M A Dimopoulos


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Publications (557)3269.66 Total impact

  • [show abstract] [hide abstract]
    ABSTRACT: Few effective treatments exist for patients with refractory or relapsed and refractory multiple myeloma not responding to treatment with bortezomib and lenalidomide. Pomalidomide alone has shown limited efficacy in patients with relapsed multiple myeloma, but synergistic effects have been noted when combined with dexamethasone. We compared the efficacy and safety of pomalidomide plus low-dose dexamethasone with high-dose dexamethasone alone in these patients. This multicentre, open-label, randomised phase 3 trial was undertaken in Australia, Canada, Europe, Russia, and the USA. Patients were eligible if they had been diagnosed with refractory or relapsed and refractory multiple myeloma, and had failed at least two previous treatments of bortezomib and lenalidomide. They were assigned in a 2:1 ratio with a validated interactive voice and internet response system to either 28 day cycles of pomalidomide (4 mg/day on days 1-21, orally) plus low-dose dexamethasone (40 mg/day on days 1, 8, 15, and 22, orally) or high-dose dexamethasone (40 mg/day on days 1-4, 9-12, and 17-20, orally) until disease progression or unacceptable toxicity. Stratification factors were age (≤75 years vs >75 years), disease population (refractory vs relapsed and refractory vs bortezomib intolerant), and number of previous treatments (two vs more than two). The primary endpoint was progression-free survival (PFS). Analysis was by intention to treat. This trial is registered with ClinicalTrials.gov, number NCT01311687, and with EudraCT, number 2010-019820-30. The accrual for the study has been completed and the analyses are presented. 302 patients were randomly assigned to receive pomalidomide plus low-dose dexamethasone and 153 high-dose dexamethasone. After a median follow-up of 10·0 months (IQR 7·2-13·2), median PFS with pomalidomide plus low-dose dexamethasone was 4·0 months (95% CI 3·6-4·7) versus 1·9 months (1·9-2·2) with high-dose dexamethasone (hazard ratio 0·48 [95% CI 0·39-0·60]; p<0·0001). The most common grade 3-4 haematological adverse events in the pomalidomide plus low-dose dexamethasone and high-dose dexamethasone groups were neutropenia (143 [48%] of 300 vs 24 [16%] of 150, respectively), anaemia (99 [33%] vs 55 [37%], respectively), and thrombocytopenia (67 [22%] vs 39 [26%], respectively). Grade 3-4 non-haematological adverse events in the pomalidomide plus low-dose dexamethasone and high-dose dexamethasone groups included pneumonia (38 [13%] vs 12 [8%], respectively), bone pain (21 [7%] vs seven [5%], respectively), and fatigue (16 [5%] vs nine [6%], respectively). There were 11 (4%) treatment-related adverse events leading to death in the pomalidomide plus low-dose dexamethasone group and seven (5%) in the high-dose dexamethasone group. Pomalidomide plus low-dose dexamethasone, an oral regimen, could be considered a new treatment option in patients with refractory or relapsed and refractory multiple myeloma. Celgene Corporation.
    The Lancet Oncology 09/2013; · 25.12 Impact Factor
  • Meletios A Dimopoulos, Efstathios Kastritis, Evangelos Terpos
    Oncology (Williston Park, N.Y.) 09/2013; 27(9):930-2. · 3.19 Impact Factor
  • Journal of Clinical Oncology 07/2013; 31(21):2750-1. · 18.04 Impact Factor
  • Meletios A Dimopoulos, Evangelos Terpos, Ruben Niesvizky
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    ABSTRACT: Lenalidomide is a distinct second-generation immunomodulatory compound with multiple anticancer and immunomodulatory effects against haematological malignancies, in particular multiple myeloma (MM). Dexamethasone synergistically enhances the anticancer effects of lenalidomide, and the combination of lenalidomide and dexamethasone (Len/Dex) is approved for the treatment of patients with relapsed and/or refractory MM. Results from pivotal phase III trials in this setting have demonstrated that Len/Dex extends overall survival compared with dexamethasone alone. Optimal clinical benefits are seen when Len/Dex is initiated at first relapse and continued, beyond best treatment response, until disease progression. Lenalidomide based regimens are also effective as induction therapy in patients with newly diagnosed MM. Importantly, lenalidomide has a predictable and manageable tolerability profile, with minimal neurotoxicity, allowing long-term administration. As the paradigm of myeloma disease continues to change, future studies will determine the efficacy of lenalidomide in novel combinations with potentially complimentary agents.
    Critical reviews in oncology/hematology 06/2013; · 5.27 Impact Factor
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    ABSTRACT: Background:Accurate prediction of outcome for metastatic renal cell carcinoma (mRCC) patients receiving targeted therapy is essential. Most of the available models have been developed in patients treated with cytokines, while most of them are fairly complex, including at least five factors. We developed and externally validated a simple model for overall survival (OS) in mRCC. We also studied the recently validated International Database Consortium (IDC) model in our data sets.Methods:The development cohort included 170 mRCC patients treated with sunitinib. The final prognostic model was selected by uni- and multivariate Cox regression analyses. Risk groups were defined by the number of risk factors and by the 25th and 75th percentiles of the model's prognostic index distribution. The model was validated using an independent data set of 266 mRCC patients (validation cohort) treated with the same agent.Results:Eastern Co-operative Oncology Group (ECOG) performance status (PS), time from diagnosis of RCC and number of metastatic sites were included in the final model. Median OS of patients with 1, 2 and 3 risk factors were: 24.7, 12.8 and 5.9 months, respectively, whereas median OS was not reached for patients with 0 risk factors. Concordance (C) index for internal validation was 0.712, whereas C-index for external validation was 0.634, due to differences in survival especially in poor-risk populations between the two cohorts. Predictive performance of the model was improved after recalibration. Application of the mRCC International Database Consortium (IDC) model resulted in a C-index of 0.574 in the development and 0.576 in the validation cohorts (lower than those recently reported for this model). Predictive ability was also improved after recalibration in this analysis. Risk stratification according to IDC model showed more similar outcomes across the development and validation cohorts compared with our model.Conclusion:Our model provides a simple prognostic tool in mRCC patients treated with a targeted agent. It had similar performance with the IDC model, which, however, produced more consistent survival results across the development and validation cohorts. The predictive ability of both models was lower than that suggested by internal validation (our model) or recent published data (IDC model), due to differences between observed and predicted survival among intermediate and poor-risk patients. Our results highlight the importance of external validation and the need for further refinement of existing prognostic models.British Journal of Cancer advance online publication 27 June 2013; doi:10.1038/bjc.2013.341 www.bjcancer.com.
    British Journal of Cancer 06/2013; · 5.08 Impact Factor
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    ABSTRACT: Background: Lenalidomide has significant antimyeloma activity but it is associated with a significant risk of venous thromboembolism(VTE). In this study we assessed clinical and genetic risk factors that may predispose for VTE in myeloma patients who were treated with lenalidomide-based regimens. Methods: we analyzed common clinical and selected genetic factors in 200 consecutive, unselected myeloma patients who were treated with lenalidomide-based regimens in a single institution. Results: Twelve patients (6%) developed a VTE (9 deep venous thrombosis and 3 pulmonary embolism). All VTEs occurred in patients who were receiving aspirin prophylaxis; no patient who received LMWH or acenocoumarol had a VTE. The frequency of VTEs was 9.4% in previously untreated and 4.5% in previously treated patients. VTEs were more frequent in patients >65 years (8.1% vs. 1.6%) especially among patients receiving aspirin as prophylaxis (10.4% vs. 1.8% for patients ≤65 years). In patients who received prophylaxis with low dose aspirin a single-nucleotide polymorphism in NFκB1 (rs3774968) gene was associated with increased risk of VTE (OR 3.76, 95%CI 1-16, p=0.051). None of the patients who developed VTEs had common genetic variations that are associated with increased risk of VTEs in the general population, such as FVLeiden and FIIG20210A. Conclusions: our data indicated that LMWH or vitamin K antagonists (with a target INR 2-3) effectively reduce the risk of VTEs. In patients who received prophylaxis with aspirin genetic variants of genes that are involved directly or indirectly in inflammatory response may be associated with increased risk of VTE.
    American Journal of Hematology 06/2013; · 4.00 Impact Factor
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    ABSTRACT: The ubiquitin-proteasome system is central to the regulation of cellular proteostasis. Nevertheless, the impact of in vivo proteasome dysfunction on the proteostasis networks and the aging processes remains poorly understood. We found that RNAi-mediated knockdown of 20S proteasome subunits in Drosophila melanogaster resulted in larval lethality. We therefore studied the molecular effects of proteasome dysfunction in adult flies by developing a model of dose-dependent pharmacological proteasome inhibition. Impaired proteasome function promoted several "old-age" phenotypes and markedly reduced flies' lifespan. In young somatic tissues and in gonads of all ages, loss of proteasome activity induced higher expression levels and assembly rates of proteasome subunits. Proteasome dysfunction was signaled to the proteostasis network by reactive oxygen species that originated from malfunctioning mitochondria and triggered an Nrf2-dependent upregulation of the proteasome subunits. RNAi-mediated Nrf2 knockdown reduced proteasome activities, flies resistance to stress, as well as longevity. Conversely, inducible activation of Nrf2 in transgenic flies, upregulated basal proteasome expression and activity independently of age, and conferred resistance to proteotoxic stress. Interestingly, prolonged Nrf2 over-expression reduced longevity, indicating that excessive activation of the proteostasis pathways can be detrimental. Our in vivo studies add new knowledge on the proteotoxic stress-related regulation of the proteostasis networks in higher metazoans. Proteasome dysfunction triggers the activation of an Nrf2-dependent tissue- and age-specific regulatory circuit aiming to adjust the cellular proteasome activity according to temporal and/or spatial proteolytic demands. Prolonged deregulation of this proteostasis circuit accelerates aging. This article is protected by copyright. All rights reserved.
    Aging cell 06/2013; · 7.55 Impact Factor
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    ABSTRACT: In this phase 2 study, the first prospective evaluation of bortezomib-dexamethasone as second-line therapy for relapsed/refractory multiple myeloma, 163 patients were enrolled to receive four cycles of bortezomib-dexamethasone. Patients were investigator-assessed for response at cycle 5 day 1, then treated as follows: responding patients received another four cycles of bortezomib-dexamethasone, while patients with stable disease were subsequently randomized to sequential treatment with a further four cycles of bortezomib-dexamethasone alone or with added cyclophosphamide or lenalidomide. The primary endpoint was response to sequential therapy; however this could not be evaluated as investigator-assessed response rates to bortezomib-dexamethasone after four cycles were high, and an insufficient number of patients were randomized to sequential treatment per protocol. Among all 163 patients, validated best confirmed response rate was 66%, including 37% complete/very good partial responses; median response duration was 9.7 months. After median follow-up of 16.9 months, median time to progression and progression-free survival were 9.5 and 8.6 months, respectively; estimated 1-year overall survival was 81%. Median glomerular filtration rate improved from baseline during treatment. Among 58 patients with baseline glomerular filtration rate <50 mL/min, 24 had renal responses. Grade 3/4 adverse events included thrombocytopenia (17%), anemia (10%), constipation (6%), peripheral sensory neuropathy (5%), and polyneuropathy (5%). Overall, 57% of neuropathy events improved/resolved; median time to improvement was 2.1 months. These findings suggest bortezomib-dexamethasone represents an active, feasible second-line treatment option for patients with relapsed/refractory myeloma. This trial is registered with ClinicalTrials.gov (NCT00908232), and EudraCT (2007-001462-33).
    Haematologica 05/2013; · 5.94 Impact Factor
  • Efstathios Kastritis, Evangelos Terpos, Meletios A Dimopoulos
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    ABSTRACT: Introduction: Renal impairment (RI) is a common complication of symptomatic myeloma; 20 - 40% of newly diagnosed patients present with moderate or severe RI and 10% of them may require dialysis. Immediate initiation of specific antimyeloma therapy is crucial in order to improve RI. Areas covered: There has been a significant improvement in the outcome of patients with RI over the past 15 years. The authors review current data on the role of antimyeloma therapy on the improvement or resolution of RI and the importance of novel regimens, especially those based on bortezomib. IMiDs-based regimens, conventional chemotherapy and high-dose therapy is also reviewed. The role of extrarenal free light chain removal, by means of plasma exchange or extended hemodialysis with the use of high cutoff dialysis membranes, is also discussed. Expert opinion: Bortezomib/dexamethasone-based regimens are the preferred regimens for most patients with multiple myeloma (MM) who present with RI, especially for newly diagnosed patients; however, other novel agents (thalidomide, lenalidomide) in combination with dexamethasone may also improve RI in several patients. Further investigation is needed for the clarification of the role of plasma exchange or extended high cutoff dialysis. Carfilzomib, which was recently approved, may also be a treatment choice for selected patients with relapsed MM and RI.
    Expert Opinion on Pharmacotherapy 05/2013; · 2.86 Impact Factor
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    ABSTRACT: PURPOSEThe aim of the International Myeloma Working Group was to develop practice recommendations for the management of multiple myeloma (MM) -related bone disease.MethodologyAn interdisciplinary panel of clinical experts on MM and myeloma bone disease developed recommendations based on published data through August 2012. Expert consensus was used to propose additional recommendations in situations where there were insufficient published data. Levels of evidence and grades of recommendations were assigned and approved by panel members.RecommendationsBisphosphonates (BPs) should be considered in all patients with MM receiving first-line antimyeloma therapy, regardless of presence of osteolytic bone lesions on conventional radiography. However, it is unknown if BPs offer any advantage in patients with no bone disease assessed by magnetic resonance imaging or positron emission tomography/computed tomography. Intravenous (IV) zoledronic acid (ZOL) or pamidronate (PAM) is recommended for preventing skeletal-related events in patients with MM. ZOL is preferred over oral clodronate in newly diagnosed patients with MM because of its potential antimyeloma effects and survival benefits. BPs should be administered every 3 to 4 weeks IV during initial therapy. ZOL or PAM should be continued in patients with active disease and should be resumed after disease relapse, if discontinued in patients achieving complete or very good partial response. BPs are well tolerated, but preventive strategies must be instituted to avoid renal toxicity or osteonecrosis of the jaw. Kyphoplasty should be considered for symptomatic vertebral compression fractures. Low-dose radiation therapy can be used for palliation of uncontrolled pain, impending pathologic fracture, or spinal cord compression. Orthopedic consultation should be sought for long-bone fractures, spinal cord compression, and vertebral column instability.
    Journal of Clinical Oncology 05/2013; · 18.04 Impact Factor
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    ABSTRACT: ABSTRACT Clinical outcomes for patients with multiple myeloma (MM) have improved substantially since the introduction of novel agents, including the proteasome inhibitor bortezomib and the immunomodulatory drugs thalidomide and lenalidomide. However, most patients with MM eventually relapse and prognosis remains poor among patients with relapsed and/or refractory disease. Combination therapy using agents with different mechanisms of action is emerging as an attractive treatment approach in oncology to increase efficacy and/or overcome resistance to standard treatment regimens. This review discusses unmet needs in the treatment of MM and the development of histone deacetylase inhibitors as a treatment modality for MM.
    Leukemia & lymphoma 04/2013; · 2.40 Impact Factor
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    ABSTRACT: Medullary thyroid carcinoma (MTC) is a rare tumour which frequently occurs in the context of the multiple endocrine neoplasia syndromes, where it coexists with other usually benign tumours. The clinical picture varies and distant metastases are frequently present at diagnosis. Calcitonin levels are elevated in the presence of metastatic disease. Two MTC cases are presented, which had elevated postoperative calcitonin levels. Imaging revealed lung lesions which were originally attributed to metastatic disease from the MTC. However, at follow-up, these cases presented unusual features. The rapid increase in the lung lesions and the development of hypercalcaemia in the first patient suggested a second unrelated tumour. Biopsy of the lung lesion was compatible with lung adenocarcinoma. In the second patient, the appearance of a liver mass, although calcitonin levels remained stable, led to biopsy of the lesion: this was negative for calcitonin and compatible with metastatic lung adenocarcinoma. These MTC cases show that further malignancies may coexist with MTC and may obscure the clinical picture and influence the therapeutic decisions, especially in the case of metastatic disease. Features such as unusual imaging characteristics and the development of hypercalcemia, never encountered in MTC outside the MEN2 syndromes, as well as 'disproportionately' low calcitonin levels, incompatible with extensive metastatic disease, were the factors that led to further work-up. Both the cases subsequently proved to carry an unsuspected second malignancy. It is crucial to discriminate the metastatic lesion attributed to MTC from another coexisting primary malignancy, because different therapeutic strategies are needed for each setting.
    Endocrine 04/2013; · 1.42 Impact Factor
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    ABSTRACT: Histone deacetylases (HDACs) mediate protein acetylation states, which in turn regulate normal cellular processes often dysregulated in cancer. These observations led to the development of HDAC inhibitors that target tumors through multiple effects on protein acetylation. Clinical evidence demonstrates that treatment with HDAC inhibitors (such as vorinostat, panobinostat, and romidepsin) in combination with other antimyeloma agents (such as proteasome inhibitors and immunomodulatory drugs) has promising antitumor activity in relapsed/refractory multiple myeloma patients. This mini-review highlights the role of protein acetylation in the development of cancers and the rationale for the use of HDAC inhibitors in this patient population.
    Leukemia research 04/2013; · 2.36 Impact Factor
  • Meletios A Dimopoulos, Evangelos Terpos, Efstathios Kastritis
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    ABSTRACT: Proteasome inhibitors effectively kill tumor cells in myeloma and other plasma cell-related diseases. Preclinical data indicated that lymphoplasmatic cells are also vulnerable to proteasome inhibition and proteasome-targeting therapies have proved their clinical activity in Waldenström's macroglobulinemia (WM). Bortezomib is the first in class proteasome inhibitor (PI), and has been used in several clinical trials either alone or in combination with rituximab. Bortezomib treatment alone might induce major responses in 25%-60% of patients with WM but in combination with rituximab major responses might be as high as 50%-83%. Bortezomib might reduce immunoglobulin M levels rapidly and is not myelotoxic. However, peripheral neuropathy remains a major toxicity of bortezomib therapy; alternative schedules and dosing or route of administration (subcutaneous) might reduce neurotoxicity. Second generation PIs, such as carfilzomib, are also promising but further investigation is needed.
    Clinical lymphoma, myeloma & leukemia 04/2013;
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    ABSTRACT: BACKGROUND: The HER2 gene has been established as a valid biological marker for the treatment of breast cancer patients with trastuzumab and probably other agents, such as paclitaxel and anthracyclines. The TOP2A gene has been associated with response to anthracyclines. Limited information exists on the relationship of HER2/TOP2A gene status in the presence of centromere 17 (CEP17) gain with outcome of patients treated with anthracycline-containing adjuvant chemotherapy. METHODS: Formalin-fixed paraffin-embedded tumor tissue samples from 1031 patients with high-risk operable breast cancer, enrolled in two consecutive phase III trials, were assessed in a central laboratory by fluorescence in situ hybridization for HER2/TOP2A gene amplification and CEP17 gain (CEP17 probe). Amplification of HER2 and TOP2A were defined as a gene/CEP17 ratio of >=2.2 and >=2.0, respectively, or gene copy number higher than 6. Additionally, HER2, TopoIIa, ER/PgR and Ki67 protein expression was assessed by immunohistochemistry (IHC) and patients were classified according to their IHC phenotype. Treatment consisted of epirubicin-based adjuvant chemotherapy followed by hormonal therapy and radiation, as indicated. RESULTS: HER2 amplification was found in 23.7% of the patients and TOP2A amplification in 10.1%. In total, 41.8% of HER2-amplified tumors demonstrated TOP2A co-amplification. The median (range) of HER2, TOP2A and CEP17 gain was 2.55 (0.70-45.15), 2.20 (0.70-26.15) and 2.00 (0.70-26.55), respectively. Forty percent of the tumors had CEP17 gain (51% of those with HER2 amplification). Adjusting for treatment groups in the Cox model, HER2 amplification, TOP2A amplification, CEP17 gain and HER2/TOP2A co-amplification were not associated with time to relapse or time to death. CONCLUSION: HER2 amplification, TOP2A amplification, CEP17 gain and HER2/TOP2A co-amplification were not associated with outcome in high-risk breast cancer patients treated with anthracycline-based adjuvant chemotherapy.Trial registration: Australian New Zealand Clinical Trials Registry (ANZCTR) ACTRN12611000506998 and ACTRN12609001036202.
    BMC Cancer 03/2013; 13(1):163. · 3.33 Impact Factor
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    ABSTRACT: Key points Deep clonal responses improve outcomes and can change the natural history of advanced (cardiac stage III) AL amyloidosis.NT-proBNP >8500 ng/L and systolic blood pressure <100 mm of Hg identify a very poor risk subgroup of stage III AL amyloidosis.
    Blood 03/2013; · 9.06 Impact Factor
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    ABSTRACT: Germline mutations in the BRCA1 and BRCA2 genes contribute to approximately 18% of hereditary ovarian cancers conferring an estimated lifetime risk from 15% to 50%. A variable incidence of mutations has been reported for these genes in ovarian cancer cases from different populations. In Greece, six mutations in BRCA1 account for 63% of all mutations detected in both BRCA1 and BRCA2 genes. This study aimed to determine the prevalence of BRCA1 mutations in a Greek cohort of 106 familial ovarian cancer patients that had strong family history or metachronous breast cancer and 592 sporadic ovarian cancer cases. All 698 patients were screened for the six recurrent Greek mutations (including founder mutations c.5266dupC, p.G1738R and the three large deletions of exon 20, exons 23–24 and exon 24). In familial cases, the BRCA1 gene was consequently screened for exons 5, 11, 12, 20, 21, 22, 23, 24. A deleterious BRCA1 mutation was found in 43/106 (40.6%) of familial cancer cases and in 27/592 (4.6%) of sporadic cases. The variant of unknown clinical significance p.V1833M was identified in 9/698 patients (1.3%). The majority of BRCA1 carriers (71.2%) presented a high-grade serous phenotype. Identifying a mutation in the BRCA1 gene among breast and/or ovarian cancer families is important, as it enables carriers to take preventive measures. All ovarian cancer patients with a serous phenotype should be considered for genetic testing. Further studies are warranted to determine the prevalence of mutations in the rest of the BRCA1 gene, in the BRCA2 gene, and other novel predisposing genes for breast and ovarian cancer.
    PLoS ONE 03/2013; · 3.73 Impact Factor
  • Evangelos Terpos, G David Roodman, Meletios A Dimopoulos
    Blood 02/2013; · 9.06 Impact Factor
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    ABSTRACT: Multiple myeloma (MM) typically follows a relapsing course with many patients requiring multiple therapies. This single-arm phase 2 study prospectively evaluated the efficacy and safety of bortezomib retreatment in MM patients who had relapsed after achieving at least a partial response (≥PR) to prior bortezomib-based therapy. Patients aged ≥18 years, with measurable, secretory MM, who relapsed ≥6 months after prior bortezomib treatment were eligible. Patients received up to eight cycles of bortezomib (±dexamethasone). The primary endpoint was best confirmed response at retreatment; secondary endpoints included duration of response (DOR), time to progression (TTP), and safety. Adverse events (AEs) were graded by National Cancer Institute Common Terminology Criteria for Adverse Events version 3.0. A total of 130 patients (median of two prior lines of therapy) were enrolled and received retreatment. At retreatment, 28% and 72% of patients received bortezomib and bortezomib-dexamethasone, respectively. Overall response rate was 40%. In patients who achieved ≥PR, median DOR and TTP were 6·5 and 8·4 months, respectively. Thrombocytopenia was the most common grade ≥3 AE (35%). Forty percent of patients experienced neuropathy events, which improved and resolved in a median of 1·5 and 8·9 months, respectively. In conclusion, bortezomib retreatment was effective and tolerable in relapsed MM patients, with no evidence of cumulative toxicities.
    British Journal of Haematology 01/2013; · 4.94 Impact Factor
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    ABSTRACT: Multiple myeloma remains an incurable disease despite the introduction of the immunomodulatory drugs (IMiDs) thalidomide and lenalidomide and the proteasome inhibitor bortezomib that have improved the outcome of patients with both newly diagnosed and relapsed/refractory disease. However, patients who relapse after treatment with these agents or are refractory to them represent an unmet need and highlight the necessity for the development of novel anti-myeloma agents. Pomalidomide is an IMiD, structurally related to thalidomide, with enhanced antiangiogenic, antineoplastic, and anti-inflammatory properties and exhibiting potent anti-myeloma activity in vitro and in vivo. Pomalidomide has shown remarkable activity in patients who were refractory to both bortezomib and lenalidomide in Phase II and III studies. This paper reviews the chemistry and mechanisms of action of pomalidomide as well as all the available data from clinical trials on pomalidomide use in patients with refractory/relapsed multiple myeloma.
    OncoTargets and Therapy 01/2013; 6:531-538. · 2.07 Impact Factor

Publication Stats

11k Citations
3,269.66 Total Impact Points


  • 1996–2014
      Athínai, Attica, Greece
  • 2013
    • Clínica Universidad de Navarra
      Madrid, Madrid, Spain
    • Sapienza University of Rome
      • Department of Cellular Biotechnology and Hematology BCE
      Roma, Latium, Italy
  • 2003–2013
    • Dana-Farber Cancer Institute
      • Department of Medical Oncology
      Boston, MA, United States
    • Hippokration General Hospital, Athens
      Athínai, Attica, Greece
  • 2001–2013
    • Θεαγένειο Αντικαρκινικό Νοσοκομείο
      Saloníki, Central Macedonia, Greece
  • 2000–2013
    • University Hospital of Ioannina
      Yannina, Epirus, Greece
      Athínai, Attica, Greece
  • 1999–2013
    • National and Kapodistrian University of Athens
      • • Division of Clinical Therapeutics
      • • Faculty of Medicine
      Athens, Attiki, Greece
  • 1996–2013
    • Athens State University
      Athens, Alabama, United States
  • 2012
    • Papageorgiou Hospital
      Saloníki, Central Macedonia, Greece
    • Roswell Park Cancer Institute
      Buffalo, New York, United States
  • 2011–2012
    • Wiener Krankenanstaltenverbund
      Wien, Vienna, Austria
    • Università degli Studi di Torino
      Torino, Piedmont, Italy
    • University Medical Center Utrecht
      • Department of Hematology
      Utrecht, Provincie Utrecht, Netherlands
  • 2000–2012
    • Evangelismos Hospital
      Athínai, Attica, Greece
  • 2010–2011
    • Universitair Ziekenhuis Leuven
      Louvain, Flanders, Belgium
    • Multiple Myeloma - Institute for Myeloma & Bone Cancer Research
      California City, California, United States
  • 1990–2011
    • General Hospital of Komotini "Sismanoglio"
      Komotina, East Macedonia and Thrace, Greece
  • 1989–2011
    • Laiko Hospital
      Athínai, Attica, Greece
  • 2008–2010
    • Hospital Universitario de Salamanca
      Helmantica, Castille and León, Spain
    • Κωνσταντοπούλειο νοσοκομείο Νέας Ιωνίας (Η Αγία Όλγα)
      Athínai, Attica, Greece
    • University of Maryland, Baltimore
      • Greenebaum Cancer Center
      Baltimore, MD, United States
  • 2009
    • Centre Hospitalier de Lens
      Lens, Nord-Pas-de-Calais, France
    • University of Barcelona
      Barcino, Catalonia, Spain
    • University of Pennsylvania
      • "Abramson" Cancer Center
      Philadelphia, PA, United States
    • Άγιος Σάββας Αντικαρκινικό Νοσοκομείο
      Athínai, Attica, Greece
  • 2006–2009
    • Yale-New Haven Hospital
      • Department of Pathology
      New Haven, Connecticut, United States
    • Imperial College London
      • Faculty of Medicine
      London, ENG, United Kingdom
    • Karolinska University Hospital
      Tukholma, Stockholm, Sweden
    • Ευρωκλινική
      Athínai, Attica, Greece
  • 2005–2009
    • Attikon University Hospital
      • Department of Internal Medicine IV
      Athens, Attiki, Greece
    • King's College London
      • School of Medicine
      London, ENG, United Kingdom
    • BMI The Alexandra Hospital
      Cheadle Hulme, England, United Kingdom
  • 2002–2008
    • Hygeia Hospital
      Athínai, Attica, Greece
  • 2000–2008
    • Hellenic Cooperative Oncology Group
      Athínai, Attica, Greece
  • 1991–2008
    • University of Texas MD Anderson Cancer Center
      • Department of Lymphoma and Myeloma
      Houston, TX, United States
  • 2007
    • Yale University
      • School of Medicine
      New Haven, CT, United States
  • 2003–2006
    • National Hellenic Research Foundation
      Athínai, Attica, Greece
  • 2001–2006
    • Aristotle University of Thessaloniki
      • • Faculty of Medicine
      • • Laboratory of Ecology
      Thessaloníki, Kentriki Makedonia, Greece
  • 2004
    • Metropolitan Hospital
      Athínai, Attica, Greece
  • 2001–2002
    • University of Ioannina
      Yannina, Epirus, Greece
  • 1999–2000
    • University of Crete
      • Department of Medical Oncology
      Réthymnon, Kriti, Greece
  • 1994
    • Royal Melbourne Hospital
      Melbourne, Victoria, Australia