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Association of overexpressed MYC gene with altered PHACTR3 and E2F4 genes contributes to non-small cell lung carcinoma pathogenesis

, optimize treatments and enable monitoring disease progression and response to therapy. Molecules that regulate cellular processes essential for maintaining malignant phenotype, such as c-Myc oncogene, stand out as promising candidates to serve as molecular markers. This nuclear phosphoprotein functions as transcriptional regulator of multiple genes and controls cell proliferation, induces apoptosis, and regulates stemness, senescence, metabolism and genome stability ( 4 ). Its expression is deregulated in number of human cancers including breast cancer, Burkitt

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Thiol-disulphide homeostasis in essential thrombocythemia patients

is high in ET patients ( 2 , 3 ). ET is a disease with bone marrow myeloproliferation in which monoclonal proliferation of megakaryocytes is more distinct. Although the pathogenesis of ET is not clearly known, 90% of cases have acquired somatic driver mutations such as JAK2, CALR, and MPL. Hypersensitivity to cytokines such as erythropoietin (EPO), thrombopoietin (TPO), interleukin 3 (IL-3) and stem cell factor (SCF) is known in the etiopathogenesis of ET. Increased free radicals are also known to increase the risk of genetic mutation in neoplastic processes ( 4

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Interaction of apelin, elabela and nitric oxide in schizophrenia patients

burden of schizophrenia in the United States was $156 billion ( 2 ). Elabela (ELA) is a peptide of 32 amino acids that activates the apelin receptor (APJ) ( 5 , 6 ). It plays a role in various biological events such as self-renewing human embryonic stem cells in embryonic and adult periods, endoderm differentiation, cardiac morphogenesis, bone formation, regulation of blood pressure, water and food intake ( 7 ). ELA appears in many tissues including the APJ such as placenta, heart, kidney, lung, liver, brain, skeletal muscle, gastrointestinal system ( 8 ). Before

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Chronic myelomonocytic leukemia “myelodysplastic type’’ in transformation to acute myeloid leukemia – diagnostic and therapeutic options: case report and literature review / Leucemie mielomonocitară cronică forma mielodisplazică în transformare spre leucemie acută mieloidă – diagnostic și opțiuni terapeutice: prezentare de caz și revizuirea literaturii

Cytogenetic Nomenclature. Basel, Switzerland: 2013: 78-79. 20. Kekre N, Ho VT. Allogeneic hematopoietic stem cell transplantation for myelofibrosis and chronic myelomonocytic leukemia. Am J Hematol. 2015 Nov;91(1):123-30. DOI: 10.1002/ajh.24215. 21. Symeonidis A, van Biezen A, de Wreede L, Piciocchi A, Finke J, Beelen D, et al. Achievement of complete remission predicts outcome of allogeneic haematopoietic stem cell transplantation in patients with chronic myelomonocytic leukaemia. A study of the chronic malignancies working party of the

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A glance on recent progresses in diagnosis and treatment of primary immunodeficiencies/ Progrese recente în diagnosticul şi tratamentul imunodeficienţelor primare

.jaci.2013.08.032 42. Takahashi K, Yamanaka S. Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors. Cell. 2006 Aug 25;126(4):663-76. DOI: 10.1016/j.cell.2006.07.024 43. Takahashi K, Tanabe K, Ohnuki M, Narita M, Ichisaka T, Tomoda K, et al. Induction of pluripotent stem cells from adult human fibroblasts by defined factors. Cell. 2007 Nov 30;131(5):861-72. DOI: 10.1016/j. cell.2007.11.019 44. Pessach IM, Ordovas-Montanes J, Zhang SY, Casanova JL, Giliani S, Gennery AR, et

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In Vivo Testing of Xenogeneic Acellular Aortic Valves Seeded with Stem Cells

Valve Scaffolds Obtained by Complete Decellularization of Porcine Aortic Roots in a Novel Differential Pressure Gradient Perfusion System. Tissue Eng Part C Methods. 2015 Dec;21(12):1284-96. DOI: 10.1089/ten.tec.2015.0170. 6. Gimble J, Guilak F. Adipose-derived adult stem cells: isolation, characterization, and differentiation potential. Cytotherapy. 2003;5(5):362-9. DOI: 10.1080/14653240310003026. 7. Schoen FJ. Heart valve tissue engineering: quo vadis? Curr Opin Biotechnol. 2011 Oct;22(5):698-705. DOI: 10.1016/j.copbio.2011

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Therapy-related myelodysplastic syndrome after successful treatment of acute promyelocytic leukemia: case report and literature review


In the 2016 revision of the World Health Organization classification the term therapy-related myeloid neoplasia (t-MN) defines a subgroup of acute myeloid leukemia (AML) comprising patients who develop myelodysplastic syndrome (MDS-t) or acute myeloid leukemia (AML-t) after treatment with cytotoxic and/or radiation therapy for various malignancies or autoimmune disorders. We report the case of a 36 year old patient with t-MN (t-MDS) after achieving complete remission (CR) of a PML-RARA positive acute promyelocytic leukemia (APL) at 32 months after diagnosis. Initially classified as low risk APL and treated according to the AIDA protocol - induction and 3 consolidation cycles - the patient achieved a complete molecular response in September 2013 and started maintenance therapy. On follow-up PML-RARA transcript remained negative. In January 2016 leukopenia and thrombocytopenia developed and a peripheral blood smear revealed hypogranular and agranular neutrophils. Immunophenotyping in the bone marrow aspirate identified undifferentiated blast cells that did not express cytoplasmic myeloperoxidase. The cytogenetic study showed normal karyotype. The molecular biology tests not identified PMLRARA transcript. A diagnosis of t-MDS (AREB-2 - WHO 2008) was established. Treatment of AML was started with 2 “3+7” regimens and 1 MEC cycle. Two months from diagnosis, while in CR, an allogeneic HSCT from an unrelated HLA compatible donor was performed after myeloablative regimen. An unfavorable clinical evolution was followed by death on day 9 after transplantation. The occurrence of t-MNs during CR of APL represents a particular problem in terms of follow-up and differential diagnosis of relapse and constitutes a dramatic complication for a disease with a favorable prognosis.

This work was supported by the grants PN 41-087 /PN2-099 from the Romanian Ministry of Research and Technology

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Exposure of Human Endothelial Progenitors to Sevoflurane Improves Their Survival Abilities

cell therapy in a porcine acute myocardial infarction model induces cardiac hypertrophy, mediated by paracrine secretion of cardiotrophic factors including TGFbeta1. Stem Cells Dev. 2008;17(5):941-51. DOI: 10.1089/scd.2007.0214. 6. Jujo K, Ii M, Losordo DW. Endothelial progenitor cells in neovascularization of infarcted myocardium. J Mol Cell Cardiol. 2008;45(4):530-44. DOI: 10.1016/j. yjmcc.2008.08.003. 7. Freyman T, Polin G, Osman H, Crary J, Lu M, Cheng L, et al. A quantitative, randomized study evaluating three methods of

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Stereological Evaluation of the Brains in Patients with Parkinson’s disease Compared to Controls

neurons in non‐Alzheimer dementia patients. Acta neurologica scandinavica. 2004;109(2):132-9. DOI: 10.1034/j.1600-0404.2003.00182.x 39. Joelving F, Billeskov R, Christensen J, West M, Pakkenberg B. Hippocampal neuron and glial cell numbers in Parkinson’s disease-a stereological study. Hippocampus. 2006;16(10):826-33. DOI: 10.1002/hipo.20212 40. Jubault T, Brambati SM, Degroot C, Kullmann B, Strafella AP, Lafontaine A-L, et al. Regional brain stem atrophy in idiopathic Parkinson’s disease detected by anatomical MRI. PloS one. 2009;4(12):e

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The importance of the new prognostic scoring system for evaluating patients with lower-risk myelodysplastic syndrome at diagnosis

, Bacigalupo A., Meloni G., Jacobsen N. et al:Haematopoietic stem cell transplantation for patients with myelodysplastic syndromes and secondary acute myeloid leukemias: A report on behalf of the Chronic Leukaemia Working Party of the European Group for Blood and Marrow Transplantation (EBMT).Br J Haematol,2000;110:620-630.

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