Vanessa Rebecca Gasparini
@burlo.trieste.it
IRCCS Burlo Garofolo
Scopus Publications
- STAT3-MEDIATED CIRCULAR RNAS DYSREGULATION IN NEUTROPENIC T-LARGE GRANULAR LYMPHOCYTE LEUKEMIA PATIENTS
Rebecca Crivellari
Haematologica, 2026
Introduction. T-Large Granular Lymphocyte Leukemia (T-LGLL) is a rare chronic lymphoproliferative disorder with unclear pathogenesis. Clonal expansion is driven by pro-inflammatory cytokines that induce JAK/STAT stimulation. Activating STAT mutations have been identified, with STAT3 lesions being typical of CD8+ T-LGLL and distinguishing symptomatic cases, mainly for neutropenia, from indolent ones. The discovery of the STAT3-miR-146b-FasL axis in STAT3-mutated CD8+ cases has highlighted the role of non-coding RNAs (ncRNAs). This study aims to clarify the role of circular RNAs (circRNAs), a class of ncRNAs, whose involvement in T-LGLL remains unexplored.Methods. We considered RNA-sequencing (RNA-seq) data (GEO GSE228868) of 20 T-LGLL cases and 5 healthy donors (HD). CircRNA identification and analysis was carried out using the CircCompara2/edgeR pipeline. Candidate circRNAs were validated in an independent cohort (n=26) through Sanger sequencing and RT-qPCR. Patient cells were treated with IL-6 (20 ng/μL) or the STAT3 inhibitor STATTIC (ST) (3.5 μM). After 24 hours cell viability, STAT3 activation, and circRNA expression were assessed via Annexin V staining, western blot, and RT-qPCR, respectively.Results. A total of 5,948 circRNAs (p-adj<0.05) were detected through RNA-seq. Principal component analysis revealed distinct circRNA expression patterns between T-LGLL patients and HD, with 358 circRNAs differentially expressed in neutropenic STAT3-mutated patients compared to asymptomatic ones. The altered expression of 11 circRNAs was validated in an independent cohort. Of these, 5 were specifically altered in STAT3-mutated CD8+ patients: 4 were up-regulated, while circZC3H12B was down-regulated. Among upregulated circRNAs, circPVT1 and circZBTB46 were previously associated with oncogenic roles in different malignancies, whereas circZC3H12B, previously known as circX, was found highly expressed in normal lymphocytes and downexpressed in Acute Lymphoblastic Leukemia. To assess the potential link between STAT3 activation and circRNA dysregulation, cells from asymptomatic patients were stimulated ex vivo with IL-6 which is known to trigger STAT3. Protein activation, confirmed by western blot (p<0.01), modulated the 5 circRNAs to levels comparable to symptomatic cases. Consistently, experiments on cells from symptomatic patients with STAT3 hyperactivating variants treated with ST, an inhibitor of STAT3 phosphorylation (p<0.05), showed an inverse modulation of circRNAs expression compared to IL-6 treatment.Conclusions. This study reveals a T-LGLL-specific circRNA signature. neutropenic CD8+ STAT3-mutated patients showed a proper distinct circRNA profile, suggesting a role of these transcripts in disease severity and clinical manifestation. Experiments demonstrated that STAT3 activation drives circRNA dysregulation, offering new insights into T-LGLL pathogenesis. Future studies will explore circRNA function through siRNA silencing and RNA pull-down assays. - Diagnostic criteria for NK cell large granular lymphocyte leukemia: validation through a multicentric international study
Cedric Pastoret, Jun Yang, David J. Feith, Mikaël Roussel, Aline Moignet, Shubha Dighe, Micheal Dimitri Solga, Tony Marchand, Garance Visser, Vanessa Rebecca Gasparini, Antonella Teramo, Renato Zambello, Thomas P. Loughran, Thierry Lamy
Blood Advances, 2026
Natural killer (NK) large granular lymphocytic leukemia (LGLL) is a rare lymphoproliferative disorder lacking definitive clonality markers, complicating diagnosis and distinction from reactive NK cell expansions. We previously proposed an NK clonality score with high diagnostic accuracy, but a subset of patients remained unclassified. In this multicenter international study, we refined and validated updated diagnostic criteria using independent training (n = 78) and validation (n = 57) cohorts from 3 national registries (United States, Italy, and France). The revised framework integrates NK score parameters with CC motif chemokine ligand 22 (CCL22) mutations and bone marrow biopsy (BMB) findings. Four major criteria were defined: NK cell count of ≥1.0 × 109/L, killer-cell immunoglobulin-like receptor restriction, CD94/NKG2A overexpression, and somatic mutations in STAT3, TET2, or CCL22, the latter newly introduced. In the training cohort, 50 patients were classified as having NK-LGLL by an NK score of &gt;4, 18 had intermediate scores (2-3), and 10 were diagnosed as reactive proliferations. CCL22 mutations were identified in 16 patients (20%), including 5 with intermediate scores who were reclassified as NK-LGLL; BMB supported the diagnosis in 2 additional cases, resulting in 57 NK-LGLL overall. These patients exhibited more cytopenias, higher treatment needs, and greater transfusion requirements than patients with alternative diagnoses. In the validation cohort (25 NK-LGLL and 32 reactive cases), CCL22 mutations were detected in 5 NK-LGLL (20%). Altogether, incorporation of CCL22 mutations reduced the fraction of unclassified patients, improved diagnostic sensitivity without compromising specificity, and may decrease reliance on invasive procedures. These revised international criteria represent a step toward standardized, molecularly guided NK-LGLL diagnosis. - Transcriptomic landscape of CD8+ and CD4 + T-LGL leukemia revealed the distinct impact of STAT3 and STAT5B activating mutations
Giulia Calabretto, Andrea Binatti, Antonella Teramo, Alessia Buratin, Gregorio Barilà, Vanessa Rebecca Gasparini, Cristina Vicenzetto, Enrico Gaffo, Elisa Rampazzo, Silvia Orsi, Elena Buson, Valentina Trimarco, Barbara Mariotti, Monica Facco, Flavia Bazzoni, Livio Trentin, Gianpietro Semenzato, Renato Zambello, Stefania Bortoluzzi
Leukemia, 2025
The biological basis of the high clinical heterogeneity of T-LGL Leukemia (T-LGLL) is not completely understood and effective therapies for this disease are lacking. Through RNA-Sequencing of purified T-LGLs we reveal gene expression profiles and pathway dysregulations in the major patient subgroups, defined by CD8+ or CD4+ phenotype and STAT3/STAT5B mutational status. Overall, T-LGLL patients exhibited a marked transcriptome dysregulation compared to controls. This was more pronounced in the most symptomatic CD8 + STAT3-mutated patients, which emerged as a distinct biological entity, separated from the other disease subgroups. Particularly, CD8 + STAT3-mutated cases displayed extensive down-regulation of genes, ultimately resulting in the de-repression of proliferation and cell cycle pathways. Among genes up-regulated in CD8 + STAT3-mutated cases we found VCAM1, the transcriptional repressor EZH2 and the p53-regulator MDM2 proto-oncogene, as well as the leukemogenesis-associated PVT1 up-regulation, representing the first report of a long-non-coding RNA alterations in leukemic T-LGLs. The impact of STAT5B mutations on T-LGLs transcriptome was more limited and the overexpression of the PIM1 serine/threonine kinase proto-oncogene was identified as one of the most relevant features of STAT5B-mutated CD4 + T-LGLL. This study significantly advances our understanding of T-LGLL pathogenesis, uncovering new oncogenic mechanisms within the distinct molecular subtypes of the disease. - Beyond the Curtains: Identification of the Genetic Cause of Foetal Developmental Abnormalities Through the Application of Molecular Autopsy
Beatrice Spedicati, Giulia Pianigiani, Aurora Santin, Vanessa Rebecca Gasparini, Ilaria Falcomer, Agnese Feresin, Maria Teresa Bonati, Daniela Mazzà, Elisa Paccagnella, Domizia Pasquetti, Elisa Rubinato, Claudio Granata, Flora Maria Murru, Maurizio Pinamonti, Rossana Bussani, Ilaria Fantasia, Tamara Stampalija, Paolo Gasparini, Stefania Zampieri, Giorgia Girotto
Genes, 2025
Background: Foetal structural abnormalities can be detected in approximately 3% of all pregnancies and frequently remain without a genetic diagnosis. This study aims to apply an integrated approach with the final goal of providing a molecular diagnosis in the challenging Italian setting of early termination of pregnancy. Methods: In a cohort of 86 foetuses, post-mortem dysmorphological examination, radiological assessments, and molecular autopsy through Whole-Exome Sequencing—WES—analysis were performed. Results: Forty-two foetuses were phenotypically classified as presenting a single major malformation (i.e., central nervous system, skeletal, urogenital, or cardiac anomalies, or fluid accumulation), while 44 foetuses presented multiple malformations and/or dysmorphic features. Overall, WES provided a diagnostic yield of 26.7%; additionally, seven Variants of Uncertain Significance (VUS) potentially liked to the foetal phenotype were identified. The highest detection rate was achieved for foetuses presenting a single major urogenital (50%) or skeletal (42.9%) malformation, followed by foetuses presenting multiple malformations (27.3%). Peculiar results of particular interest were (1) the identification of two splicing variants (within the INPPL1 and RHOA genes), functionally characterised through minigene assay, which contributed to evaluate their pathogenicity, and (2) the identification of a novel de novo missense ZNF292 variant (NM_015021.3:c.6325A>C p.(Ser2109Arg)) in a foetus affected by corpus callosum hypoplasia. The ZNF292 gene is associated with the Intellectual developmental disorder, autosomal dominant 64 and this finding represents the first report of prenatally detected anomalies of the central nervous system in a foetus carrying a ZNF292 variant. Conclusions: This study underlines the diagnostic utility of an integrated approach to achieve a precise genetic diagnosis for structural foetal abnormalities, thus providing families with precise recurrence risk estimations and detailed options about future pregnancies. Additionally, a systematic implementation of this strategy could be crucial to better characterise new variants and discover new genes involved in embryonic and foetal development. - The constitutive activation of STAT3 gene and its mutations are at the crossroad between LGL leukemia and autoimmune disorders
Gianpietro Semenzato, Giulia Calabretto, Antonella Teramo, Vanessa Rebecca Gasparini, Elisa Rampazzo, Gregorio Barilà, Renato Zambello
Blood Cancer Journal, 2024
Type T Large Granular Lymphocyte Leukemia (T-LGLL) is a chronic disorder characterized by the abnormal proliferation of clonal cytotoxic T cells. The intriguing association of T-LGLL with autoimmune and inflammatory diseases, the most prominent example being rheumatoid arthritis, raises questions about the underlying pathophysiologic relationships between these disorders which share several biological and clinical features, most notably neutropenia, which is considered as a clinical hallmark. Recent progress in molecular genetics has contributed to a better understanding of pathogenetic mechanisms, thus moving our knowledge in the field of LGL leukemias forward. Focusing on the constitutive activation of STAT3 pathway and the well-established role of STAT3 mutations in T-LGLL, we herein discuss whether the T cell clones occurring in comorbid conditions are the cause or the consequence of the immune-inflammatory associated events. Overall, this review sheds light on the intricate relationships between inflammation and cancer, emphasizing the importance of the STAT3 gene and its activation in the pathophysiology of these conditions. Gaining a deeper understanding of these underlying mechanisms seeks to pave the way for the development of novel targeted therapies for patients affected by inflammation-related cancers. - Proteasome Inhibitors Induce Apoptosis in Ex Vivo Cells of T-Cell Prolymphocytic Leukemia
Vanessa Rebecca Gasparini, Elisa Rampazzo, Gregorio Barilà, Alessia Buratin, Elena Buson, Giulia Calabretto, Cristina Vicenzetto, Silvia Orsi, Alessia Tonini, Antonella Teramo, Livio Trentin, Monica Facco, Gianpietro Semenzato, Stefania Bortoluzzi, Renato Zambello
International Journal of Molecular Sciences, 2024
Finding an effective treatment for T-PLL patients remains a significant challenge. Alemtuzumab, currently the gold standard, is insufficient in managing the aggressiveness of the disease in the long term. Consequently, numerous efforts are underway to address this unmet clinical need. The rarity of the disease limits the ability to conduct robust clinical trials, making in silico, ex vivo, and in vivo drug screenings essential for designing new therapeutic strategies for T-PLL. We conducted a drug repurposing analysis based on T-PLL gene expression data and identified proteasome inhibitors (PIs) as a promising new class of compounds capable of reversing the T-PLL phenotype. Treatment of ex vivo T-PLL cells with Bortezomib and Carfilzomib, two PI compounds, supported this hypothesis by demonstrating increased apoptosis in leukemic cells. The current lack of a suitable in vitro model for the study of T-PLL prompted us to perform similar experiments in the SUP-T11 cell line, validating its potential by showing an increased apoptotic rate. Taken together, these findings open new avenues for investigating the molecular mechanisms underlying the efficacy of PI in T-PLL and expand the spectrum of potential therapeutic strategies for this highly aggressive disease. - Pro-inflammatory cells sustain leukemic clonal expansion in T-cell large granular lymphocyte leukemia
Cristina Vicenzetto, Vanessa Rebecca Gasparini, Gregorio Barila, Antonella Teramo, Giulia Calabretto, Elisa Rampazzo, Samuela Carraro, Valentina Trimarco, Livio Trentin, Monica Facco, Gianpietro Semenzato, Renato Zambello
Haematologica, 2024
T-cell Large Granular Lymphocyte Leukemia (T-LGLL) is a chronic lymphoproliferative disorder characterized by the clonal expansion of T-LGL. Immunophenotypic and genotypic features contribute to discriminate symptomatic (CD8+ STAT3 mutated T-LGLL) from clinically indolent patients, this latter group including CD8+ wild type (wt), CD4+ STAT5B mutated and wt cases. T-LGL lymphoproliferation is sustained both by somatic gain-offunction mutations (i.e. STAT3 and STAT5B) and by pro-inflammatory cytokines, but little information is available on the activity of T-LGLL non leukemic cells. In this study, we characterized pro-inflammatory cells in peripheral blood of T-LGLL patients and analyzed their role in supporting the leukemic growth. In symptomatic patients we found that cell populations not belonging to the leukemic component showed a discrete pro-inflammatory pattern. In particular, CD8+ STAT3 mutated cases showed skewed Th17/Treg ratio and an abnormal monocyte populations’ distribution characterized by increased intermediate and non-classical monocytes. We also demonstrated that monocytes released high levels of IL-6 after CCL5 stimulation, a chemokine specifically expressed only by leukemic LGL. Conversely, in asymptomatic cases an altered distribution of monocytes populations was not detected. Moreover, T-LGLL patients’ monocytes showed abnormal activation of signaling pathways, further supporting the different pathogenetic role of monocytes in patients with discrete clinical settings. Altogether, our data contribute to deepen the knowledge on the different cell subtypes in TLGLL, particularly focusing on non-leukemic cell populations and thus offering the rationale for new therapeutic strategies. - Not all LGL leukemias are created equal
Gianpietro Semenzato, Giulia Calabretto, Gregorio Barilà, Vanessa Rebecca Gasparini, Antonella Teramo, Renato Zambello
Blood Reviews, 2023
Large Granular Lymphocyte (LGL) Leukemia is a rare, heterogeneous even more that once thought, chronic lymphoproliferative disorder characterized by the clonal expansion of T- or NK-LGLs that requires appropriate immunophenotypic and molecular characterization. As in many other hematological conditions, genomic features are taking research efforts one step further and are also becoming instrumental in refining discrete subsets of LGL disorders. In particular, STAT3 and STAT5B mutations may be harbored in leukemic cells and their presence has been linked to diagnosis of LGL disorders. On clinical grounds, a correlation has been established in CD8+ T-LGLL patients between STAT3 mutations and clinical features, in particular neutropenia that favors the onset of severe infections. Revisiting biological aspects, clinical features as well as current and predictable emerging treatments of these disorders, we will herein discuss why appropriate dissection of different disease variants is needed to better manage patients with LGL disorders. - Tγδ LGLL identifies a subset with more symptomatic disease: analysis of an international cohort of 137 patients
Gregorio Barilà, Angela Grassi, HeeJin Cheon, Antonella Teramo, Giulia Calabretto, Jasmanet Chahal, Cristina Vicenzetto, Julia Almeida, Bryna C. Shemo, Min Shi, Vanessa Rebecca Gasparini, Noemi Munoz-Garcia, Cédric Pastoret, Hideyuki Nakazawa, Kazuo Oshimi, Lubomir Sokol, Fumihiro Ishida, Thierry Lamy, Alberto Orfao, William G. Morice, Thomas P. Loughran, Gianpietro Semenzato, Renato Zambello
Blood, 2023
Tγδ large granular lymphocyte leukemia (LGLL) is a rare variant of T-cell LGLL (T-LGLL) that has been less investigated as compared with the more frequent Tαβ LGLL, particularly in terms of frequency of STAT3 and STAT5b mutations. In this study, we characterized the clinical and biological features of 137 patients affected by Tγδ LGLL; data were retrospectively collected from 1997 to 2020 at 8 referral centers. Neutropenia and anemia were the most relevant clinical features, being present in 54.2% and 49.6% of cases, respectively, including severe neutropenia and anemia in ∼20% of cases each. Among the various treatments, cyclosporine A was shown to provide the best response rates. DNA samples of 97 and 94 cases were available for STAT3 and STAT5b mutation analysis, with 38.1% and 4.2% of cases being mutated, respectively. Clinical and biological features of our series of Tγδ cases were also compared with a recently published Tαβ cohort including 129 cases. Though no differences in STAT3 and STAT5b mutational frequency were found, Tγδ cases more frequently presented with neutropenia (P = .0161), anemia (P &lt; .0001), severe anemia (P = .0065), and thrombocytopenia (P = .0187). Moreover, Vδ2− cases displayed higher frequency of symptomatic disease. Overall, Tγδ cases displayed reduced survival with respect to Tαβ cases (P = .0017). Although there was no difference in STAT3 mutation frequency, our results showed that Tγδ LGLL represents a subset of T-LGLL characterized by more frequent symptoms and reduced survival as compared with Tαβ LGLL. - Defining TCRγδ lymphoproliferative disorders by combined immunophenotypic and molecular evaluation
Antonella Teramo, Andrea Binatti, Elena Ciabatti, Gianluca Schiavoni, Giulia Tarrini, Gregorio Barilà, Giulia Calabretto, Cristina Vicenzetto, Vanessa Rebecca Gasparini, Monica Facco, Iacopo Petrini, Roberto Grossi, Nadia Pisanti, Stefania Bortoluzzi, Brunangelo Falini, Enrico Tiacci, Sara Galimberti, Gianpietro Semenzato, Renato Zambello
Nature Communications, 2022
Tγδ large granular lymphocyte leukemia (Tγδ LGLL) is a rare lymphoproliferative disease, scantily described in literature. A deep-analysis, in an initial cohort of 9 Tγδ LGLL compared to 23 healthy controls, shows that Tγδ LGLL dominant clonotypes are mainly public and exhibit different V-(D)-J γ/δ usage between patients with symptomatic and indolent Tγδ neoplasm. Moreover, some clonotypes share the same rearranged sequence. Data obtained in an enlarged cohort (n = 36) indicate the importance of a combined evaluation of immunophenotype and STAT mutational profile for the correct management of patients with Tγδ cell expansions. In fact, we observe an association between Vδ2/Vγ9 clonality and indolent course, while Vδ2/Vγ9 negativity correlates with symptomatic disease. Moreover, the 7 patients with STAT3 mutations have neutropenia and a CD56-/Vδ2- phenotype, and the 3 cases with STAT5B mutations display an asymptomatic clinical course and CD56/Vδ2 expression. All these data indicate that biological characterization is needed for Tγδ-cell neoplasm definition. - All that glitters is not LGL Leukemia
Gianpietro Semenzato, Antonella Teramo, Giulia Calabretto, Vanessa Rebecca Gasparini, Renato Zambello
Leukemia, 2022 - Hypocellular myelodysplastic syndromes (h-MDS): from clinical description to immunological characterization in the Italian multi-center experience
Giulia Calabretto, Enrico Attardi, Antonella Teramo, Valentina Trimarco, Samuela Carraro, Sandra Mossuto, Gregorio Barilà, Cristina Vicenzetto, Vanessa Rebecca Gasparini, Monica Crugnola, Pasquale Niscola, Antonella Poloni, Valentina Giai, Valentina Gaidano, Carlo Finelli, Roberta Bertorelle, Cinzia Candiotto, Marco Pizzi, Gianni Binotto, Monica Facco, Fabrizio Vianello, Livio Trentin, Gianpietro Semenzato, Renato Zambello, Valeria Santini
Leukemia, 2022 - Identification of novel STAT5B mutations and characterization of TCRβ signatures in CD4+ T-cell large granular lymphocyte leukemia
Dipabarna Bhattacharya, Antonella Teramo, Vanessa Rebecca Gasparini, Jani Huuhtanen, Daehong Kim, Jason Theodoropoulos, Gianluca Schiavoni, Gregorio Barilà, Cristina Vicenzetto, Giulia Calabretto, Monica Facco, Toru Kawakami, Hideyuki Nakazawa, Brunangelo Falini, Enrico Tiacci, Fumihiro Ishida, Gianpietro Semenzato, Tiina Kelkka, Renato Zambello, Satu Mustjoki
Blood Cancer Journal, 2022 - Neutropenia and large granular lymphocyte leukemia: From pathogenesis to therapeutic options
Giulia Calabretto, Antonella Teramo, Gregorio Barilà, Cristina Vicenzetto, Vanessa Rebecca Gasparini, Gianpietro Semenzato, Renato Zambello
Cells, 2021 - Treatment Induced Cytotoxic T-Cell Modulation in Multiple Myeloma Patients
Gregorio Barilà, Laura Pavan, Susanna Vedovato, Tamara Berno, Mariella Lo Schirico, Massimiliano Arangio Febbo, Antonella Teramo, Giulia Calabretto, Cristina Vicenzetto, Vanessa Rebecca Gasparini, Anna Fregnani, Sabrina Manni, Valentina Trimarco, Samuela Carraro, Monica Facco, Francesco Piazza, Gianpietro Semenzato, Renato Zambello
Frontiers in Oncology, 2021 - Lack of Viral Load Within Chronic Lymphoproliferative Disorder of Natural Killer Cells: What Is Outside the Leukemic Clone?
Edoardo Giussani, Andrea Binatti, Giulia Calabretto, Vanessa Rebecca Gasparini, Antonella Teramo, Cristina Vicenzetto, Gregorio Barilà, Monica Facco, Alessandro Coppe, Gianpietro Semenzato, Stefania Bortoluzzi, Renato Zambello
Frontiers in Oncology, 2021 - Large granular lymphocyte leukemia
Antonella Teramo, Cristina Vicenzetto, Gregorio Barilà, Giulia Calabretto, Vanessa Rebecca Gasparini, Gianpietro Semenzato, Renato Zambello
Hematologic Malignancies, 2021 - Stat3 mutations impact on overall survival in large granular lymphocyte leukemia: a single-center experience of 205 patients
Gregorio Barilà, Antonella Teramo, Giulia Calabretto, Cristina Vicenzetto, Vanessa Rebecca Gasparini, Laura Pavan, Matteo Leoncin, Susanna Vedovato, Anna Chiara Frigo, Monica Facco, Gianpietro Semenzato, Renato Zambello
Leukemia, 2020 - A high definition picture of somatic mutations in chronic lymphoproliferative disorder of natural killer cells
Vanessa Rebecca Gasparini, Andrea Binatti, Alessandro Coppe, Antonella Teramo, Cristina Vicenzetto, Giulia Calabretto, Gregorio Barilà, Annica Barizza, Edoardo Giussani, Monica Facco, Satu Mustjoki, Gianpietro Semenzato, Renato Zambello, Stefania Bortoluzzi
Blood Cancer Journal, 2020 - Insights Into Genetic Landscape of Large Granular Lymphocyte Leukemia
Antonella Teramo, Gregorio Barilà, Giulia Calabretto, Cristina Vicenzetto, Vanessa Rebecca Gasparini, Gianpietro Semenzato, Renato Zambello
Frontiers in Oncology, 2020 - Atypical mature T-cell neoplasms: The relevance of the role of flow cytometry
Teodora Statuto, Fiorella D'Auria, Luigi Del Vecchio, Giovanna Rosaria Mansueto, Oreste Villani, Anna Vittoria Lalinga, Luciana Possidente, Filomena Nozza, Gabriella Vona, Luciana Rago, Giovanni Storto, Vanessa Rebecca Gasparini, Renato Zambello, Giovanni D'Arena, Luciana Valvano
Oncotargets and Therapy, 2020 - T cell large granular lymphocyte leukemia and chronic NK lymphocytosis
Gregorio Barilà, Giulia Calabretto, Antonella Teramo, Cristina Vicenzetto, Vanessa Rebecca Gasparini, Gianpietro Semenzato, Renato Zambello
Best Practice and Research Clinical Haematology, 2019 - Genomic landscape characterization of large granular lymphocyte leukemia with a systems genetics approach
A Coppe, E I Andersson, A Binatti, V R Gasparini, S Bortoluzzi, M Clemente, M Herling, J Maciejewski, S Mustjoki, S Bortoluzzi
Leukemia, 2017 - High incidence of activating STAT5B mutations in CD4-positive T-cell large granular lymphocyte leukemia
Emma I. Andersson, Takahiro Tanahashi, Nodoka Sekiguchi, Vanessa Rebecca Gasparini, Sabrina Bortoluzzi, Toru Kawakami, Kazuyuki Matsuda, Takeki Mitsui, Samuli Eldfors, Stefania Bortoluzzi, Alessandro Coppe, Andrea Binatti, Sonja Lagström, Pekka Ellonen, Noriyasu Fukushima, Sayaka Nishina, Noriko Senoo, Hitoshi Sakai, Hideyuki Nakazawa, Yok-Lam Kwong, Thomas P. Loughran, Jaroslaw P. Maciejewski, Satu Mustjoki, Fumihiro Ishida
Blood, 2016
