Background High-dose therapy with melphalan can prolong survivalamong patients with multiple myeloma. We assessed whether theaddition of thalidomide, which has activity against advancedand refractory myeloma, would further improve survival.
Methods Between October 1998 and February 2004, 668 patientswith newly diagnosed multiple myeloma received two cycles ofintensive melphalan-based chemotherapy, each supported by autologoushematopoietic stem-cell transplantation. A total of 323 wererandomly assigned to receive thalidomide from the outset untildisease progression or undue adverse effects, and 345 did notreceive thalidomide. The primary end point was the five-yearevent-free survival rate. Secondary end points were completeresponse and overall survival.
Results After a median follow-up of 42 months among survivors,the thalidomide and control groups had rates of complete responseof 62 percent and 43 percent, respectively (P<0.001), andfive-year event-free survival rates of 56 percent and 44 percent(P=0.01). The five-year rate of overall survival was approximately65 percent in both groups (P=0.90). Median survival after relapsewas 1.1 years in the thalidomide group and 2.7 years in thecontrol group (P=0.001). Severe peripheral neuropathy and deep-veinthrombosis occurred more frequently in the thalidomide groupthan in the control group.
Conclusions When incorporated into high-dose therapy for myeloma,thalidomide increased the frequency of complete responses andextended event-free survival at the expense of added adverseeffects without improving overall survival. (ClinicalTrials.govnumber, NCT00083551
[ClinicalTrials.gov]
.)
The steep dose–response effect of melphalan in patientswith multiple myeloma can be used to therapeutic advantage whensupported with infusions of autologous peripheral-blood stemcells.1,2 After a pilot trial of two transplantations in patientswith multiple myeloma,3 a larger trial (the InterGroupe Francophonedu Myélome) reported seven-year event-free and overallsurvival rates of 20 and 40 percent, respectively — twicethe rates obtained with single transplantations.4,5 Our phase3 randomized trial was prompted by the demonstration of theefficacy of thalidomide (Kevadon) in multiple myeloma that isrefractory to post-transplantation salvage therapies.6,7 Wesought to determine whether the addition of thalidomide to intensivechemotherapy would improve the outcome among patients with multiplemyeloma.
Methods
Patients
Between October 1998 and February 2004, we enrolled 668 patientswho had newly diagnosed progressive or symptomatic multiplemyeloma, were 75 years old or younger, and had received no morethan one cycle of prior therapy. All patients provided writteninformed consent in keeping with the guidelines of the participatinginstitution and the National Cancer Institute. The protocolwas approved by the institutional review board and the Foodand Drug Administration and was monitored by a data and safetymonitoring board as required by the National Cancer Institutefor phase 3 trials. Data on eligibility, dosing, response, andadverse effects were checked by a certified independent auditingteam, usually every six months; each audit involved at least50 patients (a total of 350 were audited).
Prior local radiotherapy for pain control or cord compressionwas permitted. Patients had to have a Southwest Oncology Groupperformance status of less than 3, unless the score was basedsolely on bone pain. Cardiopulmonary function had to be adequate;renal failure, even that requiring hemodialysis, was not anexclusion criterion.
Treatment
The study design (Figure 1) required stratification of patientsaccording to serum beta2-microglobulin levels (less than 4 mgper liter vs. 4 mg per liter or more). Table 1 lists the fourphases of the protocol and the regimens and doses used.8,9,10
At enrollment, patients were randomly assigned either to a controlgroup (no thalidomide) or to the experimental group (thalidomide).The thalidomide doses were 400 mg daily during induction chemotherapy(withheld on day 5 of cycle 3 of chemotherapy for the collectionof peripheral-blood stem cells), 100 mg daily between transplantations,200 mg daily with consolidation therapy, 100 mg daily duringthe first year of maintenance therapy, and then 50 mg on alternatingdays; the drug was given until relapse or adverse events occurred.All patients proceeded to the transplantation phase regardlessof the level of response or the lack of response to inductionchemotherapy.
Filgrastim was administered to support induction and consolidationchemotherapy regimens, such as dexamethasone, cyclophosphamide,etoposide, and cisplatin; cyclophosphamide, doxorubicin, anddexamethasone; and dexamethasone, cisplatin, doxorubicin, cyclophosphamide,and etoposide (Table 1), along with prophylactic antibiotics,histamine H2 blockers, and recombinant erythropoietin as needed.Unless required for the management of pain, renal failure, seriousinfection, or lack of a caregiver, all treatments includingtransplantations were given in the outpatient setting by experiencedmembers of the nursing staff. Low-molecular-weight heparin wasgiven prophylactically to all patients in the thalidomide groupstarting in July 2001 to reduce the incidence of deep-vein thrombosis,since the incidence of this complication had not been reducedby treatment with low-dose warfarin.
Laboratory Evaluation
Evaluations included serum and urinary protein electrophoresis;quantitation of serum immunoglobulin levels, 24-hour urinaryprotein excretion, and serum levels of beta2-microglobulin andC-reactive protein; morphologic interpretation of bone marrowaspirates and biopsy specimens; and flow cytometry to evaluatenuclear DNA content and cytoplasmic immunoglobulin.11 Thesetests were performed before protocol therapy was begun, monthlyuntil the initiation of consolidation therapy, and every threeto six months thereafter.
Other laboratory studies included peripheral-blood counts andchemistry analyses. Multiple gated acquisition scanning or echocardiographywas used for cardiac evaluations; pulmonary status was evaluatedby determining the forced expiratory volume in one second andcarbon monoxide diffusion capacity; all test results had tobe within the institutional range of normal before enrollmentand before each of the two transplantation regimens. Standardskeletal surveys and magnetic resonance imaging (MRI) studiesof the skeleton were also performed.
Criteria for Response and Relapse
A complete response required the absence of a monoclonal immunoglobulinor light chain on immunofixation analysis of serum and urine,a normal morphologic appearance of bone marrow aspirates andbiopsy specimens, and the absence, on flow cytometry, of aneuploidor light-chain–restricted cells.11 A partial responsewas defined as a reduction in serum monoclonal immunoglobulinlevels by at least 75 percent and in urinary light chains byat least 90 percent and a normal morphologic appearance of bonemarrow aspirates and biopsy specimens. For each definition,the criteria had to be met on at least two occasions at leasttwo months apart.
Relapse after a complete response was diagnosed on the reappearanceof a monoclonal protein in serum or urine. Relapse after a partialresponse was diagnosed on the basis of an increase in serummonoclonal immunoglobulin levels or in urinary light chainsby at least 50 percent or a doubling from the lowest level,whichever occurred first. Disease progression was defined asan increase in serum levels of myeloma protein or in 24-hoururinary excretion of light chains by at least 25 percent.
In patients with nonsecretory or hyposecretory disease, baselinebone marrow plasmacytosis had to exceed 30 percent or multiplebone lesions had to be detected by MRI (fine-needle aspiratesfrom lesions detected in this manner had to contain at least30 percent monoclonal plasma cells). A response in patientswith nonsecretory multiple myeloma required a complete bonemarrow response or resolution of MRI-defined bone lesions. Relapseof nonsecretory multiple myeloma was defined by the reemergenceof monoclonal marrow plasmacytosis or focal lesions on MRI.The development of new osteolytic lesions and extramedullarymultiple myeloma also constituted relapse or progression inpatients with secretory and those with nonsecretory multiplemyeloma.
Statistical Analysis
The primary objective of the study was to demonstrate an increasein the five-year event-free survival rate from 40 percent inthe control group to 50 percent in the thalidomide group, givena statistical power of 82 percent and a two-sided P value ofless than 0.05 by the log-rank test. Interim analyses were performedafter the enrollment of 480 patients and once enrollment ended(with the use of tandem one-sided tests for the null and alternativehypotheses and a P value of 0.0025). The data and safety monitoringboard approved release of the results in March 2005, one yearafter study closure. A P value of 0.0225 was considered to indicatestatistical significance in the final analysis.12 In accordancewith the policy of the Journal, we report only two-sided P values.
The analyses of outcomes in the two groups were conducted accordingto the intention-to-treat principle. Treatment-related deathwas defined as a death that was attributable to a treatmentgiven within two months before death. The cumulative incidenceof treatment-related mortality was estimated according to themethod of Gooley et al.13 and compared with the use of the log-ranktest. The Kaplan–Meier method14 was used to estimate event-freesurvival, overall survival, and survival after relapse. Event-freesurvival was measured from the date of enrollment until diseaseprogression, relapse, or death from any cause. Data on patientswho had no events were censored at the time of last contact.Overall survival was measured from the date of enrollment untildeath from any cause; data on survivors were censored at thetime of last contact. Post-relapse survival was measured fromthe date of progression or relapse to death from any cause,with censoring of data at the time of last contact. The log-ranktest was used to compare event-free, overall, and post-relapsesurvival in the two groups.15 Cox regression analysis16 wasused to examine multivariate models of prognostic factors. Completeresponse was examined as a time-dependent covariate. Standardprognostic factors of event-free and overall survival were dichotomizedwith the use of cutoff points reported as part of the InternationalStaging System for multiple myeloma.17
All investigators had full access to the data, which were analyzedby Cancer Research and Biostatistics in Seattle.
Results
Outcome
The baseline characteristics of the 323 patients who were randomlyassigned to thalidomide and the 345 controls were similar (Table 2).As of August 15, 2005, the median follow-up of 478 survivingpatients was 42 months (range, 21 to 81), 270 patients had hadan event, and 190 had died. There were no significant differencesbetween the two groups in the number who participated in thevarious phases of treatment or in the reasons for leaving thestudy (details are given in Table 1 of the Supplementary Appendix,available with the full text of this article at www.nejm.org).Overall, 85 percent of patients received one transplant, 67percent received two transplants, 65 percent started consolidationtherapy, and 56 percent began the maintenance phase (Table 1of the Supplementary Appendix). The time to completion of treatmentwas also similar in the two groups (Figure 2A).
Figure 2. Percentages of Patients Who Entered Each Phase of Treatment (Panel A); Overall and Event-free Survival, Treatment-Related Mortality, and Percentage of Patients in the Thalidomide Group Who Discontinued Thalidomide (Panel B); Survival after Relapse or Progression (Panel C); and Survival According to Age (Panel D).
In Panel A, there was no significant difference among groups in the speed of progression through the protocol or in the rate of completion of the protocol. In Panel B, the nine patients who never started thalidomide therapy were excluded from the analysis of patients who discontinued taking thalidomide because of adverse effects or other reasons. CI denotes confidence interval.
As compared with the control group, the thalidomide group hada higher rate of complete response (62 percent vs. 43 percent,P<0.001), a similar rate of complete response at four years(64 percent in both groups), and a higher rate of five-yearevent-free survival (56 percent vs. 44 percent, P=0.01) (Figure 2B).The cumulative 12-month treatment-related mortality rate was8 percent in both groups, but it was significantly higher amongpatients 65 years of age or older than among younger patients(13 percent vs. 6 percent, P=0.004), independently of treatmentgroup. Despite a superior event-free survival rate in the thalidomidegroup, there was no significant difference between the two groupsin overall survival, owing in part to significantly shortersurvival after relapse in the thalidomide group than in thecontrol group (median, 1.1 years vs. 2.7 years; P=0.001) (Figure 2C).Since the rate of insurance denial for transplantation was higheramong patients who were at least 65 years old than among youngerpatients (24 percent vs. 4 percent, P<0.001), younger patientshad a higher rate of completion of the first transplantation(87 percent vs. 77 percent, P=0.003) and second transplantation(72 percent vs. 47 percent, P<0.001) and a higher overallsurvival rate at five years (68 percent vs. 50 percent, P=0.008)(Figure 2D).
Prognostic Factors
The probability of event-free and overall survival was significantlylower among patients with cytogenetic abnormalities, those witha lactate dehydrogenase level that exceeded the upper limitof normal, and those with a serum albumin level of less than3.5 g per deciliter (Table 3). Event-free survival and overallsurvival were significantly longer among patients who had acomplete response than among those who had a partial or no response(evaluated as a time-dependent covariate). Independently ofthese features, randomization to the thalidomide group was associatedwith longer event-free survival but not overall survival.
Table 3. Multivariate Analysis of Features Associated with the Clinical Outcome.
Adverse Events
The occurrence of clinically significant adverse events (Table 4)necessitated changes in the dose of thalidomide in a sizablefraction of patients, especially elderly patients. Thalidomidewas discontinued within two years after enrollment in 30 percentof patients, and within four years in more than 60 percent (Figure 2B).Especially during induction chemotherapy, thromboembolic eventswere almost twice as common among patients assigned to the thalidomidegroup as among those assigned to the control group. The highincidence of deep-vein thrombosis in the initial phase of thestudy (34 percent among the first 162 patients randomly assignedto thalidomide, as compared with 18 percent among the first174 patients enrolled in the control group; P<0.001) (Figure1A of the Supplementary Appendix) was not eliminated by prophylacticadministration of low-molecular-weight heparin later in thestudy (24 percent among the last 152 patients enrolled in thethalidomide group, as compared with 15 percent among the last163 patients enrolled in the control group; P=0.064) (Figure1B of the Supplementary Appendix). Syncopal episodes relatedto sinus bradycardia occurred in 12 percent of patients in thethalidomide group and in only 4 percent of patients in the controlgroup.
Table 4. Incidence of Severe Adverse Events of More Than Grade 2, According to Treatment Group and Phase of Therapy.
Because of concern about drug safety, cardiac pacemakers wereimplanted in nearly one third of the 38 patients with symptomaticsinus bradycardia. Tremor was encountered twice as frequentlyin the thalidomide group as in the control group (13 percentvs. 6 percent). Most debilitating was peripheral neuropathywith a grade of more than 2 (i.e., more than moderate) accordingto the Common Toxicity Criteria of the National Cancer Institute;this adverse event was more common in the thalidomide groupthan in the control group (27 percent vs. 17 percent, P<0.001)(Table 4) and among patients at least 65 years old than amongyounger patients (29 percent vs. 20 percent, P=0.02). Forty-onepercent of patients who were at least 65 years old and who werereceiving thalidomide had peripheral neuropathy, as comparedwith 17 percent of younger patients in the control group (P<0.001)(Figure 1C of the Supplementary Appendix). Peripheral neuropathyimproved to less than grade 2 within three to four months aftera dose reduction or cessation of thalidomide in nearly 90 percentof affected patients. Severe constipation leading to bowel obstructionwas noted in 14 percent of patients receiving thalidomide andin 8 percent of patients in the control group (P=0.02) (Table 4).Neutropenia of more than grade 2 was recorded in 46 percentof patients in the thalidomide group during the consolidationand maintenance phases but in only 28 percent of patients inthe control group (P<0.001) (Table 4). Despite the higherincidence of various adverse events in the thalidomide group,the treatment-related mortality rate was similar in the twogroups (Figure 2B).
Management after Relapse in Relation to Prior Thalidomide Therapy
Of 164 events (deaths excluded), multiple myeloma progressedafter transplantation in 136 patients; 107 of these patientsreceived salvage therapies. The proportions of patients receivingspecific salvage regimens did not differ significantly in thetwo groups (44 in the thalidomide group and 63 in the controlgroup). These salvage treatments included further thalidomideor thalidomide (75 percent of the thalidomide group and 83 percentof the control group), bortezomib18 (45 percent and 37 percent,respectively), thalidomide or bortezomib (84 percent and 92percent, respectively), lenalidomide19 (9 percent and 11 percent,respectively), and dexamethasone, thalidomide, cisplatin, doxorubicin,cyclophosphamide, and etoposide chemotherapy (Table 1) (23 percentand 22 percent, respectively), and further high-dose therapy(7 percent and 2 percent, respectively). Even though the twogroups had similar features at baseline and relapse, the incidenceof partial responses was higher (71 percent vs. 55 percent,P=0.029) and survival after relapse was longer (2.7 vs. 1.1years, P=0.001) among patients initially assigned to receiveno thalidomide than among those assigned to receive thalidomide(Figure 2C). Neither the cumulative dose of thalidomide northe duration of treatment interruption because of adverse eventsbefore relapse influenced survival after relapse.
Discussion
The addition of thalidomide to intensive melphalan-based chemotherapysupported with two peripheral-blood hematopoietic stem-celltransplantations improved the rate of complete response andevent-free survival among patients with newly diagnosed multiplemyeloma. The drug failed, however, to prolong overall survivaland was associated with considerable adverse effects. Attalet al. also reported longer event-free survival but not overallsurvival when thalidomide was given after two transplantationsas maintenance therapy in lower doses than the ones we used.20
Relapses in the thalidomide group appeared to be more drug-resistantthan relapses in the control group. A higher failure rate withsalvage therapy and shorter survival after relapse can partiallyexplain the similar overall survival times in the two groups.Our results indicate that a complete response is not a validsurrogate for survival in myeloma clinical trials. The definitionof a complete response in patients with multiple myeloma reliesin part on the presence of immunoglobulin-producing plasma cells,although the presence of nonsecretory or hyposecretory plasmacells often accounts for relapses among patients with high lactatedehydrogenase levels21; such cells may be present at diagnosisand preferentially expand during disease progression. Furthermore,as compared with the relatively rapid reduction in levels ofthe myeloma protein, MRI-defined focal lesions (which harbormyeloma cells) take one or two years to regress and are oftenthe first sites of relapse.22 When multiple myeloma evolvesfrom a documented monoclonal gammopathy of uncertain significance(MGUS), or a smoldering phase, a complete response is infrequent,but when one does occur, it has no effect on the likelihoodof survival.23 This phenomenon presumably reflects the reestablishmentof a stable MGUS-like condition.
Superior response rates have been reported for thalidomide plusdexamethasone as compared with dexamethasone alone for inductiontherapy in patients with multiple myeloma.24,25 Since many patientsin these trials received high-dose therapy after induction therapywith thalidomide and dexamethasone, the long-term benefit ofthis combination cannot be ascertained. Reserving thalidomidefor maintenance therapy after transplantation, as was done inthe pilot and larger trials conducted by the InterGroupe Francophonedu Myélome,4,5 has several advantages: resistance maybe avoided; the risk of thromboembolic complications can bereduced, since this risk is highest during induction therapy,when the burden of tumor is high26; and the incidence of neurotoxiceffects should be reduced with the later introduction of thalidomideat lower doses (50 to 100 mg) during maintenance therapy. Highrates of complete response approaching the rates observed withhigh-intensity treatment plus stem-cell transplantation haverecently been found in trials of thalidomide combined with standardtreatment with melphalan and prednisone.27,28 Similarly, combinationsof bortezomib and dexamethasone,29,30 plus pegylated doxorubicin31or thalidomide,32,33 have shown promise. Little is known, however,about the durability of the responses induced by these treatments,especially after the discontinuation of the drugs. Althoughstandard high-dose melphalan therapy with stem-cell transplantationhas considerable acute adverse effects, its low mortality andinfrequent chronic adverse effects have to be balanced againstthe potential of the newer agents for irreversible and incapacitatingchronic adverse effects. Acute complications (thromboembolismwith thalidomide and lenalidomide) and chronic sequelae (polyneuropathywith thalidomide and bortezomib) may be minimized by combining"old" and "new" therapies, especially since the genomic heterogeneityof multiple myeloma may require a multifaceted approach to treatmentto achieve lasting control.34
Supported in part by a Program Project Grant (CA55819) fromthe National Cancer Institute and Celgene Corporation.
No potential conflict of interest relevant to this article wasreported.
Source Information
From the Myeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock (B.B., G.T., E.A., J.S., F.R., A.F., M.Z., K.H., M.P.-R., C.L., G.T., R.T., E.K., S.K., M.F.); and Cancer Research and Biostatistics, University of Washington, Seattle (E.R., J.C.).
Address reprint requests to Dr. Barlogie at the Myeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, 4301 W. Markham St., Mail Slot 816, Little Rock, AR 72205, or at barlogiebart{at}uams.edu.
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Nair, B., Shaughnessy, J. D. Jr, Zhou, Y., Astrid-Cartron, M., Qu, P., van Rhee, F., Anaissie, E., Alsayed, Y., Waheed, S., Hollmig, K., Szymonifka, J., Petty, N., Hoering, A., Barlogie, B.
(2009). Gene expression profiling of plasma cells at myeloma relapse from tandem transplantation trial Total Therapy 2 predicts subsequent survival. Blood
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Harousseau, J.-L., Moreau, P.
(2009). Autologous Hematopoietic Stem-Cell Transplantation for Multiple Myeloma. NEJM
360: 2645-2654
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Ocio, E. M., Maiso, P., Chen, X., Garayoa, M., Alvarez-Fernandez, S., San-Segundo, L., Vilanova, D., Lopez-Corral, L., Montero, J. C., Hernandez-Iglesias, T., de Alava, E., Galmarini, C., Aviles, P., Cuevas, C., San-Miguel, J. F., Pandiella, A.
(2009). Zalypsis: a novel marine-derived compound with potent antimyeloma activity that reveals high sensitivity of malignant plasma cells to DNA double-strand breaks. Blood
113: 3781-3791
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Spencer, A., Prince, H. M., Roberts, A. W., Prosser, I. W., Bradstock, K. F., Coyle, L., Gill, D. S., Horvath, N., Reynolds, J., Kennedy, N.
(2009). Consolidation Therapy With Low-Dose Thalidomide and Prednisolone Prolongs the Survival of Multiple Myeloma Patients Undergoing a Single Autologous Stem-Cell Transplantation Procedure. JCO
27: 1788-1793
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Ludwig, H., Hajek, R., Tothova, E., Drach, J., Adam, Z., Labar, B., Egyed, M., Spicka, I., Gisslinger, H., Greil, R., Kuhn, I., Zojer, N., Hinke, A.
(2009). Thalidomide-dexamethasone compared with melphalan-prednisolone in elderly patients with multiple myeloma. Blood
113: 3435-3442
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Stewart, A. K.
(2009). Reduced-intensity allogeneic transplantation for myeloma: reality bites. Blood
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Lahuerta, J. J., Mateos, M. V., Martinez-Lopez, J., Rosinol, L., Sureda, A., de la Rubia, J., Garcia-Larana, J., Martinez-Martinez, R., Hernandez-Garcia, M. T., Carrera, D., Besalduch, J., de Arriba, F., Ribera, J. M., Escoda, L., Hernandez-Ruiz, B., Garcia-Frade, J., Rivas-Gonzalez, C., Alegre, A., Blade, J., San Miguel, J. F.
(2008). Influence of Pre- and Post-Transplantation Responses on Outcome of Patients With Multiple Myeloma: Sequential Improvement of Response and Achievement of Complete Response Are Associated With Longer Survival. JCO
26: 5775-5782
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Barlogie, B., Epstein, J., Shaughnessy, J. D. Jr
(2008). Going with the flow, and beyond, in myeloma. Blood
112: 3917-3918
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Xiong, W., Wu, X., Starnes, S., Johnson, S. K., Haessler, J., Wang, S., Chen, L., Barlogie, B., Shaughnessy, J. D. Jr, Zhan, F.
(2008). An analysis of the clinical and biologic significance of TP53 loss and the identification of potential novel transcriptional targets of TP53 in multiple myeloma. Blood
112: 4235-4246
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Moreau, P., Garban, F., Attal, M., Michallet, M., Marit, G., Hulin, C., Benboubker, L., Doyen, C., Mohty, M., Yakoub-Agha, I., Leyvraz, S., Casassus, P., Avet-Loiseau, H., Garderet, L., Mathiot, C., Harousseau, J.-L., on behalf of the IFM group,
(2008). Long-term follow-up results of IFM99-03 and IFM99-04 trials comparing nonmyeloablative allotransplantation with autologous transplantation in high-risk de novo multiple myeloma. Blood
112: 3914-3915
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Dispenzieri, A.
(2008). Biology, treatment, and time. Blood
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Barlogie, B., Pineda-Roman, M., van Rhee, F., Haessler, J., Anaissie, E., Hollmig, K., Alsayed, Y., Waheed, S., Petty, N., Epstein, J., Shaughnessy, J. D. Jr, Tricot, G., Zangari, M., Zeldis, J., Barer, S., Crowley, J.
(2008). Thalidomide arm of Total Therapy 2 improves complete remission duration and survival in myeloma patients with metaphase cytogenetic abnormalities. Blood
112: 3115-3121
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Rajkumar, S. V.
(2008). Treatment of Myeloma: Cure vs Control. Mayo Clin Proc.
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Tai, Y.-T., Dillon, M., Song, W., Leiba, M., Li, X.-F., Burger, P., Lee, A. I., Podar, K., Hideshima, T., Rice, A. G., van Abbema, A., Jesaitis, L., Caras, I., Law, D., Weller, E., Xie, W., Richardson, P., Munshi, N. C., Mathiot, C., Avet-Loiseau, H., Afar, D. E. H., Anderson, K. C.
(2008). Anti-CS1 humanized monoclonal antibody HuLuc63 inhibits myeloma cell adhesion and induces antibody-dependent cellular cytotoxicity in the bone marrow milieu. Blood
112: 1329-1337
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van Rhee, F., Dhodapkar, M., Shaughnessy, J. D. Jr, Anaissie, E., Siegel, D., Hoering, A., Zeldis, J., Jenkins, B., Singhal, S., Mehta, J., Crowley, J., Jagannath, S., Barlogie, B.
(2008). First thalidomide clinical trial in multiple myeloma: a decade. Blood
112: 1035-1038
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Burington, B., Barlogie, B., Zhan, F., Crowley, J., Shaughnessy, J. D. Jr.
(2008). Tumor Cell Gene Expression Changes Following Short-term In vivo Exposure to Single Agent Chemotherapeutics are Related to Survival in Multiple Myeloma. Clin. Cancer Res.
14: 4821-4829
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Barlogie, B., Shaughnessy, J. D. Jr., Crowley, J.
(2008). Duration of Survival in Patients with Myeloma Treated with Thalidomide. NEJM
359: 210-212
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San-Miguel, J., Harousseau, J.-L., Joshua, D., Anderson, K. C.
(2008). Individualizing Treatment of Patients With Myeloma in the Era of Novel Agents. JCO
26: 2761-2766
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Palumbo, A., Gay, F., Bringhen, S., Falcone, A., Pescosta, N., Callea, V., Caravita, T., Morabito, F., Magarotto, V., Ruggeri, M., Avonto, I., Musto, P., Cascavilla, N., Bruno, B., Boccadoro, M.
(2008). Bortezomib, doxorubicin and dexamethasone in advanced multiple myeloma. Ann Oncol
19: 1160-1165
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Geerts, W. H., Bergqvist, D., Pineo, G. F., Heit, J. A., Samama, C. M., Lassen, M. R., Colwell, C. W.
(2008). Prevention of Venous Thromboembolism: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest
133: 381S-453S
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Hsi, E. D., Steinle, R., Balasa, B., Szmania, S., Draksharapu, A., Shum, B. P., Huseni, M., Powers, D., Nanisetti, A., Zhang, Y., Rice, A. G., van Abbema, A., Wong, M., Liu, G., Zhan, F., Dillon, M., Chen, S., Rhodes, S., Fuh, F., Tsurushita, N., Kumar, S., Vexler, V., Shaughnessy, J. D. Jr., Barlogie, B., van Rhee, F., Hussein, M., Afar, D. E.H., Williams, M. B.
(2008). CS1, a Potential New Therapeutic Antibody Target for the Treatment of Multiple Myeloma. Clin. Cancer Res.
14: 2775-2784
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Palumbo, A., Facon, T., Sonneveld, P., Blade, J., Offidani, M., Gay, F., Moreau, P., Waage, A., Spencer, A., Ludwig, H., Boccadoro, M., Harousseau, J.-L.
(2008). Thalidomide for treatment of multiple myeloma: 10 years later. Blood
111: 3968-3977
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Mehta, J.
(2008). One or two autografts for myeloma?. Blood
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Brenner, H., Gondos, A., Pulte, D.
(2008). Recent major improvement in long-term survival of younger patients with multiple myeloma. Blood
111: 2521-2526
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Abdelkefi, A., Ladeb, S., Torjman, L., Othman, T. B., Lakhal, A., Romdhane, N. B., Omri, H. E., Elloumi, M., Belaaj, H., Jeddi, R., Aissaoui, L., Ksouri, H., Hassen, A. B., Msadek, F., Saad, A., Hsairi, M., Boukef, K., Amouri, A., Louzir, H., Dellagi, K., Abdeladhim, A. B., on behalf of the Tunisian Multiple Myeloma Study G,
(2008). Single autologous stem-cell transplantation followed by maintenance therapy with thalidomide is superior to double autologous transplantation in multiple myeloma: results of a multicenter randomized clinical trial. Blood
111: 1805-1810
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Bensinger, W.
(2008). Stem-Cell Transplantation for Multiple Myeloma in the Era of Novel Drugs. JCO
26: 480-492
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Lokhorst, H. M., Schmidt-Wolf, I., Sonneveld, P., van der Holt, B., Martin, H., Barge, R., Bertsch, U., Schlenzka, J., Bos, G. M.J., Croockewit, S., Zweegman, S., Breitkreutz, I., Joosten, P., Scheid, C., van Marwijk-Kooy, M., Salwender, H.-J., van Oers, M. H.J., Schaafsma, R., Naumann, R., Sinnige, H., Blau, I., Delforge, M., de Weerdt, O., Wijermans, P., Wittebol, S., Duersen, U., Vellenga, E., Goldschmidt, H., for Dutch-Belgian HOVON and German GMMG,
(2008). Thalidomide in induction treatment increases the very good partial response rate before and after high-dose therapy in previously untreated multiple myeloma. haematol
93: 124-127
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Harousseau, J.-L.
(2008). Induction Therapy in Multiple Myeloma. ASH Education Book
2008: 306-312
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Rajkumar, S. V., Hayman, S. R.
(2008). Controversies Surrounding the Initial Treatment of Multiple Myeloma. Am Soc Clin Oncol Ed Book
2008: 369-374
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Fermand, J.-P.
(2008). Initial Therapy for Multiple Myeloma: Role of Stem Cell Transplantation. Am Soc Clin Oncol Ed Book
2008: 375-379
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Haessler, J., Shaughnessy, J. D. Jr., Zhan, F., Crowley, J., Epstein, J., van Rhee, F., Anaissie, E., Pineda-Roman, M., Zangari, M., Hollmig, K., Mohiuddin, A., Alsayed, Y., Hoering, A., Tricot, G., Barlogie, B.
(2007). Benefit of Complete Response in Multiple Myeloma Limited to High-Risk Subgroup Identified by Gene Expression Profiling. Clin. Cancer Res.
13: 7073-7079
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Palumbo, A., Falco, P., Corradini, P., Falcone, A., Di Raimondo, F., Giuliani, N., Crippa, C., Ciccone, G., Omede, P., Ambrosini, M. T., Gay, F., Bringhen, S., Musto, P., Foa, R., Knight, R., Zeldis, J. B., Boccadoro, M., Petrucci, M. T.
(2007). Melphalan, Prednisone, and Lenalidomide Treatment for Newly Diagnosed Myeloma: A Report From the GIMEMA Italian Multiple Myeloma Network. JCO
25: 4459-4465
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van de Velde, H. J.K., Liu, X., Chen, G., Cakana, A., Deraedt, W., Bayssas, M.
(2007). Complete response correlates with long-term survival and progression-free survival in high-dose therapy in multiple myeloma. haematol
92: 1399-1406
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Katzel, J. A., Hari, P., Vesole, D. H.
(2007). Multiple Myeloma: Charging Toward a Bright Future. CA Cancer J Clin
57: 301-318
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Plasmati, R., Pastorelli, F., Cavo, M., Petracci, E., Zamagni, E., Tosi, P., Cangini, D., Tacchetti, P., Salvi, F., Bartolomei, I., Michelucci, R., Tassinari, C. A.
(2007). Neuropathy in multiple myeloma treated with thalidomide: A prospective study. Neurology
69: 573-581
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Manochakian, R., Miller, K. C., Chanan-Khan, A. A.
(2007). Clinical Impact of Bortezomib in Frontline Regimens for Patients with Multiple Myeloma. The Oncologist
12: 978-990
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van Rhee, F., Bolejack, V., Hollmig, K., Pineda-Roman, M., Anaissie, E., Epstein, J., Shaughnessy, J. D. Jr, Zangari, M., Tricot, G., Mohiuddin, A., Alsayed, Y., Woods, G., Crowley, J., Barlogie, B.
(2007). High serum-free light chain levels and their rapid reduction in response to therapy define an aggressive multiple myeloma subtype with poor prognosis. Blood
110: 827-832
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van Rhee, F., Crowley, J., Barlogie, B., Rajkumar, S. V., Kyle, R. A., Moreau, P., Harousseau, J.-L., Attal, M., Bruno, B., Ciccone, G., Boccadoro, M.
(2007). Allografting or Autografting for Myeloma. NEJM
356: 2646-2648
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Cavo, M., Tosi, P., Zamagni, E., Cellini, C., Tacchetti, P., Patriarca, F., Di Raimondo, F., Volpe, E., Ronconi, S., Cangini, D., Narni, F., Carubelli, A., Masini, L., Catalano, L., Fiacchini, M., de Vivo, A., Gozzetti, A., Lazzaro, A., Tura, S., Baccarani, M.
(2007). Prospective, Randomized Study of Single Compared With Double Autologous Stem-Cell Transplantation for Multiple Myeloma: Bologna 96 Clinical Study. JCO
25: 2434-2441
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Richardson, P. G., Mitsiades, C., Schlossman, R., Munshi, N., Anderson, K.
(2007). New Drugs for Myeloma. The Oncologist
12: 664-689
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Carlo-Stella, C., Guidetti, A., Di Nicola, M., Lavazza, C., Cleris, L., Sia, D., Longoni, P., Milanesi, M., Magni, M., Nagy, Z., Corradini, P., Carbone, A., Formelli, F., Gianni, A. M.
(2007). IFN-{gamma} Enhances the Antimyeloma Activity of the Fully Human Anti-Human Leukocyte Antigen-DR Monoclonal Antibody 1D09C3. Cancer Res.
67: 3269-3275
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Palumbo, A., Ambrosini, M. T., Benevolo, G., Pregno, P., Pescosta, N., Callea, V., Cangialosi, C., Caravita, T., Morabito, F., Musto, P., Bringhen, S., Falco, P., Avonto, I., Cavallo, F., Boccadoro, M., for the Italian Multiple Myeloma Network, Gruppo I,
(2007). Bortezomib, melphalan, prednisone, and thalidomide for relapsed multiple myeloma. Blood
109: 2767-2772
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Walker, R., Barlogie, B., Haessler, J., Tricot, G., Anaissie, E., Shaughnessy, J. D. Jr, Epstein, J., van Hemert, R., Erdem, E., Hoering, A., Crowley, J., Ferris, E., Hollmig, K., van Rhee, F., Zangari, M., Pineda-Roman, M., Mohiuddin, A., Yaccoby, S., Sawyer, J., Angtuaco, E. J.
(2007). Magnetic Resonance Imaging in Multiple Myeloma: Diagnostic and Clinical Implications. JCO
25: 1121-1128
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Fonseca, R., Stewart, A. K.
(2007). Targeted therapeutics for multiple myeloma: The arrival of a risk-stratified approach. Molecular Cancer Therapeutics
6: 802-810
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Muto, A., Hori, M., Sasaki, Y., Saitoh, A., Yasuda, I., Maekawa, T., Uchida, T., Asakura, K., Nakazato, T., Kaneda, T., Kizaki, M., Ikeda, Y., Yoshida, T.
(2007). Emodin has a cytotoxic activity against human multiple myeloma as a Janus-activated kinase 2 inhibitor. Molecular Cancer Therapeutics
6: 987-994
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Dispenzieri, A., Rajkumar, S. V., Gertz, M. A., Lacy, M. Q., Kyle, R. A., Greipp, P. R., Witzig, T. E., Lust, J. A., Russell, S. J., Hayman, S. R., Kumar, S., Zeldenrust, S. R., Fonseca, R., Bergsagel, P. L., Reeder, C. B., Stewart, A. K., Roy, V., Dalton, R. J.
(2007). Treatment of Newly Diagnosed Multiple Myeloma Based on Mayo Stratification of Myeloma and Risk-Adapted Therapy (mSMART): Consensus Statement. Mayo Clin Proc.
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Zhan, F., Barlogie, B., Arzoumanian, V., Huang, Y., Williams, D. R., Hollmig, K., Pineda-Roman, M., Tricot, G., van Rhee, F., Zangari, M., Dhodapkar, M., Shaughnessy, J. D. Jr
(2007). Gene-expression signature of benign monoclonal gammopathy evident in multiple myeloma is linked to good prognosis. Blood
109: 1692-1700
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Sekimoto, E., Ozaki, S., Ohshima, T., Shibata, H., Hashimoto, T., Abe, M., Kimura, N., Hattori, K., Kawai, S., Kinoshita, Y., Yamada-Okabe, H., Tsuchiya, M., Matsumoto, T.
(2007). A Single-Chain Fv Diabody against Human Leukocyte Antigen-A Molecules Specifically Induces Myeloma Cell Death in the Bone Marrow Environment. Cancer Res.
67: 1184-1192
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Auwerda, J. J.A., Sonneveld, P., de Maat, M. P.M., Leebeek, F. W.G.
(2007). Prothrombotic coagulation abnormalities in patients with newly diagnosed multiple myeloma. haematol
92: 279-280
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Fonseca, R.
(2007). Strategies for Risk-Adapted Therapy in Myeloma. ASH Education Book
2007: 304-310
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Suvannasankha, A., Fausel, C., Juliar, B. E., Yiannoutsos, C. T., Fisher, W. B., Ansari, R. H., Wood, L. L., Smith, G. G., Cripe, L. D., Abonour, R.
(2007). Final Report of Toxicity and Efficacy of a Phase II Study of Oral Cyclophosphamide, Thalidomide, and Prednisone for Patients with Relapsed or Refractory Multiple Myeloma: A Hoosier Oncology Group Trial, HEM01-21. The Oncologist
12: 99-106
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Merlini, G.
(2006). Exciting new agents in multiple myeloma. Blood
108: 3235-3236
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Attal, M., Harousseau, J.-L., Leyvraz, S., Doyen, C., Hulin, C., Benboubker, L., Agha, I. Y., Bourhis, J.-H., Garderet, L., Pegourie, B., Dumontet, C., Renaud, M., Voillat, L., Berthou, C., Marit, G., Monconduit, M., Caillot, D., Grobois, B., Avet-Loiseau, H., Moreau, P., Facon, T., for the Inter-Groupe Francophone du Myelome (IFM),
(2006). Maintenance therapy with thalidomide improves survival in patients with multiple myeloma. Blood
108: 3289-3294
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Barlogie, B., Tricot, G.
(2006). Complete response in myeloma: a Trojan horse?. Blood
108: 2134-2134
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Zhan, F., Huang, Y., Colla, S., Stewart, J. P., Hanamura, I., Gupta, S., Epstein, J., Yaccoby, S., Sawyer, J., Burington, B., Anaissie, E., Hollmig, K., Pineda-Roman, M., Tricot, G., van Rhee, F., Walker, R., Zangari, M., Crowley, J., Barlogie, B., Shaughnessy, J. D. Jr
(2006). The molecular classification of multiple myeloma. Blood
108: 2020-2028
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Hanamura, I., Stewart, J. P., Huang, Y., Zhan, F., Santra, M., Sawyer, J. R., Hollmig, K., Zangarri, M., Pineda-Roman, M., van Rhee, F., Cavallo, F., Burington, B., Crowley, J., Tricot, G., Barlogie, B., Shaughnessy, J. D. Jr
(2006). Frequent gain of chromosome band 1q21 in plasma-cell dyscrasias detected by fluorescence in situ hybridization: incidence increases from MGUS to relapsed myeloma and is related to prognosis and disease progression following tandem stem-cell transplantation. Blood
108: 1724-1732
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Naumann, F., Weingart, O., Kruse, E., Schulz, H., Bohlius, J., Hulsewede, H., Engert, A.
(2006). Fifth biannual report of the cochrane haematologic malignancies group--focus on multiple myeloma.. JNCI J Natl Cancer Inst
98: E2-EE
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Folkman, J., Rogers, M. S., Barlogie, B., Shaughnessy, J., Tricot, G.
(2006). Thalidomide for multiple myeloma.. NEJM
354: 2389-2390
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(2006). More Data on Thalidomide for Multiple Myeloma. JWatch General
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Cavo, M., Baccarani, M.
(2006). The Changing Landscape of Myeloma Therapy. NEJM
354: 1076-1078
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Zonder, J. A.
(2006). Thrombotic Complications of Myeloma Therapy. ASH Education Book
2006: 348-355
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