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Circulating Polymorphonuclear Myeloid-Derived Suppressor Cells (PMN-MDSCs) Have a Biological Role in Patients with Primary Myelofibrosis.
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- Cancers, 2024, v. 16, n. 14, p. 2556, doi. 10.3390/cancers16142556
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- Article
Circulating Mesenchymal Stromal Cells in Patients with Infantile Hemangioma: Evaluation of Their Functional Capacity and Gene Expression Profile.
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- Cells (2073-4409), 2024, v. 13, n. 3, p. 254, doi. 10.3390/cells13030254
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- Article
Type 1 CALR mutation allele frequency correlates with CD34/CXCR4 expression in myelofibrosis-type megakaryocyte dysplasia: A mechanism of disease progression?
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- Blood Cancer Journal, 2024, v. 14, n. 1, p. 1, doi. 10.1038/s41408-024-00991-2
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- Article
VEGFA rs3025039 is associated with phenotype severity of myelofibrosis‐type megakaryocyte dysplasia.
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- EJHaem, 2023, v. 4, n. 3, p. 756, doi. 10.1002/jha2.708
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- Article
Clonal Megakaryocyte Dysplasia with Isolated Thrombocytosis Is a Distinct Myeloproliferative Neoplasm Phenotype.
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- Acta Haematologica, 2023, v. 146, n. 1, p. 14, doi. 10.1159/000527284
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Clonal Megakaryocyte Dysplasia with Normal Blood Values Is a Distinct Myeloproliferative Neoplasm.
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- Acta Haematologica, 2022, v. 145, n. 1, p. 30, doi. 10.1159/000517207
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Bone Marrow Microenvironment in Light-Chain Amyloidosis: In Vitro Expansion and Characterization of Mesenchymal Stromal Cells.
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- Biomedicines, 2021, v. 9, n. 11, p. 1523, doi. 10.3390/biomedicines9111523
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New Markers of Disease Progression in Myelofibrosis.
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- Cancers, 2021, v. 13, n. 21, p. 5324, doi. 10.3390/cancers13215324
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Clinical Relevance of VEGFA (rs3025039) +936 C>T Polymorphism in Primary Myelofibrosis: Susceptibility, Clinical Co-Variates, and Outcomes.
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- Genes, 2021, v. 12, n. 8, p. 1271, doi. 10.3390/genes12081271
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Impact of the rs1024611 Polymorphism of CCL2 on the Pathophysiology and Outcome of Primary Myelofibrosis.
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- Cancers, 2021, v. 13, n. 11, p. 2552, doi. 10.3390/cancers13112552
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- Article
Clinical Applications of Mesenchymal Stem/Stromal Cell Derived Extracellular Vesicles: Therapeutic Potential of an Acellular Product.
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- Diagnostics (2075-4418), 2020, v. 10, n. 12, p. 999, doi. 10.3390/diagnostics10120999
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Constitutive STAT5 phosphorylation in CD34<sup>+</sup> cells of patients with primary myelofibrosis: Correlation with driver mutation status and disease severity.
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- PLoS ONE, 2019, v. 14, n. 8, p. 1, doi. 10.1371/journal.pone.0220189
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The spleen of patients with myelofibrosis harbors defective mesenchymal stromal cells.
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- American Journal of Hematology, 2018, v. 93, n. 5, p. 615, doi. 10.1002/ajh.25047
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Increased plasma nicotinamide phosphoribosyltransferase is associated with a hyperproliferative phenotype and restrains disease progression in MPN-associated myelofibrosis.
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- American Journal of Hematology, 2016, v. 91, n. 7, p. 709, doi. 10.1002/ajh.24388
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- Article
Tie2 Expressing Monocytes in the Spleen of Patients with Primary Myelofibrosis.
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- PLoS ONE, 2016, v. 11, n. 6, p. 1, doi. 10.1371/journal.pone.0156990
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Increase of circulating endothelial cells in patients with Hereditary Hemorrhagic Telangiectasia.
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- International Journal of Hematology, 2015, v. 101, n. 1, p. 23, doi. 10.1007/s12185-014-1698-4
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<i>JAK2</i> V617F Genotype Is a Strong Determinant of Blast Transformation in Primary Myelofibrosis.
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- PLoS ONE, 2013, v. 8, n. 3, p. 1, doi. 10.1371/journal.pone.0059791
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Evidence that Prefibrotic Myelofibrosis Is Aligned along a Clinical and Biological Continuum Featuring Primary Myelofibrosis.
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- PLoS ONE, 2012, v. 7, n. 4, p. 1, doi. 10.1371/journal.pone.0035631
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- Article
Splenectomy produces a rapid but transient decrease of the frequency of circulating CD34.
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- British Journal of Haematology, 2011, v. 152, n. 5, p. 665, doi. 10.1111/j.1365-2141.2010.08527.x
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High Frequency of Endothelial Colony Forming Cells Marks a Non-Active Myeloproliferative Neoplasm with High Risk of Splanchnic Vein Thrombosis.
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- PLoS ONE, 2010, v. 5, n. 12, p. 1, doi. 10.1371/journal.pone.0015277
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Phase I/II study of single-agent bortezomib for the treatment of patients with myelofibrosis. Clinical and biological effects of proteasome inhibition.
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- American Journal of Hematology, 2010, v. 85, n. 8, p. 616, doi. 10.1002/ajh.21754
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research paper Spleen neoangiogenesis in patients with myelofibrosis with myeloid metaplasia.
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- British Journal of Haematology, 2004, v. 124, n. 5, p. 618, doi. 10.1111/j.1365-2141.2004.04829.x
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- Article
Molecular and Functional Bases of Self-Antigen Recognition in Long-Term Persistent Melanocyte-Specific CD8<sup>+</sup> T Cells in One Vitiligo Patient.
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- Journal of Investigative Dermatology, 2003, v. 121, n. 2, p. 308, doi. 10.1046/j.1523-1747.2003.12368.x
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Human CD8 co–receptor is strictly involved in MHC–peptide tetramer–TCR binding and T cell activation.
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- International Immunology, 2002, v. 14, n. 1, p. 39, doi. 10.1093/intimm/14.1.39
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Specific Cytotoxic T Lymphocyte Responses Against Melan-A/MART1, Tyrosinase and Gp100 in Vitiligo by the Use of Major Histocompatibility Complex/Peptide Tetramers: the Role of Cellular Immunity in the Etiopathogenesis of Vitiligo.
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- Journal of Investigative Dermatology, 2001, v. 117, n. 2, p. 326, doi. 10.1046/j.1523-1747.2001.01408.x
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Diverse expansion potential and heterogeneous avidity in tumor-associated antigen-specific T lymphocytes from primary melanoma patients.
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- European Journal of Immunology, 2001, v. 31, n. 2, p. 412, doi. 10.1002/1521-4141(200102)31:2<412::AID-IMMU412>3.0.CO;2-4
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Increased frequency of RAG-expressing, CD4.
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- European Journal of Immunology, 2000, v. 30, n. 5, p. 1520, doi. 10.1002/(SICI)1521-4141(200005)30:5<1520::AID-IMMU1520>3.0.CO;2-D
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- Article