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  • 1
    Keywords: carcinoma ; RISK ; SAMPLES ; INFECTION ; antibodies ; LYMPHOMA ; CANCERS ; EPILYMPH ; MCPYV
    Abstract: Merkel cell polyomavirus (MCPyV) has been suspected to cause chronic lymphocytic leukaemia (CLL) but previous data are inconsistent. We measured seroreactivities of nine polyomaviruses (MCPyV, BKPyV, JCPyV, LPyV, KIPyV, WUPyV, HPyV-6, HPyV-7 and TSPyV) in 359 CLL cases and 370 controls using bead-based multiplex serology technology. We additionally tested two herpesviruses (HSV-1 and CMV). Associations between disease and viral seroreactivities were assessed using logistic regression. All human viruses showed high seroprevalences (69-99 %) against structural proteins in controls but significantly lower viral seroprevalences in cases (58-94 %; OR range = 0.21-0.70, P value 〈 0.05), except for MCPyV (OR = 0.79, 95 % CI = 0.54-1.16). Lower seroreactivity levels were observed among CLL subjects, with significant differences already observed at early stages of disease, unrelated to treatment status. Seroreactivities against polyomavirus related oncoproteins were almost null. Our data suggest no association for MCPyV polyomavirus with CLL development and an unlikely association for other polyomaviruses tested.
    Type of Publication: Journal article published
    PubMed ID: 25920529
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  • 2
    Abstract: T-cell prolymphocytic leukaemia (T-PLL) is an aggressive leukaemia. The primary genetic alteration in T-PLL are the inv(14)(q11q32)/t(14;14)(q11;q32) leading to TRD/TRA-TCL1A fusion, or the t(X;14)(q28;q11) associated with TRD/TRA-MTCP1 fusion. However, additional cooperating abnormalities are necessary for emergence of the full neoplastic phenotype. Though the pattern of secondary chromosomal aberrations is remarkably conserved, targets of the changes are largely unknown. We analysed a cohort of 43 well-characterized T-PLL for hotspot mutations in the genes JAK3, STAT5B and RHOA. Additionally, we selected a subset of 23 T-PLL cases for mutational screening of 54 genes known to be recurrently mutated in T-cell and other haematological neoplasms. Activating mutations in the investigated regions of the JAK3 and STAT5B genes were detected in 30% (13/43) and 21% (8/39) of the cases, respectively, and were mutually exclusive. Further, we identified mutations in the genes encoding the epigenetic regulators EZH2 in 13% (3/23), TET2 in 17% (4/23) and BCOR in 9% (2/23) of the cases. We confirmed that the JAK-STAT pathway is a major mutational target, and identified epigenetic regulators recurrently mutated in T-PLL. These findings complement the mutational spectrum of secondary aberrations in T-PLL and underscore the potential therapeutical relevance of epigenetic regulators in T-PLL.
    Type of Publication: Journal article published
    PubMed ID: 26917488
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  • 3
    ISSN: 1432-0584
    Keywords: Key words Anaplastic large-cell lymphoma ; leukemia ; ALK-1
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Anaplastic large-cell lymphoma (ALCL) is a lymphoproliferative disorder that frequently presents with disseminated disease and extranodal involvement. Rare atypical cells have been detected in the peripheral blood in occasional cases. However, the presence of a prominent leukemic phase is extremely rare in these patients. We describe a patient with a small-cell variant of ALCL of T-cell phenotype, ALK-1 positive, who developed a rapid leukemic phase in association with the progression of the disease. Similar to the nodal biopsy, the predominant cells in bone marrow and peripheral blood were small atypical lymphoid cells. The large tumor cells expressed ALK immunoreactivity with a cytoplasmic and nuclear pattern, whereas some of the small cells showed only a nuclear-restricted pattern of staining. An RT-PCR study detected the NPM-ALK chimeric product in the nodal biopsy and in a peripheral blood sample in the early phase of the disease, but it became negative in a peripheral blood sample obtained after completion of the chemotherapy treatment, suggesting that this assay may be useful in the follow-up of these patients. This case indicates that a prominent leukemic phase may develop in ALCL as a manifestation of tumor dissemination and that it may be composed of a predominant small-cell atypical component.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Empirical eradication therapy of H. pylori has been proposed as a therapeutic alternative for duodenal ulcer.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To identify the cost-effectiveness of empirical eradication therapy vs. test-and-treatment for the management of patients already diagnosed with a duodenal ulcer.〈section xml:id="abs1-3"〉〈title type="main"〉Methods:A decision analysis was performed to compare the cost-effectiveness of empirical eradication therapy of H. pylori diagnosed duodenal ulcer vs. eradication therapy after confirmatory diagnosis of Helicobacter pylori infection by means of several diagnostic tests.〈section xml:id="abs1-4"〉〈title type="main"〉Results:The empirical eradication therapy of duodenal ulcer was found to be the most effective and cost-effective strategy of all the alternatives. Amongst the alternatives, which included the previous performance of confirmatory diagnostic tests, the best cost-effectiveness ratio used a serology test. The model was robust in the face of changes in the values of therapeutic effectiveness, sensitivity and specificity of the diagnostic tests, prevalence of H. pylori infection in duodenal ulcer, duration of the antisecretory therapy, and number of medical visits.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusions:Based on our cost-effectiveness analysis, a treat approach is more effective and cost-effective than a test-and-treat approach in the clinical management of already diagnosed duodenal ulcer.
    Type of Medium: Electronic Resource
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  • 5
    Publication Date: 2018-07-27
    Description: Mantle cell lymphoma (MCL) is an aggressive B-cell malignancy, but some patients have a very indolent evolution. This heterogeneous course is related, in part, to the different biological characteristics of conventional MCL (cMCL) and the distinct subgroup of leukemic nonnodal MCL (nnMCL). Robust criteria to distinguish these MCL subtypes and additional biological parameters that influence their evolution are not well defined. We describe a novel molecular assay that reliably distinguishes cMCL and nnMCL using blood samples. We trained a 16-gene assay (L-MCL16 assay) on the NanoString platform using 19 purified leukemic samples. The locked assay was applied to an independent cohort of 70 MCL patients with leukemic presentation. The assay assigned 37% of cases to nnMCL and 56% to cMCL. nnMCL and cMCL differed in nodal presentation, lactate dehydrogenase, immunoglobulin heavy chain gene mutational status, management options, genomic complexity, and CDKN2A / ATM deletions, but the proportion with 17p/ TP53 aberrations was similar in both subgroups. Sequential samples showed that assay prediction was stable over time. nnMCL had a better overall survival (OS) than cMCL (3-year OS 92% vs 69%; P = .006) from the time of diagnosis and longer time to first treatment. Genomic complexity and TP53 / CDKN2A aberrations predicted for shorter OS in the entire series and cMCL, whereas only genomic complexity was associated with shorter time to first treatment and OS in nnMCL. In conclusion, the newly developed assay robustly recognizes the 2 molecular subtypes of MCL in leukemic samples. Its combination with genetic alterations improves the prognostic evaluation and may provide useful biological information for management decisions.
    Keywords: Lymphoid Neoplasia
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 6
    Publication Date: 2015-07-23
    Description: Chronic lymphocytic leukaemia (CLL) is a frequent disease in which the genetic alterations determining the clinicobiological behaviour are not fully understood. Here we describe a comprehensive evaluation of the genomic landscape of 452 CLL cases and 54 patients with monoclonal B-lymphocytosis, a precursor disorder. We extend the number of CLL driver alterations, including changes in ZNF292, ZMYM3, ARID1A and PTPN11. We also identify novel recurrent mutations in non-coding regions, including the 3' region of NOTCH1, which cause aberrant splicing events, increase NOTCH1 activity and result in a more aggressive disease. In addition, mutations in an enhancer located on chromosome 9p13 result in reduced expression of the B-cell-specific transcription factor PAX5. The accumulative number of driver alterations (0 to 〉/=4) discriminated between patients with differences in clinical behaviour. This study provides an integrated portrait of the CLL genomic landscape, identifies new recurrent driver mutations of the disease, and suggests clinical interventions that may improve the management of this neoplasia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Puente, Xose S -- Bea, Silvia -- Valdes-Mas, Rafael -- Villamor, Neus -- Gutierrez-Abril, Jesus -- Martin-Subero, Jose I -- Munar, Marta -- Rubio-Perez, Carlota -- Jares, Pedro -- Aymerich, Marta -- Baumann, Tycho -- Beekman, Renee -- Belver, Laura -- Carrio, Anna -- Castellano, Giancarlo -- Clot, Guillem -- Colado, Enrique -- Colomer, Dolors -- Costa, Dolors -- Delgado, Julio -- Enjuanes, Anna -- Estivill, Xavier -- Ferrando, Adolfo A -- Gelpi, Josep L -- Gonzalez, Blanca -- Gonzalez, Santiago -- Gonzalez, Marcos -- Gut, Marta -- Hernandez-Rivas, Jesus M -- Lopez-Guerra, Monica -- Martin-Garcia, David -- Navarro, Alba -- Nicolas, Pilar -- Orozco, Modesto -- Payer, Angel R -- Pinyol, Magda -- Pisano, David G -- Puente, Diana A -- Queiros, Ana C -- Quesada, Victor -- Romeo-Casabona, Carlos M -- Royo, Cristina -- Royo, Romina -- Rozman, Maria -- Russinol, Nuria -- Salaverria, Itziar -- Stamatopoulos, Kostas -- Stunnenberg, Hendrik G -- Tamborero, David -- Terol, Maria J -- Valencia, Alfonso -- Lopez-Bigas, Nuria -- Torrents, David -- Gut, Ivo -- Lopez-Guillermo, Armando -- Lopez-Otin, Carlos -- Campo, Elias -- England -- Nature. 2015 Oct 22;526(7574):519-24. doi: 10.1038/nature14666. Epub 2015 Jul 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departamento de Bioquimica y Biologia Molecular, Instituto Universitario de Oncologia (IUOPA), Universidad de Oviedo, 33006 Oviedo, Spain. ; Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), 08036 Barcelona, Spain. ; Unitat de Hematologia, Hospital Clinic, IDIBAPS, Universitat de Barcelona, 08036 Barcelona, Spain. ; Departament d'Anatomia Patologica, Microbiologia i Farmacologia, Universitat de Barcelona, 08036 Barcelona, Spain. ; Programa Conjunto de Biologia Computacional, Barcelona Supercomputing Center (BSC), Institut de Recerca Biomedica (IRB), Spanish National Bioinformatics Institute, Universitat de Barcelona, 08028 Barcelona, Spain. ; Research Unit on Biomedical Informatics, Department of Experimental and Health Sciences, Universitat Pompeu Fabra, 08003 Barcelona, Spain. ; Unidad de Genomica, IDIBAPS, 08036 Barcelona, Spain. ; Servicio de Hematologia, Hospital Clinic, IDIBAPS, 08036 Barcelona, Spain. ; Institute for Cancer Genetics, Columbia University, New York 10032, USA. ; Servicio de Hematologia, Hospital Universitario Central de Asturias, 33011 Oviedo, Spain. ; Center for Genomic Regulation (CRG), Pompeu Fabra University (UPF), Hospital del Mar Research Institute (IMIM), 08003 Barcelona, Spain. ; Servicio de Hematologia, IBSAL-Hospital Universitario de Salamanca, Centro de Investigacion del Cancer, Universidad de Salamanca-CSIC, 37007 Salamanca, Spain. ; Centro Nacional de Analisis Genomico, Parc Cientific de Barcelona, 08028 Barcelona, Spain. ; Catedra Inter-Universitaria de Derecho y Genoma Humano, Universidad de Deusto, Universidad del Pais Vasco, 48007 Bilbao, Spain. ; Structural Biology and Biocomputing Programme, Spanish National Cancer Research Centre (CNIO), Spanish National Bioinformatics Institute, 28029 Madrid, Spain. ; Institute of Applied Biosciences, Center for Research and Technology Hellas, 57001 Thermi, Thessaloniki, Greece. ; Department of Molecular Biology, Faculty of Science, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen, 6500 HB Nijmegen, The Netherlands. ; Servicio de Hematologia, Hospital Clinico de Valencia, 46010 Valencia, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26200345" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/genetics ; Alternative Splicing/genetics ; B-Cell-Specific Activator Protein/biosynthesis/genetics ; B-Lymphocytes/metabolism ; Carrier Proteins/genetics ; Chromosomes, Human, Pair 9/genetics ; DNA Mutational Analysis ; DNA, Neoplasm/genetics ; Enhancer Elements, Genetic/genetics ; Genomics ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell/*genetics/metabolism/pathology ; Mutation/*genetics ; Nerve Tissue Proteins/genetics ; Nuclear Proteins/genetics ; Protein Tyrosine Phosphatase, Non-Receptor Type 11/genetics ; Receptor, Notch1/genetics/metabolism ; Transcription Factors/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2011-06-07
    Description: Chronic lymphocytic leukaemia (CLL), the most frequent leukaemia in adults in Western countries, is a heterogeneous disease with variable clinical presentation and evolution. Two major molecular subtypes can be distinguished, characterized respectively by a high or low number of somatic hypermutations in the variable region of immunoglobulin genes. The molecular changes leading to the pathogenesis of the disease are still poorly understood. Here we performed whole-genome sequencing of four cases of CLL and identified 46 somatic mutations that potentially affect gene function. Further analysis of these mutations in 363 patients with CLL identified four genes that are recurrently mutated: notch 1 (NOTCH1), exportin 1 (XPO1), myeloid differentiation primary response gene 88 (MYD88) and kelch-like 6 (KLHL6). Mutations in MYD88 and KLHL6 are predominant in cases of CLL with mutated immunoglobulin genes, whereas NOTCH1 and XPO1 mutations are mainly detected in patients with unmutated immunoglobulins. The patterns of somatic mutation, supported by functional and clinical analyses, strongly indicate that the recurrent NOTCH1, MYD88 and XPO1 mutations are oncogenic changes that contribute to the clinical evolution of the disease. To our knowledge, this is the first comprehensive analysis of CLL combining whole-genome sequencing with clinical characteristics and clinical outcomes. It highlights the usefulness of this approach for the identification of clinically relevant mutations in cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3322590/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3322590/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Puente, Xose S -- Pinyol, Magda -- Quesada, Victor -- Conde, Laura -- Ordonez, Gonzalo R -- Villamor, Neus -- Escaramis, Georgia -- Jares, Pedro -- Bea, Silvia -- Gonzalez-Diaz, Marcos -- Bassaganyas, Laia -- Baumann, Tycho -- Juan, Manel -- Lopez-Guerra, Monica -- Colomer, Dolors -- Tubio, Jose M C -- Lopez, Cristina -- Navarro, Alba -- Tornador, Cristian -- Aymerich, Marta -- Rozman, Maria -- Hernandez, Jesus M -- Puente, Diana A -- Freije, Jose M P -- Velasco, Gloria -- Gutierrez-Fernandez, Ana -- Costa, Dolors -- Carrio, Anna -- Guijarro, Sara -- Enjuanes, Anna -- Hernandez, Lluis -- Yague, Jordi -- Nicolas, Pilar -- Romeo-Casabona, Carlos M -- Himmelbauer, Heinz -- Castillo, Ester -- Dohm, Juliane C -- de Sanjose, Silvia -- Piris, Miguel A -- de Alava, Enrique -- San Miguel, Jesus -- Royo, Romina -- Gelpi, Josep L -- Torrents, David -- Orozco, Modesto -- Pisano, David G -- Valencia, Alfonso -- Guigo, Roderic -- Bayes, Monica -- Heath, Simon -- Gut, Marta -- Klatt, Peter -- Marshall, John -- Raine, Keiran -- Stebbings, Lucy A -- Futreal, P Andrew -- Stratton, Michael R -- Campbell, Peter J -- Gut, Ivo -- Lopez-Guillermo, Armando -- Estivill, Xavier -- Montserrat, Emili -- Lopez-Otin, Carlos -- Campo, Elias -- 088340/Wellcome Trust/United Kingdom -- 093867/Wellcome Trust/United Kingdom -- England -- Nature. 2011 Jun 5;475(7354):101-5. doi: 10.1038/nature10113.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departamento de Bioquimica y Biologia Molecular, Instituto Universitario de Oncologia, Universidad de Oviedo, 33006 Oviedo, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21642962" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Carrier Proteins/genetics ; DNA Mutational Analysis ; Genome, Human/*genetics ; Humans ; Karyopherins/genetics ; Leukemia, Lymphocytic, Chronic, B-Cell/*genetics ; Molecular Sequence Data ; Mutation/*genetics ; Myeloid Differentiation Factor 88/chemistry/genetics ; Receptor, Notch1/genetics ; Receptors, Cytoplasmic and Nuclear/genetics ; Reproducibility of Results
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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