Refine
Has Fulltext
- yes (95)
Is part of the Bibliography
- yes (95)
Year of publication
Document Type
- Journal article (95)
Language
- English (95) (remove)
Keywords
- multiple myeloma (23)
- Aspergillus (6)
- cytokines (5)
- Aspergillus fumigatus (4)
- T cells (4)
- allogeneic stem cell transplantation (4)
- fungal infection (4)
- immunotherapy (4)
- refractory (4)
- relapse (4)
- CXCR4 (3)
- NK cells (3)
- cancer (3)
- invasive aspergillosis (3)
- medicine (3)
- survival (3)
- 18F-FDG PET/CT (2)
- B cells (2)
- Bone marrow transplantation (2)
- CCL4 (2)
- COVID-19 (2)
- GVHD (2)
- Multiple myeloma (2)
- T cell (2)
- adaptive immunity (2)
- amplicon sequencing (2)
- aspergillus fumigatus (2)
- autologous transplantation (2)
- biomarker (2)
- cell staining (2)
- dendritic cells (2)
- extramedullary disease (2)
- galactomannan (2)
- immunoassay (2)
- inflammation (2)
- lenalidomide (2)
- leukemia (2)
- pomalidomide (2)
- quality of life (2)
- regulatory T cells (2)
- stem-cell transplantation (2)
- theranostics (2)
- transplantation (2)
- 11C-Methionine PET/CT (1)
- 68Ga-Pentixafor PET/CT (1)
- ABL gene (1)
- AKT-signaling (1)
- AML (1)
- Active disease (1)
- Acute lymphoblastic leukemia (1)
- Acute myeloid leukemia (1)
- Acute myeloid leukemia (AML) (1)
- Akt (1)
- Allogeneic stem cell transplantation (1)
- Allogeneic transplantation (1)
- Alpha therapy (1)
- Ascaris lumbricoides (1)
- Autoimmune diseases (1)
- B cell (1)
- B cell receptors (1)
- BCOR (1)
- BCORL1 (1)
- BRAF mutation (1)
- Bacteria (1)
- Bioluminescence (1)
- Bioluminescence imaging (1)
- Blood (1)
- Bone marrow cells (1)
- Bone marrow transplantantation (1)
- Bone-marrow-transplantation (1)
- C-X-C motif chemokine receptor 4 (1)
- CAPA (1)
- CAR T cell (1)
- CAR T cells (1)
- CAR-T-cell (1)
- CCL3 (1)
- CCL5 (1)
- CD11b+ myeloid cells (1)
- CD319 (1)
- CD38 (1)
- CD4(+) (1)
- CMV (1)
- CS1 (1)
- CXCR4/SDF-1 (1)
- Cancer genetics (1)
- Cancer risk factors (1)
- Cancer treatment (1)
- Candida albicans (1)
- Capicua transcriptional repressor (1)
- Chronic lymphoblastic leukemia (1)
- Chronic myeloid leukaemia (1)
- Chronic myeloid leukemia (1)
- Conditioning regimen (1)
- Dara-KDT-P(A)CE (1)
- Dendritische Zelle (1)
- Drug resistance (1)
- European experts (1)
- European group (1)
- Expression (1)
- Extramedullary disease (1)
- FDG (1)
- FDG PET/CT (1)
- Factor receptor (1)
- Fludarabine (1)
- Fludarabine-treosulfan (FT) (1)
- Fungal (1)
- Fusarium (1)
- GVL (1)
- Genome-wide association studies (1)
- Graft versus Tumor (1)
- Graft-versus-host disease (1)
- Graft-versus-leukemia (1)
- Gruppo-italiano (1)
- GvHD (1)
- HBV (1)
- HCV (1)
- HD (1)
- HIV (1)
- HLA antigens (1)
- HLA-E matching (1)
- HSTC outcome (1)
- Haematology (1)
- Hematopoietic stem cell transplantation (1)
- Hepatitis B virus (1)
- Hepatitis B virus reactivation (1)
- Herpes simplex virus (1)
- Hsp90 (1)
- Human immunodefiency virus (1)
- Immune receptor signaling (1)
- Infections (1)
- Infectious Diseases (1)
- Influenzae type B (1)
- Interleukin-2 (1)
- Invasive Aspergillosis (1)
- KRAS (1)
- Killer cell immunoglobulin-like receptors (1)
- LATE DEATHS (1)
- LPS (1)
- Late mortality (1)
- Low-dose acyclovir (1)
- Lymphomas (1)
- MAPKAPK2 (1)
- MEK/ERK-signaling (1)
- MIP-1β (1)
- MOR202 (1)
- MTB (1)
- MTX (1)
- MUST-Score (1)
- Medizin (1)
- Midollo-Osseo (1)
- Minor histocompatibility antigen mismatch transplantation (1)
- Molecularly targeted therapy (1)
- Multivariate analysis (1)
- Myeloma (1)
- NF-κB/NFAT reporter cells (1)
- NFkB-relatedgenes (1)
- NK-cells (1)
- PET (1)
- PET/CT (1)
- Pneumocystis-carinii-pneumonia (1)
- Pom‐PAD‐Dara (1)
- Prognostic scoring system (1)
- R-CHOP (1)
- RNA extraction (1)
- ROR1 (1)
- Regulatory-cells (1)
- Respiratory syncytial virus (1)
- Rheumatoid arthritis (1)
- Rhizopus (1)
- Risk factors (1)
- Ruxolitinib (1)
- SLAMF7 (1)
- Sibling donor (MSD) (1)
- Societe Francaise (1)
- Spleen (1)
- Stem cell transplantation (1)
- Suppression (1)
- Survival (1)
- T-cells (1)
- TNF (1)
- TNFR2 (1)
- TNFSF14 (1)
- TNFSF4 (1)
- TSLP (1)
- Thiotepa-busulfan-fludarabine (TBF) (1)
- Translational research (1)
- Tumor-necrosis-factor (1)
- Unrelated donor (UD) (1)
- Varicella-Zoster-Virus (1)
- Viral (1)
- [177Lu]PentixaTher (1)
- [68Ga]PentixaFor (1)
- [90Y]PentixaTher (1)
- \(^{11}\)C-methionine (1)
- actin (1)
- activation (1)
- acute Graft versus Host Disease (1)
- acute graft-versus-host disease (1)
- acute kidney injury (1)
- acute leukemia (AL) (1)
- acute lymphoblastic leukaemia (1)
- acute lymphoblastic leukemia (1)
- acute myeloid leukaemia (1)
- acute myeloid leukemia (1)
- acute myeloid-leukemia (1)
- adoptive cell therapy (1)
- adoptive transfer (1)
- adrenocortical carcinoma (1)
- agonist (1)
- alloSCT patients (1)
- allogeneic hematopoietic stem cell transplantation (1)
- alloreactive T cells (1)
- alveolar epithelium (1)
- amsacrine (1)
- antigen loss (1)
- antigens (1)
- apoptosis (1)
- artificial intelligence (1)
- aspergillosis (1)
- bacterial infection (1)
- beta-D-glucan (1)
- biophosphonate (1)
- bispecific antobodies (1)
- blinatumomab (1)
- blinatumoman (1)
- bone disease (1)
- bone marrow transplantation (1)
- bone remineralization (1)
- bone-disease (1)
- bone-mineral density (1)
- bortezomib (1)
- bortezomib plus dxamethasone (1)
- breakpoint (1)
- bridge-to-transplant (1)
- bronchoalveolar lavage fluid (1)
- cancer care (1)
- cancer immunotherapy (1)
- cancer treatment (1)
- carfilzomib (1)
- caspase-3 (1)
- cell binding (1)
- cells (1)
- cereblon expression (1)
- chemokine receptor (1)
- chemokines (1)
- chimeric antigen receptor (1)
- chronic myelogenous leukemia (1)
- chronic myeloid leukemia (1)
- chronic phase (1)
- clinical trial (1)
- combination therapy (1)
- complement system (1)
- computed tomography (1)
- consensus statement (1)
- corticosteroids (1)
- corticosteroids and cyclophosphamide (1)
- cyclophosphamide (FLAMSA) (1)
- cytogenetic response (1)
- cytotoxicity (1)
- daratumumab (1)
- daratumumab monotherapy (1)
- denritic cells (1)
- depression (1)
- diagnostics (1)
- different imatinib dose regimens (1)
- disorders (1)
- donor-cell leukemia (1)
- downstream (1)
- early applied higher imatinib dosages (1)
- elderly patients (1)
- elotuzumab (1)
- enal impairment (1)
- endoradiotherapy (1)
- enzyme-linked immunoassays (1)
- erythropoiesis-stimulating agents (1)
- fungal host response (1)
- fungal molecular diagnostics (1)
- fungi (1)
- galectin-2 (1)
- gene expression (1)
- gene expression data (1)
- gene regulation (1)
- gene regulation in immune cells (1)
- gene therapy (1)
- genetic polymorphisms (1)
- genetic susceptibility (1)
- granulocytes (1)
- group consensus statement (1)
- haploidentical γδ T lymphocytes (1)
- health care (1)
- hematologic malignancies (1)
- hematological malignancies (1)
- hematology (1)
- hematopoietic (1)
- hematopoietic cell transplantation (1)
- hematopoietic stem cell transplantation (1)
- hematopoietic stem cell transplantation (HSCT) (1)
- host defense (1)
- host response (1)
- human biomarker (1)
- human cytomegalovirus (HCMV) (1)
- human leukocyte antigen-E (HLA-E) (1)
- humans (1)
- hybrid messenger RNA (1)
- hypersensitivity (1)
- immune cell recruitment (1)
- immune cells (1)
- immune control (1)
- immune impairment (1)
- immune receptors (1)
- immune reconstitution (1)
- immune response (1)
- immunohistochemistry techniques (1)
- in vitro model (1)
- in vivo cell expansion (1)
- in vivo imaging (1)
- incidence (1)
- individual mind state (1)
- induction regimen (1)
- infectious diseases (1)
- infusion (1)
- inhibition (1)
- innate immune response (1)
- innate immunity (1)
- interaction (1)
- intermediate dose Ara-C (1)
- invasive fungal infections (1)
- invasive pulmonary aspergillosis (1)
- involvement (1)
- isoforms (1)
- kidney (1)
- library screening (1)
- life-threatening side-effects (1)
- lifestyle habits (1)
- loss-of-function (1)
- lymphoma (1)
- mAb engineering (1)
- malignancies (1)
- malignant transformation (1)
- malnutrition (1)
- management (1)
- mantle cell lymphoma (1)
- marrow plasma cells (1)
- matrix metallopeptidase-1 (1)
- mebendazole (1)
- mechanism (1)
- metastasis (1)
- microenvironment (1)
- mismatch (1)
- mold exposure (1)
- monoclonal antibody (1)
- monoclonal gammopathy (1)
- monocytes (1)
- mortality (1)
- motivational level (1)
- mouse models (1)
- mucormycosis (1)
- multiparameter flow-cytometry (1)
- multiparameter flow-cytpmetry (1)
- multiparametric flow cytometry (1)
- multiplicity of infection (1)
- murine model (1)
- mycophenolic acid (1)
- natural killer cell (1)
- natural killer cells (1)
- natural language processing (1)
- network (1)
- newly-diagnosed myeloma (1)
- no correlation (1)
- novel therapies (1)
- nutritional counseling (1)
- nutritional medical needs (1)
- nutritional risk screening (1)
- obinutuzumab (1)
- observational (1)
- older patients (1)
- oncology (1)
- oncology outpatients (1)
- ontology (1)
- outcomes research (1)
- outreach (1)
- panobinostat (1)
- participation in clinical trials (1)
- pathogen-associated molecular patterns (1)
- pathophysiology (1)
- pathway (1)
- patient access (1)
- pattern (1)
- pattern recognition receptors (1)
- pediatric (1)
- phosphatidylinositol 3-kinase/Akt (1)
- phosphorylation (1)
- plasma cells (1)
- polymerase-chain-reaktion (1)
- population-based cohort (1)
- positron emission tomography (1)
- precision medicine (1)
- precision oncology (1)
- prediction (1)
- probe-based real-time PCR (1)
- progression (1)
- public health (1)
- radiogenomics (1)
- randomized controlled trial (1)
- randomized phase-3 trial (1)
- rare SNP (1)
- real life setting (1)
- real world data (1)
- real world evidence (1)
- real-time PCR (1)
- receptor tyrosine kinases (1)
- recombinant-human-erythropoietin (1)
- relapsed (1)
- relapsed and refractory (1)
- renal failure (1)
- respiratory virus (1)
- risk stratification (1)
- salvage (1)
- serum biomarkers (1)
- serum retention (1)
- significance MGUS (1)
- sirolimus (1)
- smoldering multiple-myeloma (1)
- smoldering myeloma (1)
- stem cell transplantation (1)
- stimulation (1)
- stress (1)
- susceptibility (1)
- symptom burden (1)
- term-follow-up (1)
- thalidomide maintenance (1)
- therapy (1)
- total body irradiation/busulfan (1)
- toxicity (1)
- transcripts (1)
- transient regulatory T-cell targeting (1)
- translational research (1)
- tumor‐specific antigen (1)
- tumour immunology (1)
- undetermined significance MGUS (1)
- venetoclax (1)
- venous thromboembolic disease (1)
- viral infection (1)
- virus (1)
- virus-specific T-cell (1)
- whole-body imaging (1)
- zoledonic acid (1)
Institute
- Medizinische Klinik und Poliklinik II (93)
- Pathologisches Institut (12)
- Klinik und Poliklinik für Nuklearmedizin (8)
- Institut für Hygiene und Mikrobiologie (7)
- Institut für Virologie und Immunbiologie (6)
- Theodor-Boveri-Institut für Biowissenschaften (6)
- Kinderklinik und Poliklinik (5)
- Medizinische Klinik und Poliklinik I (5)
- Abteilung für Molekulare Innere Medizin (in der Medizinischen Klinik und Poliklinik II) (4)
- Institut für diagnostische und interventionelle Radiologie (Institut für Röntgendiagnostik) (4)
Sonstige beteiligte Institutionen
- Center for Interdisciplinary Clinical Research, Würzburg University, Würzburg, Germany (2)
- Department of Hematology and Oncology, Sana Hospital Hof, Hof, Germany (1)
- Department of Laboratory Medicine and Medicine Huddinge, Karolinska Institutet and University Hospital, Stockholm, Sweden (1)
- Department of Medicine A, University Hospital of Münster, Münster, Germany (1)
- Interdisciplinary Center for Clinical Research (IZKF), Würzburg, Germany (1)
- Mildred Scheel Early Career Center (1)
- University of Bari Medical School, Bari, Italy (1)
EU-Project number / Contract (GA) number
- 733297 (2)
- 754658 (2)
- 037602 (1)
- 19-COP-0031 (1)
- 2016 FGR 0053 (1)
- 260338 (1)
- 847507 (1)
- 853988 (1)
Multiple myeloma (MM) is a generally fatal plasma cell cancer that often shows activation of the phosphoinositide 3-kinase/Akt (PI3K/Akt) pathway. Targeted pharmacologic therapies, however, have not yet progressed beyond the clinical trial stage, and given the complexity of the PI3K/Akt signalling system (e.g. multiple protein isoforms, diverse feedback regulation mechanisms, strong variability between patients) it is mandatory to characterise its ramifications in order to better guide informed decisions about the best therapeutic approaches. Here we explore whether serum and glucocorticoid-regulated kinase 3 (SGK3), a potential downstream effector of PI3K, plays a role in oncogenic signalling in MM cells-either in concert with or independent of Akt. SGK3 was expressed in all MM cell lines and in all primary MM samples tested. Four MM cell lines representing a broad range of intrinsic Akt activation (very strong: MM. 1s, moderate: L 363 and JJN-3, absent: AMO-1) were chosen to test the effects of transient SGK3 knockdown alone and in combination with pharmacological inhibition of Akt, PI3K-p110\(\alpha\), or in the context of serum starvation. Although the electroporation protocol led to strong SGK3 depletion for at least 5 days its absence had no substantial effect on the activation status of potential downstream substrates, or on the survival, viability or proliferation of MM cells in all experimental contexts tested. We conclude that it is unlikely that SGK3 plays a significant role for oncogenic signalling in multiple myeloma.
Background: Therapy for multiple myeloma (MM) has substantially improved in the era of immunomodulatory drugs and bortezomib. However, the prognosis of patients with progressive disease despite treatment with these ‘novel agents' remains poor. Recently, pomalidomide was approved in this setting, but a median progression-free survival of <4 months still leaves room for improvement. Pomalidomide-based combination therapies are currently under investigation, but data on long-term treatment are lacking. Case Report: We present the case of a 68-year-old woman with refractory MM who received pomalidomide in combination with various drugs including anthracyclines, alkylators and proteasome inhibitors. Initially, major hematological toxicities and infectious complications including a hepatitis B virus reactivation were encountered. With careful dose adjustments and selection of combination partners, pomalidomide treatment was maintained for over 4 years and led to a sustained partial remission. In particular, the well-tolerated regimen of bortezomib, cyclophosphamide and dexamethasone together with pomalidomide was administered for >30 cycles. Conclusion: This case illustrates the value of an individualized approach to myeloma care given an increasing availability of ‘novel agents'. Tailored treatment using these drugs as a backbone is essential to achieve long-lasting responses and minimize side effects.
Background
International collaborative research is a mechanism for improving the development of disease-specific therapies and for improving health at the population level. However, limited data are available to assess the trends in research output related to orphan diseases.
Methods and Findings
We used bibliometric mapping and clustering methods to illustrate the level of fragmentation in myeloma research and the development of collaborative efforts. Publication data from Thomson Reuters Web of Science were retrieved for 2005-2009 and followed until 2013. We created a database of multiple myeloma publications, and we analysed impact and co-authorship density to identify scientific collaborations, developments, and international key players over time. The global annual publication volume for studies on multiple myeloma increased from 1,144 in 2005 to 1,628 in 2009, which represents a 43% increase. This increase is high compared to the 24% and 14% increases observed for lymphoma and leukaemia. The major proportion (> 90% of publications) was from the US and EU over the study period. The output and impact in terms of citations, identified several successful groups with a large number of intra-cluster collaborations in the US and EU. The US-based myeloma clusters clearly stand out as the most productive and highly cited, and the European Myeloma Network members exhibited a doubling of collaborative publications from 2005 to 2009, still increasing up to 2013.
Conclusion and Perspective
Multiple myeloma research output has increased substantially in the past decade. The fragmented European myeloma research activities based on national or regional groups are progressing, but they require a broad range of targeted research investments to improve multiple myeloma health care.
CXCR4 is a G-protein-coupled receptor that mediates recruitment of blood cells toward its ligand SDF-1. In cancer, high CXCR4 expression is frequently associated with tumor dissemination andpoor prognosis. We evaluated the novel CXCR4 probe [\(^{68}\)Ga]Pentixafor for invivo mapping of CXCR4 expression density in mice xenografted with human CXCR4-positive MM cell lines and patients with advanced MM by means of positron emission tomography (PET). [\(^{68}\)Ga]Pentixafor PET provided images with excellent specificity and contrast. In 10 of 14 patients with advanced MM [\(^{68}\)Ga]Pentixafor PET/CT scans revealed MM manifestations, whereas only nine of 14 standard [\(^{18}\)F]fluorodeoxyglucose PET/CT scans were rated visually positive. Assessment of blood counts and standard CD34\(^{+}\) flow cytometry did not reveal significant blood count changes associated with tracer application. Based on these highly encouraging data on clinical PET imaging of CXCR4 expression in a cohort of MM patients, we conclude that [\(^{68}\)Ga]Pentixafor PET opens a broad field for clinical investigations on CXCR4 expression and for CXCR4-directed therapeutic approaches in MM and other diseases.
Multiple myeloma (MM) is a plasma cell malignancy with a significant heritable basis. Genome-wide association studies have transformed our understanding of MM predisposition, but individual studies have had limited power to discover risk loci. Here we perform a meta-analysis of these GWAS, add a new GWAS and perform replication analyses resulting in 9,866 cases and 239,188 controls. We confirm all nine known risk loci and discover eight new loci at 6p22.3 (rs34229995, P=1.31 × 10−8), 6q21 (rs9372120, P=9.09 × 10−15), 7q36.1 (rs7781265, P=9.71 × 10−9), 8q24.21 (rs1948915, P=4.20 × 10−11), 9p21.3 (rs2811710, P=1.72 × 10−13), 10p12.1 (rs2790457, P=1.77 × 10−8), 16q23.1 (rs7193541, P=5.00 × 10−12) and 20q13.13 (rs6066835, P=1.36 × 10−13), which localize in or near to JARID2, ATG5, SMARCD3, CCAT1, CDKN2A, WAC, RFWD3 and PREX1. These findings provide additional support for a polygenic model of MM and insight into the biological basis of tumour development.
Invasive Aspergillosis (IA) is an opportunistic infection caused by Aspergillus, a ubiquitously present airborne pathogenic mold. A growing number of studies suggest a major host genetic component in disease susceptibility. Here, we evaluated whether 14 single-nucleotide polymorphisms within NFκB1, NFκB2, RelA, RelB, Rel, and IRF4 genes influence the risk of IA in a population of 834 high-risk patients (157 IA and 677 non-IA) recruited through a collaborative effort involving the aspBIOmics consortium and four European clinical institutions. No significant overall associations between selected SNPs and the risk of IA were found in this large cohort. Although a hematopoietic stem cell transplantation (HSCT)-stratified analysis revealed that carriers of the IRF4rs12203592T/T genotype had a six-fold increased risk of developing the infection when compared with those carrying the C allele (ORREC = 6.24, 95%CI 1.25–31.2, P = 0.026), the association of this variant with IA risk did not reach significance at experiment-wide significant threshold. In addition, we found an association of the IRF4AATC and IRF4GGTC haplotypes (not including the IRF4rs12203592T risk allele) with a decreased risk of IA but the magnitude of the association was similar to the one observed in the single-SNP analysis, which indicated that the haplotypic effect on IA risk was likely due to the IRF4rs12203592 SNP. Finally, no evidence of significant interactions among the genetic markers tested and the risk of IA was found. These results suggest that the SNPs on the studied genes do not have a clinically relevant impact on the risk of developing IA.
Donor CD4\(^+\)Foxp3\(^+\) regulatory T cells (T reg cells) suppress graft-versus-host disease (GvHD) after allogeneic hematopoietic stem cell transplantation (HCT allo-HCT]). Current clinical study protocols rely on the ex vivo expansion of donor T reg cells and their infusion in high numbers. In this study, we present a novel strategy for inhibiting GvHD that is based on the in vivo expansion of recipient T reg cells before allo-HCT, exploiting the crucial role of tumor necrosis factor receptor 2 (TNFR2) in T reg cell biology. Expanding radiation-resistant host T reg cells in recipient mice using a mouse TNFR2-selective agonist before allo-HCT significantly prolonged survival and reduced GvHD severity in a TNFR2-and T reg cell-dependent manner. The beneficial effects of transplanted T cells against leukemia cells and infectious pathogens remained unaffected. A corresponding human TNFR2-specific agonist expanded human T reg cells in vitro. These observations indicate the potential of our strategy to protect allo-HCT patients from acute GvHD by expanding T reg cells via selective TNFR2 activation in vivo.
Multiple myeloma (MM) is a plasma cell disorder that is characterized by a great genetic heterogeneity. Recent next generation sequencing studies revealed an accumulation of tumor-associated mutations in receptor tyrosine kinases (RTKs) which may also contribute to the activation of survival pathways in MM. To investigate the clinical role of RTK-mutations in MM, we deep-sequenced the coding DNA-sequence of EGFR, EPHA2, ERBB3, IGF1R, NTRK1 and NTRK2 which were previously found to be mutated in MM, in 75 uniformly treated MM patients of the “Deutsche Studiengruppe Multiples Myelom”. Subsequently, we correlated the detected mutations with common cytogenetic alterations and clinical parameters. We identified 11 novel non-synonymous SNVs or rare patient-specific SNPs, not listed in the SNP databases 1000 genomes and dbSNP, in 10 primary MM cases. The mutations predominantly affected the tyrosine-kinase and ligand-binding domains and no correlation with cytogenetic parameters was found. Interestingly, however, patients with RTK-mutations, specifically those with rare patient-specific SNPs, showed a significantly lower overall, event-free and progression-free survival. This indicates that RTK SNVs and rare patient-specific RTK SNPs are of prognostic relevance and suggests that MM patients with RTK-mutations could potentially profit from treatment with RTK-inhibitors.
Panobinostat is an oral pan-histone deacetylase inhibitor developed by Novartis. Panobinostat acts via epigenetic modification and inhibition of the aggresome pathway. In August 2015, the European Commission authorized panobinostat for use in combination with bortezomib and dexamethasone for the treatment of relapsed or relapsed and refractory multiple myeloma (MM) in patients who have received aeyen2 prior regimens including bortezomib and an immunomodulatory drug. In January 2016, the National Institute for Health and Care Excellence recommended panobinostat for use in the same combination and patient population. The authorization and recommendation were based on results from the pivotal phase 3 PANORAMA 1 (NCT01023308) clinical trial, which demonstrated an improvement in median progression-free survival of 7.8 months for the three-drug combination compared with placebo plus bortezomib and dexamethasone in this patient population. This review will discuss the current treatment landscape for relapsed/refractory MM, the mechanism of action of panobinostat, clinical data supporting the European authorization, concerns about safety and strategies for mitigating toxicity, and how panobinostat fits into the current MM landscape in Europe.
Infectious complications after allogeneic haematopoietic stem cell transplantation (allo-HCT) remain a clinical challenge. This is a guideline provided by the AGIHO (Infectious Diseases Working Group) of the DGHO (German Society for Hematology and Medical Oncology). A core group of experts prepared a preliminary guideline, which was discussed, reviewed, and approved by the entire working group. The guideline provides clinical recommendations for the preventive management including prophylactic treatment of viral, bacterial, parasitic, and fungal diseases. The guideline focuses on antimicrobial agents but includes recommendations on the use of vaccinations. This is the updated version of the AGHIO guideline in the field of allogeneic haematopoietic stem cell transplantation utilizing methods according to evidence-based medicine criteria.