | Vienna, AustriaEuropean Multiple Myeloma Academy | 19 – 20 January 2018 | Vienna, Austria 4

WelCome

welcome to the 17th European Multiple Myeloma Academy meeting from 19 – 20 Janu-ary 2018 in Vienna, Austria.

The last 2 decades showed a remarkable progress in our understanding of the biology of multiple myeloma and to a series of novel treatments with significant improvement in patient outcome. understanding these new developments and careful consideration of their impact has become key for optimal patient management.

During this EMMA meeting we provide in depth information on the pathophysiology of the disease, the genetics of a high-risk disease, and on the role of the microenvi-ronment for disease control and progression. Furthermore, we provide new data from recent clinical trials including the most important ones presented at ASH. These fin-dings, as well as general treatment recommendations will be presented during the meeting. Ample time will be devoted to discussions with the delegates about the rele-vance of the recent results for every day practice.

We are pleased that you decided to participate in this stimulating event and to delve into the friendly, informal atmosphere of the meeting. Exchange your ideas, explore how your colleagues handle complex situations, find answers for difficult questions and enjoy the wealth of information provided during the Vienna EMMA meeting.

heinz ludwig and Jesús San-MiguelChairmen of the meeting

Dear Colleagues,

PRoGRAmme


PROGRAMME PROGRAMMEFriday, 19 January – Afternoon Session

13:15 – 13:40 Smoldering and early myeloma: whom to treat or not to treat Maria-Victoria Mateos

13:40 – 14:05 the best induction and consolidation approach in tE patients Philippe Moreau

14:05 – 14:30 Maintenance therapy: One size fits all? Michele cavo

14:30 – 15:00 Panel discussion: best approaches in early MM and tE patients Moderator: Philippe Moreau Participants: Michele cavo, Maria-Victoria Mateos, Joan Bladé • What are the best markers for progression of SMM? • What is the optimal number of cycles for induction and consolidation? • is there any sense in switching to another protocol if patient do not respond to the first line TX? • Who benefits from consolidation? • What is the optimal maintenance therapy for hr-disease? • Questions from the audience

15:00 – 15:30 Coffee Break

15:30 – 16:20 Workshops (programme repeated)

16:20 – 16:45 Treatment options for elderly fit patients Katja Weisel

16:45 – 17:10 Management of elderly unfit and frail patients Alessandra larocca

17:10 – 17:40 Panel discussion: Management of elderly patients Moderator: Maria-Victoria Mateos Participants: Alessandra larocca, heinz ludwig

• how to improve induction therapy? • optimal approach in high-risk patients? • Maintenance after AScT? • Strategies for patients not responding to induction? • Questions from the audience

17:40 – 18:05 Prospects of gene editing with CRISPR for prevention and treatment of multiple myeloma richard JW groen

19:00 Delegate Dinner

thursday, 18 January – Dinner Meeting

19:30 – 20:45 Dinner Buffet Meeting (limited access, registration required) the role of the bone microenvironment in propagation of myeloma growth Peter croucher

Friday, 19 January – Morning Session

08:15 – 08:20 Welcome heinz ludwig and Jesús San-Miguel

08:20 – 08:45 From MGUS to multiple myeloma: Insights into the pathophysiology charlotte Pawlyn

08:45 – 09:10 the role of epigenetics in multiple myeloma Konstantinos Dimopoulos

09:10 – 09:35 nGS in myeloma: Present evidence and prospects for the future hervé Avet-loiseau

09:35 – 10:05 Panel discussion: Bringing the evolving wealth of information into perspective Moderator: heinz ludwig Participants: charlotte Pawlyn, Konstantinos Dimopoulos, hervé Avet-loiseau, noemi Puig • What induces progression? • Which targets seem to be most relevant for future research? • Which tests should be used in every day practice? • Should tests be repeated at relapse and thereafter? • Questions from audience

10:05 – 10:35 Coffee Break

10:35 – 11:00 Lessons learned from bone marrow cell immuno-profiling noemi Puig

11:00 – 11:25 Imaging in myeloma bone disease Elena Zamagni

11:25 – 12:15 Workshops • Renal disease in multiple myeloma: Pathophysiology and treatment: Paul cockwell • Pathophysiology and Management of myeloma bone disease: Evangelos Terpos • how should patients be followed after treatment initiation and when should treatment be started at biochemical relapse? Joan Bladé

12:15 – 13:15 Lunch Buffet


PROGRAMMESaturday, 20 January – Morning Session

07:45 – 08:15 Breakfast Meeting (limited access, registration required) The role of ASCT in difficult to treat patients, with emphasis on RR/MM, PCL, EMP and Amyloidosis Mohamad Mohty

08:30 – 09:00 Keynote lecture: the roadmap to cure patients with multiple myeloma Jesús San-Miguel

09:00 – 09:25 the Role of moAb in myeloma therapy niels van de Donk

09:25 – 09:50 How I treat high risk disease Pieter Sonneveld

09:50 – 10:20 Panel discussion: How to cure more patients with myeloma? Moderators: Jesús San-Miguel, Pieter Sonneveld Participant: niels van de Donk • is there an explanation for the frequent gap between PFS and oS? • Should early treatment be recommended in case of change from MrDneg to MrDpos? • What is the evidence for prolonged TX in pts with <VGPR? • The best approach in hr disease • Questions from the audience

10:20 – 10:50 Coffee break

10:50 – 11:15 Sequencing in relapsed / refractory disease heinz ludwig

11:15 – 11:40 novel drugs in early clinical development Enrique ocio

11:40 – 12:05 novel immune therapies (other than moAb) hermann Einsele

12:05 – 12:35 Panel discussion: How to maximize the benefit of new developments? Moderator: Pieter Sonneveld Participants: niels van de Donk, hermann Einsele, Enrique ocio, heinz ludwig • immunotherapy – which one, which patients and how long? • immunotherapy combos? • The best strategy after failure to cD38 targeted therapy • What are the prospects of novel nonimmunotherapy drugs? • Questions from the audience

12:35 – 13:00 new developments in amyloidosis giampaolo Merlini

13:00 – 13:05 Closure of the meeting

from 13:05 Lunch Buffet

FACulty BioGRAPhies & KeyPoints


hervé Avet-loiseau, MD, PhD, has been head of the laboratory for genomics in Myeloma at the university hospital center of Toulouse, France, since September 2012. Before that he was the head of the haematology laboratory of the university hospital of nantes, France, a position he had held since 2008.

he received his medical degree with a spe-cialization in paediatric haematology in 1990. After pursuing a postdoctoral fellowship in the laboratory of Dr. Joe gray in San Francisco, cA, uSA, he moved into the area of biological haematology in 1995 and subsequently spe-cialized in cytogenetics. he received his PhD in 1998 and became Professor of haemato-logy in 2001.

Professor hervé Avet-loiseau is highly involved in the intergroupe Francophone du Myélome (iFM), and as the current chairman he leads all biological studies.

Most of his research studies are based on the analysis of genetic/genomic abnormali-ties observed in malignant plasma cells using different technologies, including fluorescence in situ hybridization (FiSh), gene expression profiling, single nucleotide polymorphism (SnP) arrays, and next-generation sequen-cing (ngS).

heRvé Avet-loiseAu

University Hospital toulouse, toulouse, France

Friday, 19 January, 09:10 – 09:35

nGS in myeloma: Present evidence and prospects for the future

Hervé Avet-LoiseAu

1. ngS has improved our knowledge of MM biology by discovering its mutational land-scape.

2. ngS reveals the clonal composition of tumors and informs about the dynamics of clonal evolution.

3. Several gene panels have been described which are useful to capture the mutations most frequently associated with myeloma.

4. only few mutations in genes frequently abnormal in MM are associated with poor prognosis (p53, ATM, ...).

5. There are only few actionable genes such as BrAF, iDh1/2, FggFr3, and possible rAS, AKT, but their clinical relevance is very limited at present.

6. ngS of rnA will inform about gene expression, and splice variants.

7. Applying ngS for characterization of the clonotypic cDr3 region enables the detection of minimal residual disease at a sensitivity of l10-6.

8. ngS will be approved by FDA for detec-tion of MrD and therefore will be used (among ngF) as standard technique for MrD assessment.

9. ngS will replace FiSh and karyotyping and will become widely available, produ-cing reliable results in short time at much lower costs than today.


Joan Bladé, MD, PhD, was born in Benissa-net, catalonia, Spain. he graduated from the university of Barcelona in 1976, and com-pleted his fellowship at the hospital clínic of Barcelona (1976–1980), where he is now a Senior consultant.

Dr. Bladé did his PhD on prognostic factors in multiple myeloma. Since 1981 he has been devoted to the care of patients with multiple myeloma and his research is focused on cli-nical aspects, prognosis, and treatment of this disease. in 1992, he was a visiting clinician for a year in the Dysproteinemia clinic at the Mayo clinic. he was Executive Secretary of the Spanish cooperative PEThEMA group from 1994 to 2001, and has also been chair-man of PEThEMA myeloma trials since 1985.

Dr. Bladé has been a member of the Scientific Advisory Board of the international Myeloma Foundation (iMF) since 1997. he is also the Secretary of the international Myeloma Socie-ty (iMS). he has conducted a number of trials published in high-impact journals. he has pu-blished around 280 articles in peer-reviewed journals and 40 book chapters, mainly on multiple myeloma and monoclonal gammopa-thy of undetermined significance (MGUS). In 2010, Dr. Bladé received the robert A. Kyle lifetime Achievement Award, and in 2012, he received the Joseph Michaelli Award for con-tributions to Myeloma research.

JoAn BlAdé

Hospital Clínic Universitari,Barcelona, Spain

Workshop: Friday, 19 January, 11:25 – 12:15 and 15:30 – 16:20

How should patients be followed after treatment initiation and when should treatment be started at biochemical relapse?

Joan Bladé

1. Serum and urine M-protein measure-ments should be done at each follow-up visit during active treatment.

2. once the negativity of serum and urine immunofixation is confirmed, a bone mar-row aspirate must be done in order to con-firm CR.

3. Patients off therapy and with stable res-ponse should be followed every 3 to 4 months, depending on the length of res-ponse, with serum and urine M-protein measurements.

4. During follow-up off therapy, bone marrow aspirate or imaging techniques should be only done when clinically indicated (i.e., suspicion of medullary progression or myelodisplastic syndrome; suspicion of skeletal or extramedullary progression).

5. Characteristics of oligoclonal bands: faint, non-quatifiable bands in patients in CR after AScT or treatment with novel agents, frequently multiple and fluctuating never showing a significant increase and persis-ting for all along the cr duration.

6. rescue treatment should generally be initiated at clinical relapse or significant paraproteinemic relapse.

7. Patients with previous aggressive clini-cal presentation (renal failure, hipercalce-mia) and/or high-risk features (ultra high-risk, extramedullary disease, plasma cell leukemia) at diagnosis require immediate therapy at the time of relapse or progres-sion.

8. Patients relapsing from cr have a better prognosis than those relapsing from less than cr.

9. Patients with non-aggressive clinical pre-sentation at diagnosis usually have an asymptomatic slowly evolving paraprotein relapse.

10. Patients with slowly evolving paraprotein relapse who do not require therapy within the first two years have a very good out-come with a median oS longer that 8 years from relapse.


Michele cavo, MD, is Full Professor of hae-matology at the university of Bologna, Faculty of Medicine and Surgery, Bologna, italy, and head of the “Seràgnoli” institute of haema-tology in Bologna. he received his medical degree cum laude from the university of Bolo-gna, where he was also awarded his postgra-duate degree in haematology.

in 1991 he became Assistant Professor of haematology, and in 1998 he was appointed Professor of haematology at Bologna univer-sity School of Medicine. From January 2000 to June 2005 and April 2017 to date Professor cavo has served as Director of Postgradu-ate residency in haematology at the univer-sity School of Medicine in Bologna. he was a member of the board of the italian Society of haematology from 2004 to 2009 and has served as Treasurer of the society. he is also co-chair of the italian Myeloma network giMEMA.

Main research interests of Professor cavo focus on multiple myeloma and plasma cell dyscrasias. Professor cavo has been the Principal investigator of many academic phase iii italian and European studies for newly diagnosed myeloma patients and has authored many papers published in peer-reviewed journals, including the new England Journal of Medicine, the lancet, Blood, the Journal of clinical oncology, leukemia, Bri-tish Journal of haematology, haematologica, and others. he has been a member of the Edi-torial Board of the Journal of clinical onco-logy and haematologica.

miChele CAvo

University of BolognaFaculty of Medicine and Surgery, and Seràgnoli Institute of Haematology, Bologna, Italy

Friday, 19 January, 14:05 – 14:30

Maintenance therapy: One size fits all?

Michele cavo

1. Achieving the deepest level of response to anti-myeloma therapies and sustaining the duration of response are essential prere-quisites for favorable long-term outcomes.

2. high-dose therapy with autologous stem cell transplantation for newly diagnosed disease is not curative in most of the cases and many patients will invariably experience progressive disease (PD).

3. Maintenance therapy aimed at keeping under control residual tumor cells after AScT is a widely used strategy to prevent or delay PD.

4. Due to their immunomodulatory properties and ease of oral administration, thalido-mide and lenalidomide were the first novel agents explored as maintenance therapy after AScT.

5. long-term use of thalidomide, although of benefit in prolonging PFS and perhaps oS, has been limited by its neurological toxicity with impairment in patients’quality of life.

6. Lenalidomide is the first novel agent approved by EMA for maintenance the-rapy after AScT based on the extended PFS reported in two phase iii studies com-paring lenalidomide versus (vs) placebo or observation and the longer oS reported in one of them.

7. A recent meta-analysis including a third study confirmed that the PFS and OS benefit from lenalidomide maintenance outweighted the risk of developing a second primary malignancy.

8. Although there is a lack of phase iii stu-dies of bortezomib maintenance versus placebo or observation, in one trial borte-zomib was associated with extended post-AScT PFS and oS in comparison with thalidomide, particularly in patients with del(17p) who do not seem to benefit from thalidomide therapy.

9. Studies exploring the role of the second generation oral proteasome inhibitor ixa-zomib and the monoclonal antibodies daratumumab and elotuzumab, either sin-gle or combined, are currently ongoing.

10. The optimal duration of maintenance the-rapy (fixed vs continuous) and the best choice of agents (single drug vs combined therapy) to be used in the overall patient population and/or in selected subgroups at different risk still remain unanswered questions which need to be addressed in future prospective clinical trials incorpo-rating genomics and detection of minimal residual disease as drivers of treatment options.


Paul cockwell is a consultant nephrologist at Queen Elizabeth hospital, Birmingham, uK, and professor of nephrology at the uni-versity of Birmingham. Paul has clinical and research interests in para-protein related kidney disease, including myeloma and renal disease, and has a significant publication record in the field.

PAul CoCKWell

University Hospitals Birmingham,Birmingham, United Kingdom


Renal disease in multiple myeloma: Pathophysiology and treatment

Paul CoCkwell

1. Around 50% of patients with multiple mye-loma have renal impairment at presenta-tion, and up to 5% require dialysis.

2. Most patients with moderate renal impair-ment (egFr 30-59 ml/min) at presentation will have reversible acute kidney injury.

3. in kidney biopsy series from patients with multiple myeloma and severe renal impair-ment (eGFR <30 ml/min, serum creatinine >2 mg/dl), the large majority (c90%) have myeloma cast nephropathy (Mcn).

4. Myeloma cast nephropathy is caused by the involved immunoglobulin light chain clone; the threshold serum level of invol-ved immunoglobulin light chain for Mcn is 500-1000 mg/l, although patients with Mcn usually have around 10x this level or more at presentation.

5. A range of other renal lesions can be seen in patients with multiple myeloma, inclu-ding Al amyloidosis and light chain depo-sition disease: these are usually asso-ciated with progressive chronic kidney disease and proteinuria.

6. A requirement for dialysis treatment has historically been a major determinant of poor survival for patients with multiple myeloma; recovery of renal function from dialysis is an independent determinant of better overall survival.

7. Prompt diagnosis and immediate com-mencement of novel chemotherapy, accompanied by high quality supportive care, is crucial.

8. Bortezomib and dexamethasone based chemotherapy is the current standard of care for myeloma and severe renal impair-ment. There is increasing data to guide the use of other novel chemotherapy agents in patients with severe renal impairment.

9. Studies evaluating extra-corporeal remo-val of light chains by high cut-off dialysis is being published in this current period

10. outcomes for patients who require dialy-sis treatment have improved dramatically over the past decade.


Peter undertook undergraduate and PhD trai-ning in cardiff, followed by post-doctoral trai-ning in the in Cambridge and Sheffield. Peter became a leukeamia research Fund Bennett Senior research Fellow before moving to oxford university as a Senior research Fellow in 2001. Peter returned to Sheffield in 2003 as Professor of Bone Biology. in 2009 Peter was appointed joint Direct of the Mellanby center for Bone research and the head of the Department of human Metabolism, at the University of Sheffield. In December 2011 Peter joined the garvan institute of Medical research in Sydney as a Senior Principal research Fellow and head of the Division of Bone Biology.

Peter’s research interests are in understan-ding the cellular and molecular mechanisms responsible for physiological and pathological regulation of the skeleton. he has a particular interest in tumours that grow in bone including multiple myeloma, or those that metastasise to bone, such as breast and prostate cancers. Peter has been involved in the development of therapeutic approaches to inhibit bone resorp-tion and stimulate bone formation in myeloma. More recently, Peter’s interests have focused on understanding tumour cell dormancy in the skeleton.

PeteR CRouCheR

Garvan Institute of Medical Resarch,Sydney, Australia

Dinner Meeting: Thursday, 18 January, 19:30 – 20:45

the role of the bone microenvironment in propagation of myeloma growth

Peter CrouCher

1. Multiple myeloma typically develops from a monoclonal gammopathy of undetermi-ned significance.

2. Malignant plasma cell localized to spe-cialized niches in the bone marrow micro-environment, which support their survival and long-term dormancy.

3. understanding the cellular and molecular pathways that control dormancy, and more importantly the selective reaction of dor-mant cells, will likely provide new approa-ches to prevent disease relapse and ulti-mately cure myeloma.

4. Studies of the cells of bone, including osteoclasts and osteoblast, have sugges-ted that these cells are important in influ-encing the growth and survival of mye-loma cells.

5. Whilst evidence is accumulating to sup-port a role for bone cells how they do this is unclear. This is largely due to the dif-ficulty in identifying and studying myeloma cells when they first arrive in the skeleton and enter a dormant state. however, new labeling and intravital imaging technology has allowed us to begin to address this challenge.

6. We now know that myeloma cells localize to the endosteal surface in the skeleton and cells in this environment, including cells of the osteoblast lineage, are able hold myeloma cells in a long-term dormant stage.

7. once in a dormant state these cells may be resistant to some treatments.

8. Single cells rnAseq analysis has demons-trated that dormant myeloma cells express a unique gene signature and therapeutic targeting of dormancy signature genes is able to release cells from dormancy.

9. Stimulation of osteoclastic bone resorption reduces dormant cell numbers and incre-ases myeloma burden suggesting that the stochastic switching on of bone resorption maybe one mechanism that could account for the selective reactivation of dormant cells.

10. understanding myeloma cell dormancy and reactivation may provide new approa-ches to stopping reactivation and myeloma developing in the skeleton. This includes the use of selective dormant cell targeted treatments as well as bone microenviro-ment-targeted treatments.


Working experience• January 2010 – April 2011: MD at Nykøbing

Falster hospital, Department of Medicine• May 2011 – March 2012: MD at Herlev Hos-

pital, Departments of Medicine and hema-tology

• April 2012 – August 2013: MD at Rigshospi-talet, department of hematology

• September 2013 – July 2017: PhD student at Epi-/genom lab 4041, rigshospitalet

• August 2017 – present: Post-doc at Epi-/genom lab 4041, rigshospitalet

Publications1. Dimopoulos K, Gimsing P, Grønbæk K.

Aberrant micrornA expression in mul-tiple myeloma. Eur J haematol. 2013 Aug;91(2):95-105. doi: 10.1111/ejh.12124. Epub 2013 Jun 5.

2. Dimopoulos K, Gimsing P, Grønbæk K. The role of epigenetics in the biology of multiple myeloma. Blood cancer J. 2014 May 2;4:e207. doi: 10.1038/bcj.2014.29.

3. Kristensen lS, Asmar F, Dimopoulos K, nygaard MK, Aslan D, hansen JW, ralf-kiaer E, Grønbæk K. Hypermethylation of DAPK1 is an independent prognostic factor predicting survival in diffuse large B-cell lymphoma. oncotarget. 2014 oct 30;5(20):9798-810.

4. helbo AS, Treppendahl M, Aslan D, Dimopoulos K, nandrup-Bus c, holm MS, Andersen MK, liang g, Kristensen LS, Grønbæk K. Hypermethylation of the VTrnA1-3 Promoter is Associated with Poor outcome in lower risk Myelodys-plastic Syndrome Patients. genes (Basel). 2015 Oct 14;6(4):977-90. doi: 10.3390/genes6040977.

5. Dimopoulos K, Søgaard Helbo A, Fibiger Munch-Petersen h, Sjö l, christensen J, Sommer Kristensen l, Asmar F, herman-sen E, o‘connel c, gimsing P, liang g, Grønbaek K. Dual inhibition of DNMTs and EZh2 can overcome both intrin-sic and acquired resistance of myeloma cells to iMiDs in a cereblon-independent manner. Mol Oncol. 2017 Nov 11. doi: 10.1002/1878-0261.12157.

6. Konstantinos Dimopoulos, helga Fibi-ger Munch-Petersen, christian Eskelund, lene Dissing Sjö, Elisabeth ralfkiaer, Peter Gimsing, Kirsten Grønbæk. CRBN, iKZF1 and iKZF3 expression do not pre-dict lenalidomide sensitivity in multiple myeloma, but mutations in TP53 are seen in expanding resistant clones. Submitted to leukemia and lymphoma.

KonstAntinos dimoPoulos

Rigshospitalet Copenhagen,Copenhagen, Denmark

Friday, 19 January, 08:45 – 09:10

the role of epigenetics in multiple myeloma

Konstantinos Dimopoulos

1. The presentation will start with a brief int-roduction in epigenetics, as well as defi-ning the different epigenetic modifications: DNA methylation, histone modifications and nucleosome occupancy.

2. Several studies have underlined the importance of epigenetic aberrations in the development and progression of mul-tiple myeloma.

3. Epigenetic modifications are potentially reversible and druggable, thus giving a potential for targeted therapy.

4. i will present data from studies showing the nature of epigenetic aberrations in multiple myeloma.

5. i will also show data from preclinical and clinical studies involving epigenetic drugs, such as 5-Azacytidine or Panobinostat.

6. Panobinostat is an example of an epigene-tic drug not belonging to the class of pro-teasome inhibitors or iMiDs that recently got approved for the treatment of relapsed multiple myeloma.

7. i will also present data showing the role of epigenetics in the development of drug resistance in multiple myeloma.

8. combined epigenetic therapy can resen-titize drug resistant myeloma cells to the-rapy in vitro.

9. Epigenetic drugs might have the potential to enhance the toxicity of other anti-mye-loma drugs, rather than directly inhibiting growth of myeloma cells.

10. clonal evolution might not only involve a genetic, but also an epigenetic compound, which is easier to target therapeutically.


hermann Einsele, MD, FrcP, is Full Profes-sor of internal Medicine and has been Direc-tor of the Medizinische Klinik und Poliklinik ii of the Julius Maximilian university, Würzburg, germany since 2004.

Following his medical training at the univer-sities of Tübingen, Manchester, and london, Professor Einsele became a research fellow in the Department of haematology, oncology, rheumatology, and immunology at the uni-versity of Tübingen, germany. he was board certified in Internal Medicine in 1991 and in haematology/oncology in 1996. in 1999 was promoted as an Associate Professor. he is a visiting professor at the Fred hutchinson can-cer research center in Seattle, WA, uSA, and at the city of hope hospital, Duarte, cA, uSA. 2011-2015 hermann Einsele was Vice Dean

of the Faculty of Medicine of the university of Würzburg, since 2015 he is Vice President of the university of Würzburg. in 1999, he be-came chairman of the german Study group Multiple Myeloma. in 2003, he received the van Bekkum Award, the highest Annual Euro-pean award for research in the field of stem cell transplantation. in 2011 he was elected as an honorary Fellow of the royal college of Pathologists (london), in 2012 nobel lectu-rer Stem cell Biology/ Transplantation, nobel Forum Karolinska institute, and 2014 Member of the Academy of Sciences and literature, Mainz.

Prof. Einsele is expert in the field of multiple myeloma, stem cell transplantation and ad-optive immunotherapy in haematological and oncological patients.

heRmAnn einsele

University Hospital Würzburg,Würzburg, Germany

Saturday, 20 January, 11:40 – 12:05

novel immune therapies (other than moAb)

Hermann einsele

1. immunotherapy is becoming an important part of the treatment options for patients with newly diagnosed but even more for patients with relapsed/refractory multiple myeloma.

2. Monoclonal antibodies (targeting cD 38 and SlAMF7) have already been appro-ved for the treatment of patients with relapsed or relapsed/refractory multiple myeloma and are currently studied in first line therapy of patients with multiple mye-loma.

3. Four novel strategies are currently studied in patients with relapsed and relapsed/refractory multiple myeloma: a) PD1/PD-l1 blockers in combination with immu-nomodulatory agents and/or monoclonal antibodies, b) bispecific antibodies, c) Tcr-transduced T cells, d) cAr T cells.

4. The combination of checkpoint inhibi-tors (PD1/PD-l1 blockers) and immuno-modulatory agents (lenalidomide/poma-lidomide) was effective in patients with rr/MM but 2 trials with this combination showed an increase in treatment-related mortality. Thus, the FDA-decided to put all these trials on hold.

5. Bispecific antibodies targeting CD3 on T cells and cD19 on All/lymphoma cells has been very effective and a large phase iii trial led to the approval of the cD3/cD19 Bite blinatumomab by FDA/EMA. Pilot trials are ongoing evaluating BcMA/CD3 bispecific antibody formats.

6. A pilot trial of hlA-A2 restricted ny-ESo-specific TCR expressed in autologous T cells was shown efficacious in MM pati-ents.

7. Different cAr constructs with different specificity are currently been developed. Pilot trials with BcMA directed cAr T cells have shown acceptable toxicity and a high response rate even in patients with far advanced MM.


richard groen studied Pharmacochemistry at the Vu university Amsterdam. After pursu-ing a PhD in the laboratory of Prof. Dr. Pals at the Academic Medical center in Amsterdam, where he investigated the microenvironmental regulation of multiple myeloma (MM), he con-tinued his studies on myeloma at the univer-sity Medical center utrecht (Dr. Martens and Prof. Dr. lokhorst) and Dana-Farber cancer institute (Dr. Mitsiades). During this period, he developed the „humanized“ bone marrow/bone-like scaffold model, which has proven to be suitable to study not only patient-derived MM cells but also other hematologic malig-nancies as well as to simulate bone metastatic lesions of solid tumors.

in 2015, richard joined the MM program of Vu university Medical center (headed by Prof. Dr. Zweegman) as Assistant Professor. his research focuses on the investigation of the bidirectional interaction of MM tumor cells and the bone marrow microenvironment. in particular, he studies the mechanisms through which the BM microenvironment can be mol-ded by tumor cells, and the subsequent influ-ence on tumor progression and therapy re-sistance, with an ultimate goal to inform the design of novel pharmacological and cellular therapies targeting these malignancies.

RiChARd JW GRoen

VU University Medical Center,Amsterdam, the netherlands

Friday, 19 January, 17:40 – 18:05

Prospects of gene editing with CRISPR for prevention and treatment of multiple myeloma

RichaRd JW GRoen

1. i will describe criSPr/cas9-mediated gene editing and expression manipulation.

2. i will show how this technology can be applied to screen and identify molecular targets essential for MM survival (“MM-selective” essential genes) that can be used to inform novel therapeutic interven-tions in MM.

3. I will discuss the influence of the BM mic-roenvironment on these “MM-selective” essential genes.

4. i will discuss how criSPr/cas9-mediated gene editing is entering the hematology clinic.

5. i will discuss how the criSPr/cas9-tech-nology can be used to create “of the shelf” immunotherapy.


Alessandra larocca, MD,PhD is a consultant physician of the Division of hematology at the Department of hematology-oncology of the university hospital città della Salute e della Scienza, Torino, italy.

She studied Medicine at the university of Mila-no (1996-2001), and completed her residency in hematology at the same institution (2001-2005).

in 2014 she obtained her PhD in Pathology and Experimental oncology at the university of Torino. She is coordinating and working on the design and development of clinical trials for multiple myeloma developed in the De-partment of hematology. She is author and co-author of papers and books published in peer-reviewed journals. her interest is in mul-tiple myeloma and its treatment including new drugs, with special focus on clinical trials and treatment of elderly patients.

AlessAndRA lARoCCA

University of turin,turin, Italy

Friday, 19 January, 16:45 – 17:10

Management of elderly unfit and frail patients

AlessAndrA lAroccA

1. Multiple myeloma (MM) is a neoplastic disease of older adults, with a higher inci-dence in elderly patients. The prevalence of myeloma is likely to increase due to the extended survival and the growing life expectancy of the general population.

2. Much progress has been made in the past few years thanks to the introduction of new drugs. The introduction of novel agents has considerably improved overall survival, pri-marily among patients over 65 years.

3. Aging is associated with a high prevalence of frailty, that is, a state of increased vul-nerability to stressors due to a critical dec-line in physiologic reserves. Elderly people may be categorized as fit or frail according to clinical, functional and cognitive crite-ria. The presence of frailty may complicate the management and outcome of myeloma patients.

4. To date, the choice of treatment of myeloma patients has focused primarily on chronolo-gical age and performance status as mar-kers of frailty. however, the elderly popula-tion is highly heterogeneous, and improved assessment strategies are needed to define the frailty profile of patients and provide them with the most adequate treatment, thus avoiding the overtreatment of frail pati-ents and the undertreatment of fit patients.

5. The geriatric assessment (gA) is a funda-mental tool for the evaluation of cognitive and functional status.

6. Because a full comprehensive geriatric assessment is a time-consuming proce-dure that is difficult to use in every day cli-nical practice, a simplified GA that includes Activities of daily living (ADl) scale, instru-

mental ADl (iADl) scale, and the charlson comorbidity index (cci), should be adopted for elderly patients. ADl is used to screen for disability in self-care tasks and iADl to explore tasks of household management. Many prognostic indices for the elderly that incorporate age and/or comorbidity are available. The charlson co-morbidity index is one of the most frequently used in cancer patients.

7. rd and VMP are the current standards of care for older patients with newly diagnosed myeloma. To date, there have been no pro-spective trials evaluating geriatric assess-ment–driven treatments in elderly patients with newly diagnosed MM; the best strategy for frail patients remains to be defined.

8. on the basis of the results of a geriatric assessment, patients can be stratified into a fit group, suitable for full-dose therapy with three-drug combinations, or a frail group, requiring dose-adjusted therapies.

9. Frail patients need effective tailored treat-ments to better control the disease while minimizing the risk of toxicity and treatment discontinuation. The selection of therapy should be based on the risk of toxicity and the capacity of patients to tolerate treat-ment. lenalidomide and bortezomib have an essential role in the treatment of frail patients. Two-drug regimens including low-dose steroid in combination with lenalido-mide or bortezomib should be considered in this setting.

10. Additional studies are needed to define more precise geriatric assessment–direc-ted treatment selection.


Dr. heinz ludwig is Professor of internal medi-cine and haemato-oncology and chair of the Wilhelminen cancer research institute at the Department of Medicine i, centre for onco-logy and haematology, Wilhelminenspital, Vienna, Austria.

Professor ludwig’s research interests focus on haematology and medical oncology and in particular on multiple myeloma and related disorders. he has contributed to the under-standing of mechanisms of drug response and myeloma stroma interaction, has desi-gned and conducted investigator initiated trials and actively contributed to cooperate group and industry-sponsored trials. Another major research area relates to the pathophy-siology and treatment of cancer-associated anaemia. Professor ludwig’s has a strong

interest in improving the quality of cancer care by promoting medical training and research, empowering patients, improving patient infor-mation and alerting society to patients’ needs.

Professor ludwig has published a large num-ber of scientific manuscripts in prestigious medical journals and serves as peer reviewer of several international journals. Professor ludwig has served as president of the Euro-pean Society for Medical oncology (ESMo) and has been member of the international board of ASco and is the founder of the ESMo Foundation. Professor ludwig is board mem-ber of the international Myeloma Foundation and a member of the iMWg. in recognition of his influential work, he was the recipient of the Fifth Annual robert A. Kyle lifetime Achieve-ment Award.

heinz ludWiG

Wilhelminen Cancer Research Institute, Vienna, Austria


Sequencing in relapsed / refractory disease

Heinz Ludwig

1. Patients with aggressive disease usually are symptomatic at start of first line the-rapy and at relapse. good risk patients often present with biochemical relapse, long before symptoms evolve.

2. At relapse, treatment should be initiated without delay in patients with symptoms and/or features of aggressive disease, while in those with biochemical relapse and without symptoms, treatment can be withhold, provided those patients can closely been monitored.

3. Selection of treatment for an individual patient depends on 1. Patient’s age, fitness and comorbidity, 2. Biology of the disease (aggressive, cytogenetic-high risk, or non-aggressive), 3. response, duration of res-ponse and tolerance to previous therapy, 4. Availability of drugs/treatment options.

4. At first relapse, ASCT is a reasonable option in transplant-eligible patients with long duration of response after the ini-tial AScT or as second line therapy after induction with conventional treatment. re-treatment is a feasible option in pati-ents with good response to and tolerance of previous treatment, but change of drug class is preferred, provided suitable drugs are available.

5. Several recent randomized trials revealed significant superiority of three-drug regi-mens including a novel drug compared to an established rd or Vd backbone in pati-ents with 1-3 prior treatment lines.

6. Pomalidomide with dexamethasone and panobinostat with Vd have been approved for patients with ≥ 2 prior lines of therapy including lenalidomide and bortezomib. Adding cyclophosphamide to pomalido-mide dexamethasone has been shown to be superior to the original doublet regi-men.

7. Patients with high-risk cytogenetics, as defined by FISH or gene arrays should be receive regimens incorporating a prote-asome inhibitor and possibly a monoclonal antibody.

8. Several phase ii studies showed marked activity of various combinations including one or more novel drugs as later line treat-ment.

9. There are few data on the optimal length of treatment duration and on maintenance therapy. Experts recommend continued treatment until progression or intolerance in patients with poor risk features, while in those with good prognosis, treatment may be discontinued after achievement of an excellent result.

10. in patients failing to several lines of the-rapy, alkylator-based therapy such as cyclophosphamide-prednisolone or conti-nuous infusion treatment with DcEP, DT-PAcE, or inclusion in a clinical trial may be a valuable option.


Dr. María-Victoria Mateos, MD, PhD, is con-sultant Physician in the haematology Depart-ment and Associate Professor of Medicine at the university of Salamanca, Spain. She is the director of the Myeloma Program and coordi-nates the clinical Trials unit in Salamanca’s university hospital haematology Department. She serves as coordinator of gEM (Spanish Myeloma group), with direct involvement in the design and development of clinical trials. She has coordinated many clinical trials in el-derly and smouldering MM patients that have profoundly influenced current options for trea-ting these patient populations.

She is also a member of the iMWg (interna-tional MM Working group), iMS (international MM Society), EhA and ASh. She has publis-hed over 200 papers in peer-reviewed inter-national journals, some of which have become key references in the Multiple Myeloma field. She is Associate Editor of myeloma in Annals of haematology since 2011 and has acted

as a reviewer for top journals such as nEJM, lancet and lancet oncology. Among her invi-ted presentations, she has recently contribut-ed to the educational sessions of EhA 2012, ASh 2013, ASco 2015, EhA 2016, ASco and ASh 2017.

She has served on the EHA’s Scientific Pro-gram committee and Advisory Board since 2013 until 2017, and on the ASH Scientific committee on plasma cell diseases in 2015-2017.

She is a councillor on the EhA Board since 2015 for a four-year mandate, member of the Steering committee for the Society of hema-tologic oncology (Soho), member of the iMS board and member of the European School of Haematology (ESH) Scientific committee. She has published over 200 original papers in international journals. her areas of interest in-clude multiple myeloma, the biology of plasma cells and the news drugs development.

mARiA-viCtoRiA mAteos

Hospital Universitario de Salamanca,Salamanca, Spain

Friday, 19 January, 13:15 – 13:40

Smoldering and early myeloma: whom to treat or not to treat

Maria-Victoria Mateos

1. Smoldering Myeloma is defined by the presence of a M-component of at least 3 g/dL and/or plasma cell bone marrow infil-tration between 10 and 60% without any myeloma-defining event but including dif-ferent subgroups of patients with different risk of progression to myeloma.

2. The international Myeloma Working group (IMWG) updated the definition of Myeloma in 2014 including asymptomatic patients with an imminent risk of progression to myeloma, characterized by the presence of anyone or more of the following biomar-kers: plasma cell bone marrow infiltration ≥60%, serum free-light chain ratio ≥100 and/or more than 1 focal lesion in whole body magnetic resonance imaging.

3. This update allows to identify as myeloma a small subgroup of smoldering patients but the challenge about the heterogeneity in this asymptomatic disease is present.

4. The Mayo clinic group built a model based on the size of the M-component and the plasma cell bone marrow infiltration to dis-tinguish among three different subgroups of asymptomatic patients with different risk of progression to Myeloma.

5. The Spanish group did another model based on the percentage of aberrant plasma cells in the bone marrow by flow cytometry plus immunoparesis and able to identify three different subgroups of pati-ents.

6. Both models have been so far validated in a clinical trial but, at the same time, many different models to evaluate the risk of progression to myeloma have been deve-loped over the last few years. This repre-sents a challenge and a universal model should be defined.

7. The Spanish group demonstrated that early treatment with lenalidomide plus dexamethasone in high risk smoldering myeloma patients is able to delay the progression to myeloma with a significant benefit in overall survival.

8. There are more than 50 trials currently ongoing evaluating the role of novel com-binations in the delay of the progression to active disease.

9. however, there is also another different curative approach for this population of high risk smoldering patients also cur-rently ongoing based on a more intensive scheme of therapy with promising results.

10. in the future, more high risk asymptoma-tic patients will be considered as myeloma and therefore treated accordingly. This fact will contribute to increase the number of patients with myeloma candidates to be potentially cured.


giampaolo Merlini received his medical de-gree and specialized in hematology and in laboratory Medicine at the university of Pavia. he was trained by Prof. Jan Walden-ström and Prof. Elliott osserman in the study of monoclonal gammopathies and systemic amyloidosis. he is the Director of the cen-ter for research and Treatment of Systemic Amyloidosis, university hospital Policlinico San Matteo, and the Director of research of the university hospital. he is full Professor of clinical Biochemistry, Department of Mole-cular Medicine, university of Pavia, italy. he was President of the international Society of Amyloidosis from 2005 to 2010. he received several awards, including the Jan g. Walden-ström Award and the 2017 ham-Wasserman lecture of the American Society of hemato-logy.

Dr. Merlini’s research interests include the pathogenesis, natural history, diagnosis and treatment of monoclonal gammopathies, in particular immunoglobulin light chain amyloidosis. his recent research focuses on the investigation of biomarkers for assessing prognosis and response to therapy and on the development of novel therapeutic agents and treatment designed in the light of advances in the understanding of the molecular mechanisms of these diseases. he is principal investigator for several research projects in this field.

GiAmPAolo meRlini

Fondazione IRCCS Policlinico San Matteo,Pavia, Italy


new developments in amyloidosis

Giampaolo merlini

1. The molecular mechanisms underlying amyloid formation offer clinical clues.

2. Due to the progressive organ damage caused by Al amyloidosis, early diagno-sis is essential in order to improve the out-come.

3. Early diagnosis, risk assessment and treatment monitoring are based on bio-markers and imaging.

4. Unequivocal identification of the amyloid protein is essential for defining the appro-priate treatment.

5. The amyloidogenic clone is usually small, indolent and particularly sensitive to prote-asome inhibitors. iFiSh may help in direc-ting therapy.

6. The mainstay of therapy is the rapid and profound suppression of the production of the amyloidogenic light chain. Minimal residual disease may play a role in impe-ding the recovery of organ damage.

7. immunotherapy targeting the clone provi-des unprecedented hematology response rate and is a game changer.

8. immunotherapies targeting the amyloid deposits have shown promising results, indicating that future treatment will com-bine precursor-depleting agents and anti-bodies promoting amyloid clearance.


Philippe Moreau, MD, serves as Professor of clinical hematology and head of the Depart-ment of hematology, at the university hos-pital of nantes at the university of nantes in France.

Professor Moreau is a member of the admi-nistration council of the intergroupe Franco-phone du Myélome (iFM), which he chaired from 2006 through 2009. he is also a member of the international Myeloma Working group (iMWg). Professor Moreau’s clinical interests are focused on multiple myeloma and its treat-ment with high-dose therapy and novel agents. he has served as the principal investigator of many international randomized phase 3 clini-cal trials and his research is widely published.

Professor Moreau has authored or coautho-red more than 300 peer-reviewed articles that have appeared in high impact factor journals including, the new England Journal of Medici-ne, Journal of clinical oncology, The lancet oncology, and Blood. he is a member of the editorial boards of the Journal of clinical on-cology, Blood, and Blood cancer Journal and is frequently invited to speak at international hematologic oncology meetings.

PhiliPPe moReAu

Department of Hematology University Hospital of nantesUniversity of nantes nantes, France

Friday, 19 January, 13:40 – 14:05

the best induction and consolidation approach in tE patients

PhiliPPe Moreau

1. Three-drug combinations including at least bortezomib and dexamethasone are currently the standard of care prior to AScT.

2. in Europe, VTD and VcD are the most preferred regimens. VrD, when approved, will be probably widely used.

3. KrD, currently being evaluated in ongoing phase iii trials, is associated with high res-ponse rates, but is not available in the Eu.

4. Four to six courses of induction are recom-mended before proceeding to stem cell collection.

5. The combination of monoclonal antibo-dies, either elotuzumab or daratumumab, to standard induction regimens, is currently bieng evaluated in ongoing phase iii trials.

6. consolidation following AScT is improving the depth of response.

7. ongoing trials (EMn02/h095 evaluating the role of 2 VrD cycles; and BMT cTn 0702 evaluating the role of 4 VrD cycles, or tandem AScT) will clarify the impact of consolidation.

8. Patients with high-risk cytogenetics bene-fit from tandem ASCT.


Mohamad Mohty is full Professor of hemato-logy and head of the hematology and cellu-lar therapy Department at the Saint-Antoine hospital and university Pierre & Marie curie (Paris, France).

Professor Mohty obtained his medical degree from the university of Montpellier, France, and his PhD from the university of Marseille, France. he also undertook post-doctoral work at the hematology Department, imperial col-lege, hammersmith hospital, london, uK.Professor Mohty’s is also head of a transla-tional research team (inSErM team n°7) at the Saint-Antoine research centre in Paris and his research is focused on the pathophy-siology and immunobiology of normal and pathological antigen-presenting cells, espe-cially the impact of novel immunomodulatory agents such as proteasome inhibitors, iMiDs and hypomethylating agents.

he has a special clinical focus on the deve-lopment of reduced-toxicity conditioning regi-mens, immunotherapy and different aspects of therapy of acute leukemia and multiple myeloma.

Professor Mohty is currently president of the European Society for Blood and Marrow Transplantation (EBMT). he serves on the board of the EBMT, and the „intergroupe Fran-cophone du Myelome“ (iFM). he is a member of the American Society of hematology, Ame-rican Society for clinical oncology, American Society for Blood and Marrow Transplanta-tion, European hematology Association, and EBMT.

Professor Mohty has published almost 500 peer-reviewed articles in the field of stem cell transplantation, leukemia and myeloma, in dif-ferent hematology and immunology journals.

he also serves as Editor-in-chief of the jour-nal Bone Marrow Transplantation, as Associ-ate Editor for Leukemia, European Journal of Haematology and Blood Cancer Journal, as member of the editorial board of Haemato-logica, and as a regular reviewer in different immunology, hematology, and cancer journals such as Blood, J Clin Oncol, The Lancet, and Nature Reviews.

mohAmAd mohty

Saint-Antoine Hospital,Paris, France

Breakfast Meeting: Saturday, 20 January, 07:45 – 08:15

The role of ASCT in difficult to treat patients, with emphasis on RR/MM, PCL, EMP and Amyloidosis

MohaMad Mohty

1. Some so-called elderly but fit myeloma patients can receive high dose therapy similar to younger patients. Age per se is not a contra-indication to the use of AScT.

2. Treatment of patients with high risk cyto-genetics remains very challenging despite the advent of second generation novel drugs. recent trials (sub-group analyzes) suggested some benefit with some of these modern agents, but the overall out-come remains dismal.

3. high dose chemotherapy (including tan-dem AScT) remains a backbone for pati-ents with high risk cytogenetics.

4. The role of allogeneic stem cell transplan-tation is under considerable debate. how-ever, cellular therapies, especially cAr-T cells are currently actively investigated.

5. Plasma cell leukemia belongs to the “ultra-high risk” group. high dose therapy and conventional chemotherapy agents conti-nue to play a major role. Allogeneic stem cell transplantation may be beneficial in some patients.

6. The frequency of extra-medullary disease is likely increasing in heavily treated mye-loma patients who have received several lines of therapy. The biology of this phe-nomenon is still not well understood, but the emergence of highly resistant clones is likely playing a role. improvement of ima-ging techniques facilitated the diagnosis of extra-medullary disease.

7. As for plasma cell leukemia, high dose therapy and conventional chemotherapy agents continue to play a major role. irra-diation may be also indicated in some situ-ations.

8. Amyloidosis diagnosis and staging have dramatically improved over the last few years.

9. Triplet combinations (e.g. Vel-Mel-Dex) are replacing doublet combinations for the treatment of Al amyloidosis. A few selec-ted patients may still benefit from ASCT.

10. novel agents, especially novel monoclonal antibodies, are proving to be promising in amyloidosis: organ response rates compa-red favorably with traditional chemotherapy.


enRique oCio

Hospital Clínico Universitario de Salamanca Salamanca, Spain


novel drugs in early clinical development

EnriquE OciO

1. Treatment of MM has substantially chan-ged in the last years with the recent appro-val of drugs with novel mechanisms of action such as monoclonal antibodies and deacetylase inhibitors. however, novel drugs with novel mechanisms are still nee-ded for refractory patients.

2. The improvement in the understanding of MM pathogenesis would lead to the disco-very of novel targets that could be active against MM plasma cells.

3. The microenvironment has a key influence in the development and progression of MM and it should be considered as a key target for novel agents.

4. novel generation of the already approved ones are being explored both preclinically and clinically. Some examples are novel alkylators such as melflufen, novel IMiDs derivatives such as the so called “celM-ods” or novel proteasome inhibitors such as oprozomib or marizomib.

5. rAS pathway is mutated in around 50% of patients and it seems to be a promi-sing therapeutic target. Therefore, some downstream effects are targets for the-rapeutic intervention with ErK inhibitors, AKT inhibitors or PiM kinase inhibitors.

6. one of the strategies with more promise is the targeting of Bcl-2 family members. in this regard, the Bcl-2 inhibitor venetoclax has demonstrated activity in heavily pret-reated patients, both alone and in combi-nation with bortezomib.

7. Selinexor in combination with dexa-metha-sone, has demonstrated activity in penta-refractory patients, through the inhibition of XPO1, a protein that exports different proteins from the nucleus of the tumor cell.

8. Another field of development with good preliminary results, consists on the novel immunotherapeutic approaches such as MM targeted ADc, cAr-T cells or agents designed to activate the immune system or block immune checkpoints.

9. The search for biomarkers predicting sensitivity or resistance to a given agent is of upmost importance, in the current scenario. in line with this, venetoclax has demonstrated to be particularly effective in patients carrying the t(11;14).

10. The future of MM treatment looks promi-sing and probably will rely in the use of the optimization of the currently available backbones, in combination with novel tar-geted agents, probably in selected popu-lation based on the use of biomarkers.

Dr. Enrique M. ocio, MD, PhD, is a consultant Physician in the haematology Department of the university hospital of Salamanca. he graduated in Medicine in the university of Salamanca and completed his residency in haematology in the university hospital of Salamanca.

in 2005 he obtained his PhD in the univer-sity of Salamanca with a study entitled “Mul-tiparametric study of the tumoral clone in Waldenström’s Macroglobulinaemia”. later on he enjoyed a post-doctoral stay in Dana Far-ber cancer institute (harvard university, Bos-ton, MA. uSA), working in the development of novel drugs for multiple myeloma. currently he combines his tasks as a physician in the university hospital with his research work in the cancer research center of the university of Salamanca as the responsible of the new Drugs Development unit in hematologic Mali-gnancies.

he has published over 90 original papers in international journals. his main areas of inte-rest are the study of the biology and the deve-lopment of novel antitumoral drugs from the preclinical setting to early phases clinical trials of multiple myeloma and other haematological malignancies such as acute myeloid leukemia or B lymphoproliferative disorders. Among these he has focused on the study of the acti-vity and mechanism of action and resistance of several drugs such as proteasome inhibi-tors, iMiDs or deacetylase inhibitors.


ChARlotte PAWlyn

Clinical Lecturer, the Institute of Cancer Research and Royal Marsden Hospital, London

clinical lecturer, The institute of cancer research and royal Marsden hospital, lon-don.

charlotte received her degrees in pharma-cology and medicine from St John’s college, cambridge university. She completed initial medical training in the East Anglian and north london deaneries before starting haema-tology specialty training with an Academic clinical Fellowship at the royal Marsden hos-pital and The institute of cancer research, london. in 2016 she completed a Wellcome Trust funded PhD Fellowship, undertaking

laboratory research to identify novel epige-netic targets for myeloma therapy. During her PhD charlotte was awarded a ‘Women in cancer research Scholar Award’ from the American Association of cancer research. in addition to her laboratory studies charlotte is actively involved in several clinical trials inclu-ding the large UK national study, Myeloma XI. She has published numerous peer-reviewed research papers and is pursuing her labora-tory research interests alongside her clinical career, with a focus on therapeutic targets to improve outcomes for patients with high-risk myeloma.

Friday, 19 January, 08:20 – 08:45

From MGUS to multiple myeloma: Insights into the pathophysiology

Charlotte Pawlyn

1. Multiple myeloma is the end stage of a progression system comprising benign monoclonal gammopathy (MguS), an intermediate stage lacking clinical damage (SMM) and multiple myeloma itself, which has a range of clinical behaviors.

2. This progression system is driven by sub-clonal competition and selective pressu-res within the bone marrow microenviron-ment, the end result of which is a high-risk disease state.

3. Despite the dramatic improvement in ove-rall myeloma patient outcomes with the advent of novel therapeutic strategies, the high-risk subgroup of patients have not benefitted to the same extent.

4. genetic lesions underlie the key hallmarks of all myeloma disease states and may occur as tumour initiating or progression events. no single lesion explains either all high-risk disease or delineates which patients will progress from MguS/SMM to myeloma.

5. Although myeloma initiating events are clo-nal, subsequent driver lesions often occur in a subclone of cells facilitating progres-sion by Darwinian selection processes.

6. in order to effectively target disease pro-gression to high-risk states we need to understand how these drivers arise, inter-act with each other and mediate their downstream effects.

7. critically, myeloma cells are key compo-nents of a complex “ecosystem” within the bone marrow micro-environment, which co-evolves over time in concert with the malignant cells.


noemi Puig, MD, PhD earned her medical degree from the universidad complutense in Madrid and she completed her residency in internal Medicine and hematology at the university hospital la Fe in Valencia, Spain. She completed a 3-year fellowship in lymphoma, Myeloma and Autologous Stem cell Transplantation at the Princess Mar-garet hospital in the university of Toronto, in Toronto, canada. She earned a doctoral degree at the Medicine Department of the university of Salamanca, in Spain, with a thesis entitled “optimization and critical Analysis of Minimal residual Disease Moni-toring with ASo rQ-Pcr in Patients with Multiple Myeloma and comparison with Multiparameter Flow cytometry”. Dr. Puig currently serves as a consultant Physician at the hematology Department in the univer-sity hospital of Salamanca. She also works in the Flow cytometry laboratory of the uni-versity hospital of Salamanca, where she is responsible for the studies developed by the Spanish Myeloma group.

Dr. Puig is a member of the Programa para el Estudio de la Terapéutica en hemopatías Malignas (PEThEMA) and the Spanish Mye-loma group (gEM) as well as of the Euro-Flow group.

Dr. Puig´s main research interests include the role of multiparameter flow cytometry in diagnosis, risk stratification and minimal residual disease monitoring in patients with monoclonal gammopathies. She is an author or co-author in several research articles, reviews and book chapters.

noemi PuiG

Hematology DepartmentFlow Cytometry LaboratoryUniversity Hospital of SalamancaSalamanca, Spain

Friday, 19 January, 10:35 – 11:00

Lessons learned from bone marrow cell immuno-profiling

Noemi Puig

1. All cases of multiple myeloma (MM) are preceded by precursor states termed monoclonal gammopathy of undetermined significance (MGUS) or smoldering mye-loma (SMM).

2. genetic analyses of MguS cells have provided evidence that it is a genetically advanced lesion, wherein tumor cells carry many of the genetic changes found in MM cells. intraclonal heterogeneity is also established early during the MguS phase.

3. Although the genetic features of MguS or SMM cells at baseline may predict disease risk, transition to MM involves altered growth of preexisting clones.

4. interactions of MguS and SMM tumor cells with immune cells, bone cells, and others in the bone marrow niche may be key regulators of malignant transforma-tion.

5. Bone marrow cell immuno-profiling of the entire spectrum of these disorders may have broader implications beyond preven-tion of clinical malignancy or progressive disease after complete response (cr) to treatment in active MM.

6. i will show data indicating that high-risk SMM patients have an impaired immune system that could be re-activated by the immunomodulatory effects of lenalidomide even when combined with low-dose dexa-methasone, and support the value of the-rapeutic immunomodulation to delay the progression to MM.

7. I will also show that immune profiling con-comitant to MrD monitoring may contri-bute to identify patients with poor, interme-diate, and favorable outcomes.

8. i will present data suggesting that MM pati-ents with long-term disease control have a constellation of unique immune chan-ges favoring both immune cytotoxicity and recovery of B-cell production and homing, suggesting improved immune surveillance.

9. There is a clear unmet need to develop accurate immune monitoring to select pati-ents with both pre-malignant as well per-sistent MRD that could benefit from speci-fic immunotherapy approaches.

10. The development of big datasets is a criti-cal step to bring next-generation immune monitoring from bench to bedside, and foster precision immunotherapy in MM.


Jesús San-Miguel, MD, PhD, is a professor of medicine-hematology and director of clinical and translational medicine at the university of navarra in Spain. he served as director of the hematology Department of the university hospital of Salamanca in Spain, for over 22 years (1991-2013).

Dr San-Miguel has published over 780 origi-nal papers in international journals. he has made important contributions to myeloma cell biology in areas such as immunepheno-typing, risk of progression from monoclonal gammopathy of undetermined significance or smouldering MM into active MM, and minimal residual disease, as well as, making important contributions in the area of therapeutics, inclu-ding studies for new antimyeloma drugs at the preclinical and clinical levels, including prote-asome inhibitors, immunomodulatory drugs, and histone deacetylases.

he is currently President of the international Myeloma Society and member of the Advisory Board of the international Myeloma Foun-dation and the Multiple Myeloma research Foundation. he has served as board council-lor for the European Association, chairman of the Scientific Committee for the IXth Congress (2004), and president of the 15th European hematology Association (EhA) congress. he has been associate editor for Blood and hematologica. he has received numerous awards, including the Waldenstöm Award, EBMT lecture, celgene career Achievement Award, Kyle lifetime Achievement Award, Jose carreras EhA Award, ham-Wasserman lecture Award, rey Jaime i Award in clinical Medicine, and the Spanish Prizes in both oncology and translational research.

Jesús sAn-miGuel

Clínica Universidad de navarra, Pamplona, Spain

Keynote lecture: Saturday, 20 January, 08:30 – 09:00

the roadmap to cure patients with multiple myeloma

Jesússan-Miguel

1. The first reports of cure in multiple mye-loma (MM) were with allogeneic trans-plant, but this remains as an investigatio-nal approach for a very small fraction of patients.

2. in the era of chemotherapy with Autolo-gous stem cell transplant only 5-10% of MM patients remain in cr > 10 years and can be considered operationally cured. however, to consider MM a potentially curable disease the fraction of patients in ccr (at 10y) should increase to 40-50%.

3. in most malignancies to achieve cure require to eradicate all malignant clones and this imply to integrate all active treat-ment tolls through induction, consolidation & maintenance.

4. To offer intensive therapies to high-risk patients and a gentle treatment to stan-dard risk patients is a wrong philosophical approach. if cure is the goal, the risk of undertreating low risk patients by conclu-ding they are in conventional cr may be a serious error.

5. in high risk patients experimental approa-ches should be investigated. Effective treatment may not be a matter of dose intensity, but of dose density.

6. A pre-requisite for cure is to achieve and maintain the best possible response early in the course of the disease.

7. Minimal residual disease (MrD) assess by next generation flow cytometry or sequencing (with a sensitivity of 10-6) are the most sensitive biomarkers for long term survival a potentially cure.

8. cT-PET is complemamtary tool to evalu-ate MrD outside the BM.

9. To treat the disease early on. in most mali-gnancies (lung, colon, prostate, breast…) early detection and intervention is associ-ated with a high cure rate. high risk smol-dering myeloma are candidate for investi-gational studies.

10. To achieve cure, MM should not be consi-dered a single entity, and treatment stra-tegies should be adapted to the MM sub-types.


Pieter Sonneveld is Professor of hemato-logy at the Erasmus Mc cancer institute and the Erasmus university of rotterdam, The netherlands. he received his medical degree from the Erasmus university rotterdam and completed his PhD at the university of leiden, The netherlands, and received a Fogarty Fel-lowship at the national cancer institute in the united States for 2 years.

Professor Sonneveld is chair of the Dutch hoVon Myeloma group. he was one of the founders of the European Myeloma net-work (EMn) and is currently the chair. Within EMn, he organized a cooperative network for clinical trials, which has resulted in nine large European Intergroup trials and scientific work-shops for the standardization of diagnostic

methods in Europe. Within the European hematology Association (EhA), Professor Sonneveld has been chosen President and he serves on the Fellowships & grants review Committee, is chair of the Scientific Working group on ‘Multiple Myeloma’ and has been a reviewer for many years. he served on the scientific advisory boards of the International Myeloma Foundation (iMF), the international Myeloma Working group, and the internatio-nal Myeloma Society, and has been a member of the Editorial Boards of Blood, leukemia, leukemia research, haematologica, and Annals of haematology. Professor Sonneveld is the author of more than 400 scientific pub-lications and several book chapters. in 2015 Professor Sonneveld received the robert F. Kyle lifetime Achievement Award.

PieteR sonneveld

Erasmus Medical Centre Rotterdam, Rotterdam, the netherlands


How I treat high risk disease

Pieter Sonneveld

1. high-risk disease in newly diagnosed pati-ents with MM is defined by cytogenetic abnormalities, molecular subgroups, iSS stage and patient factors like age and comorbidities.

2. high-risk disease in the refractory/relapsed situation is defined by lack of chemo-sen-sitivity, short duration of response and the evolution of refractory subclones.

3. in younger patients with high-risk disease optimal treatment should consist of triple combination therapy including a prote-asome inhibitor and an imid for induction and consolidation followed by mainte-nance therapy.

4. Patients with multiple cytogenetic abnor-malities may benefit from a double autolo-gous transplant.

5. in older patients the preferred treatment is triple therapy, for example Vrd followed by maintenance therapy.

6. in general, patients with high-risk disease benefit from continuous treatment in order to prevent relapse or progression.


evAnGelos teRPos

General Hospital of Athens,Athens, Greece

Evangelos Terpos, MD, PhD is an Associate Professor of hematology in the Department of clinical Therapeutics in the university of Athens, School of Medicine, Athens, greece. he has also been appointed as honorary Senior lecturer in the Department of haema-tology, Faculty of Medicine imperial college london, uK.

his main research interest is the biology of plasma cell dyscrasias and especially the biology of bone disease in multiple myeloma (MM). in more than 400 papers in peer-revie-wed journals, Dr. Terpos has reported the signi-ficant role of RANKL and osteoprotegerin axis, CCL-3 (MIP-1α), Wnt and TGF-beta signalling in myeloma bone disease and myeloma cell growth. he has studied the predictive value of markers of bone remodelling and osteoclast function in myeloma progression and pati-ents’ survival. he has evaluated the effect of bisphosphonates and different anti-myeloma therapies including AScT, iMiDs- and borte-zomib-based regimens on bone metabolism. he has studied the biology and prevalence of osteonecrosis of the jaw in myeloma patients who receive bisphosphonates. Dr. Terpos also works on the role of modern imaging (including

whole-body low-dose cT and Mri) for MM, of angiogenesis in MM and Waldenstrom’s Macroglobulinemia, and of renal impairment in MM. in the clinical research era, Dr. Terpos participates in several important clinical trials with novel agents (pomalidomide, carfilzo-mib, ixazomib, daratumumab, elotuzumab, isatuximab, panobinostat, etc) in the field of multiple myeloma.

Dr. Terpos is co-chairing the Bone Subgroup of the international Myeloma Working group and the guideline Subgroup of the European Myeloma network. he is member of the Board of the greek Society of hematology since 2015 and Vice-President of this Society for 2016-2018. Dr. Terpos has given lectures at ASh, ASco & EhA meetings, international Myeloma Workshops, international Mee-tings on cancer-induced Bone Disease and in several national meetings. he is reviewer of scientific papers in more than 50 medical journals and has reviewed abstracts for ASh, EhA & EBMT meetings. he is Associate Edi-tor of HemaSphere (official journal of EHA) for Myeloma and member of the editorial board of haematologica.


Pathophysiology and Management of myeloma bone disease

EvangElos TErpos

1. osteolytic bone disease is the most com-mon complication of multiple myeloma. Bisphosphonate remain the cornerstone of the management of myeloma-related bone disease.

2. All myeloma patients with normal renal function and osteolytic disease at diagno-sis should be treated with zoledronic acid (preferably) or pamidronate, intravenously, in addition to specific anti-myeloma the-rapy. Symptomatic patients, without bone disease assessed by conventional radio-graphy, should also receive zoledronic acid, but its advantage is not clear for patients with no bone involvement on Mri or PET/cT. in asymptomatic MM, bisphos-phonates are not recommended.

3. Zoledronic acid should be given for more than two years only in patients with active MM. For patients who have achieved cr or VgPr, 12-24 months of therapy with bisphosphonates should be adequate. At relapse, bisphosphonates have to be rein-itiated.

4. in cases of osteonecrosis of the jaw (onJ), bisphosphonates should be discontinued and can be re-administered if onJ has healed. In patients with CrCl <30 mL/min bisphosphonates are not recommen-ded. Denosumab is a logical approach for these patients. however, until denosumab is fully approved for myeloma, patients with renal impairment have to be treated with a proteasome inhibitor-based regi-men and when renal function is reversed and crcl is >30 ml/min, bisphosphonates should be given.

5. in the largest placebo-controlled trial for myeloma patients to-date, denosumab was compared to zoledronic acid. Alt-hough, there was no difference regarding time to first skeletal-related event (SRE) was not different between the two drugs, a landmark analysis at 15 months showed a superiority of denosumab in terms of SrEs. Furthermore, denosumab showed a better renal safety profile along with a remarkable advantage in progression-free survival. Thus, denosumab is possibly another standard of care for myeloma-related bone disease.

6. low-dose radiation therapy (up to 30 gy) can be used as palliative treatment for uncontrolled pain, for impending patho-logic fracture, or impending spinal cord compression. Balloon kyphoplasty should be considered for symptomatic vertebral compression fractures, while surgery is recommended for long-bone fractures, bony compression of the spinal cord, or vertebral column instability.


niels van de Donk, MD, PhD is a hematolo-gist at the Vu university Medical center in Amsterdam, The netherlands. he completed his medical degree at the university Medical center utrecht. Prior to this he had obtai-ned a Bachelor’s degree in Pharmacy and a Master’s degree from the university Medi-cal center utrecht, where he also completed his PhD studies, which were focused on new treatment strategies for multiple myeloma by targeting Bcl-2 and the mevalonate pathway.

he trained as an internist at the university Me-dical center utrecht, where he also pursued his specialization in hematology. Following a fellowship at the Jerome lipper Multiple My-eloma center, Dana-Farber cancer institute in Boston, uSA, he became a hematologist in

the Department of hematology at the univer-sity Medical center utrecht before assuming his current post at the Vu university Medical center in Amsterdam.

Dr. van de Donk’s special interest is the treatment of patients with multiple myeloma and he is involved in translational research towards finding new targets for therapy with a focus on immune therapy. he is author or co-author of a number of books and many papers published in peer-reviewed journals and a reviewer for several journals including Blood, leukemia, and haematologica, as well as associate editor of the netherlands Journal of hematology. he is also secretary of the hoVon multiple myeloma working party.

niels vAn de donK

VU University Medical Center,Amsterdam, the netherlands


the Role of moAb in myeloma therapy

Niels vaN de doNk

1. Monoclonal antibodies are transforming multiple myeloma treatment.

2. cD38-targeting antibodies have potent single agent activity by inducing classic Fc receptor-mediated activities such as complement-dependent cytotoxicity (cDc), antibody-dependent cellular cyto-toxicity (ADcc) and antibody-dependent cellular phagocytosis (ADcP). in addition, cD38 antibodies have immunomodula-tory effects by eliminating cD38-positive regulatory T cells, regu-latory B cells, and myeloid-derived suppressor cells.

3. cD38 antibodies synergize with lenali-domide, pomalidomide, and proteasome inhibitors.

4. SlAMF7-targeting agents induce ADcc, and also activate nK cells.

5. SlAMF7-targeting agents have no marked single agent activity, but combined with standard of care regimens lenalidomide-dexamethasone and bortezomib-dexa-methasone results in improved outcome as compared to standard of care alone.

6. Both cD38 antibodies and SlAMF7-targe-ting antibodies are incorporated in first-line regimens; early results will be discussed during the meeting.

7. These antibodies are also promising agents for high-risk SMM patients.

8. new management aspects concerning these antibodies include: 1) response eva-luation, 2) infusion reactions; and 3) blood transfusion typing.


Katja Weisel, MD, is an Associate Professor in haematology/oncology in the department of hematology, oncology, immunology, rheu-matology and Pulmonology at the university of Tübingen, germany.

Prof. Weisel received her medical degree from the Medical School of the university of ulm, germany, and did her clinical residency in in-ternal medicine at the university of Tübingen. She did a postdoctoral research fellowship in the laboratory of Developmental hematopoi-esis at the Memorial Sloan-Kettering cancer center in new york, ny, uSA, She comple-ted her medical fellowship in internal medicine and hematology, oncology at the university of Tübingen. here, she is heading the outpa-tient care unit of the department. Prof. Weisel is since 2006 leading the Tübingen myeloma program. her myeloma research interests

focus on treatment optimization for high-risk myeloma, renally impaired myeloma patients, refractory myeloma patients and radiographic methods monitoring myeloma disease. She is member of the steering committee of the german speaking multiple myeloma group (gMMg).

Prof. Weisel is coinvestigator in all gMMg trials and is the lead investigator of 3 gMMg trials, including the gMMg-concEPT trial investigating a novel first-line treatment in high-risk myeloma patients. Furthermore, she was the principle investigator in several national and international phase i-iii trials.

Prof. Weisel participated in more than 80 publications on multiple myeloma treatment and biology.

KAtJA Weisel

University Hospital tübingen,tübingen, Germany

Friday, 19 January, 16:20 – 16:45

Treatment options for elderly fit patients

Katja Weisel

1. in general, patients should be determined as transplant-eligible (TE) or transplant non-eligible (TnE) according to the biolo-gical age and comorbidities. however, in many countries, patients are assigned to the TnE/elderly subgroup when older than 65 years of age, often due to reimburse-ment issues.

2. in the Eu approved treatment options for this patient group are either proteasome inhibitor based or iMiD based. The most widely used regimens are Bortezomib, Melphalan, Predinsone (VMP) and con-tinuous treatment with lenalidomide and Dexamethasone (rd).

3. in the largest Phase iii trial ever conduc-ted in this indication (FirST trial) it was recently shown that continuous treatment with Rd has significant superiority in pro-gression-free (PFS) and overall survival (oS) compared to the combination treat-ment of Melphalan, Prednisone and Tha-lidomide (MPT).

4. currently, the combination treatment with both, proteasome inhibitor and iMiD seems to be the most effective treatment regarding response rate and overall prog-nosis in TE, but also in TnE patients.

5. in the SWog S0777 trial, it was demons-trated, that treatment with lenalidomide, Bortezomib and Dexamethasone (rVd) followed by rd maintenance is superior to rd alone in PFS and oS. however, so far, the rVd combination is not approved by FDA and EMA despite widely used in the uS and integrated in the current mSMArT and ESMo guidelines.

6. Strategies to optimize the VMP standard were recently also evaluated in large phase iii trials. in the clArion trial, treat-ment with VMP was compared to treat-ment with Carfilzomib-MP (KMP). Howe-ver, there was no difference in PFS.

7. Very recently, it was shown that the addi-tion of the monoclonal Anti cD38 Anti-body Daratumumab to the VMP backbone results in significant improvement in PFS and response rates compared to VMP alone (Alcyone tial).

8. Further phase iii trials are currently inves-tigating the addition of monoclonal Anti-bodies to the rd or to the rVd standard. results of these trials are expected in the near future.

European Multiple Myeloma Academy | 19 – 20 January 2018 | Vienna, Austria 54 55 European Multiple Myeloma Academy | 19 – 20 January 2018 | Vienna, Austria

Elena Zamagni MD, PhD, is Assistant Professor of hematology at the university of Bologna, italy. She received her medical degree from university of Bologna, where she also served her residency in haematology. She got PhD in clinical hematology at the university of Bologna in May 2005.

her research interests include areas related to multiple myeloma, in particular on the role of high dose therapy with stem cell support , of prognostic factors and of imaging techniques.

She has published over 90 papers in peer-reviewed journals, mainly in the field of

plasma cell dyscrasia. She has contributed to the educational session of the italian Society of haematology. She is an active member of the board of the giMEMA myeloma working party and she has cooperated in the Scientific secretary and as principal investigator in several national randomized trials in multiple myeloma. She is a member of the italian Society of haematology and of the international Myeloma Working group. She is serving on the EHA’s Scientific Program committee since 2017.

elenA zAmAGni

Seragnoli Institute of Hematology,Bologna, Italy

Friday, 19 January, 11:00 – 11:25

Imaging in myeloma bone disease

ElEna Zamagni

1. novel imaging techniques are nowadays recommended both at diagnosis and after the end of treatment in MM (iMWg new diagnostic criteria, rajkumar V, lancet oncology 2014).

2. Whole-Body low-Dose computed Tomo-graphy (WBlDcT) is superior to conven-tional radiography for the detection of osteolytic lesions and it has replaced it in the work-up of myeloma patients. The cT part of PET/cT can be considered as a valid alternative when available.

3. Magnetic resonance imaging (Mri) is the best imaging method for the depiction of marrow infiltration by myeloma cells.

4. WB-Mri (or Mri of the spine and pelvis if WB-Mri is not available) should be perfor-med in all patients with no lytic lesions at diagnosis for the exclusion of symptomatic myeloma (iMWg new diagnostic criteria, rajkumar V, lancet oncology 2014).

5. Functional imaging techniques are nowa-days required to evaluate minimal residual disease (MrD) after the end of treatment (iMWg new response criteria, Kumar S, lancet oncology 2016).

6. FDg PET/cT is the best imaging tech-nique for evaluating and monitoring res-ponse to therapy outside the BM and is recommended by the iMWg (cavo M, lancet oncology 2017).

7. PET/cT has an independent prognostic value both at diagnosis and after treat-ment.

8. Functional whole-body Mri techniques (dynamic contrast enhanced, DcE and dif-fusion weighted imaging, DWi) seem pro-mising for response evaluation, but need further studies.

9. Standardization of PET/cT is on-going.10. A prospective comparison between PET/

cT and DWi- Mri for the evaluation of MrD is desirable.

supported by unrestricted grants by

19–20 january 2018 vienna, austria - stil_ cd · participants: michele cavo, maria-victoria...

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