Giulia Calabretto

ORCID: 0000-0001-8646-2932
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About
Contact & Profiles
Research Areas
  • Chronic Lymphocytic Leukemia Research
  • Lymphoma Diagnosis and Treatment
  • Immune Cell Function and Interaction
  • Immunodeficiency and Autoimmune Disorders
  • T-cell and Retrovirus Studies
  • Acute Lymphoblastic Leukemia research
  • Multiple Myeloma Research and Treatments
  • Acute Myeloid Leukemia Research
  • RNA modifications and cancer
  • Protein Degradation and Inhibitors
  • RNA Research and Splicing
  • Protein Tyrosine Phosphatases
  • Mycobacterium research and diagnosis
  • Viral-associated cancers and disorders
  • Peptidase Inhibition and Analysis
  • CAR-T cell therapy research
  • Immunotherapy and Immune Responses
  • NF-κB Signaling Pathways
  • Ubiquitin and proteasome pathways
  • Fungal Infections and Studies
  • Cytomegalovirus and herpesvirus research
  • T-cell and B-cell Immunology
  • Hematological disorders and diagnostics
  • Galectins and Cancer Biology
  • Cancer Mechanisms and Therapy

Sidney Kimmel Cancer Center
2024-2025

Thomas Jefferson University
2024-2025

University of Padua
2015-2024

Veneto Institute of Molecular Medicine
2015-2024

Consorci Institut D'Investigacions Biomediques August Pi I Sunyer
2019

Centro de Investigación Biomédica en Red de Cáncer
2019

The University of Texas MD Anderson Cancer Center
2019

Institute of Molecular Medicine
2019

// Antonella Teramo 1, 2, * , Gregorio Barilà Giulia Calabretto 2 Chiara Ercolin Thierry Lamy 3 Aline Moignet Mikael Roussel 4 Cédric Pastoret Matteo Leoncin 1 Cristina Gattazzo Anna Cabrelle Elisa Boscaro Sara Teolato Pagnin Tamara Berno Elena De March Monica Facco Francesco Piazza Livio Trentin Gianpietro Semenzato and Renato Zambello Padua University School of Medicine, Department Hematology Clinical Immunology Branch, Padua, Italy Venetian Institute Molecular Medicine (VIMM), Hematology,...

10.18632/oncotarget.18711 article EN Oncotarget 2017-06-27

Abstract CD4+ T-cell large granular lymphocyte leukemia (T-LGLL) is a rare subtype of T-LGLL with unknown etiology. In this study, we molecularly characterized cohort patients ( n = 35) by studying their receptor (TCR) repertoire and the presence somatic STAT5B mutations. addition to previously described gain-of-function mutations (N642H, Y665F, Q706L, S715F), discovered six novel (Q220H, E433K, T628S, P658R, P702A, V712E). Multiple were present in 22% (5/23) mutated cases, either coexisting...

10.1038/s41408-022-00630-8 article EN cc-by Blood Cancer Journal 2022-02-24

Abstract Cutaneous T-Cell Lymphoma (CTCL) is a non-Hodgkin’s lymphoma involving malignant skin-homing T-cells, characterized by variable severity and limited treatment options. Our study shows that patient samples derived cell lines express CD38 on CTCL cells, αCD38 antibodies effectively target in mouse model. In vivo antibody led to the loss of expression residual tumor highlighting need for innovative strategies improve outcomes despite cells. To investigate role pathology, we used...

10.1038/s41375-025-02551-4 article EN cc-by Leukemia 2025-03-08

Abstract The molecular pathogenesis of chronic lymphoproliferative disorder natural killer (NK) cells (CLPD‐NK) is poorly understood. Following the screening 57 CLPD-NK patients, only five presented STAT3 mutations. WES profiling 13 cases negative for STAT3/STAT5B mutations uncovered an average 18 clonal, population rare and deleterious somatic variants per patient. mutational landscape showed that most patients carry a heavy burden, with major subclonal co-existing in leukemic clone....

10.1038/s41408-020-0309-2 article EN cc-by Blood Cancer Journal 2020-04-22

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 frequency STAT3 and STAT5b mutations. In this study, we characterized clinical biological features 137 patients affected by LGLL; data were retrospectively collected from 1997 to 2020 at 8 referral centers. Neutropenia anemia most relevant features, being present 54.2% 49.6% cases, respectively, including...

10.1182/blood.2021013489 article EN cc-by-nc-nd Blood 2022-09-12

Type T Large Granular Lymphocyte Leukemia (T-LGLL) is a chronic disorder characterized by the abnormal proliferation of clonal cytotoxic cells. The intriguing association T-LGLL with autoimmune and inflammatory diseases, most prominent example being rheumatoid arthritis, raises questions about underlying pathophysiologic relationships between these disorders which share several biological clinical features, notably neutropenia, considered as hallmark. Recent progress in molecular genetics...

10.1038/s41408-024-00977-0 article EN cc-by Blood Cancer Journal 2024-01-18

Tlarge granular lymphocyte leukemia (T-LGLL) is characterized by the expansion of several large clones, among which a subset lymphocytes showing constitutively activated STAT3, specific CD8+/CD4− phenotype and presence neutropenia has been identified. Although STAT3 an inducer transcription number oncogenes, so far its relationship with miRNAs not evaluated in T-LGLL patients. Here, we investigated whether could carry out pathogenetic role through altered expression miRNAs. The level 756...

10.3324/haematol.2019.225060 article EN cc-by-nc Haematologica 2019-08-29

Abstract Tγδ large granular lymphocyte leukemia (Tγδ LGLL) is a rare lymphoproliferative disease, scantily described in literature. A deep-analysis, an initial cohort of 9 LGLL compared to 23 healthy controls, shows that dominant clonotypes are mainly public and exhibit different V-(D)-J γ/δ usage between patients with symptomatic indolent neoplasm. Moreover, some share the same rearranged sequence. Data obtained enlarged (n = 36) indicate importance combined evaluation immunophenotype STAT...

10.1038/s41467-022-31015-x article EN cc-by Nature Communications 2022-06-08

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 wt cases. T-LGL lymphoproliferation sustained both somatic gain-offunction mutations (i.e. STAT5B) pro-inflammatory cytokines, but little information...

10.3324/haematol.2022.282306 article EN cc-by-nc Haematologica 2023-07-13

Clonal expansions of large granular lymphocytes (LGL) have been reported in a wide spectrum conditions, with LGL leukemia (LGLL) being the most extreme. However, boundaries between LGLL and clones are often subtle, both conditions can be detected several clinical scenarios, particularly patients cytopenias. The intricate overlap clonal expansion other disease entities characterized by unexplained cytopenias makes their classification challenging. Indeed, precisely assigning whether might...

10.3390/cancers14215236 article EN Cancers 2022-10-25

Finding an effective treatment for T-PLL patients remains a significant challenge. Alemtuzumab, currently the gold standard, is insufficient in managing aggressiveness of disease long term. Consequently, numerous efforts are underway to address this unmet clinical need. The rarity limits ability conduct robust trials, making silico, ex vivo, and vivo drug screenings essential designing new therapeutic strategies T-PLL. We conducted repurposing analysis based on gene expression data...

10.3390/ijms252413573 article EN International Journal of Molecular Sciences 2024-12-18

Large granular lymphocyte leukemias (LGLL) are sustained by proliferating cytotoxic T cells or NK cells, as happens in Chronic Lymphoproliferative Disorder of Natural Killer (CLPD-NK), whose etiology is only partly understood. Different hypotheses have been proposed on the original events triggering cell hyperactivation and transformation, including a role viral agents. In this perspective, we revise lines evidence that suggested pathogenetic LGLL exposure to retroviruses identified Epstein...

10.3389/fonc.2020.613570 article EN cc-by Frontiers in Oncology 2021-01-18

The biology of plasma cell dyscrasias (PCD) involves both genetic and immune-related factors. Since lesions are necessary but not sufficient for Multiple Myeloma (MM) evolution, several authors hypothesized that immune dysfunction involving B T counterparts plays a key role in the pathogenesis disease. aim this study is to evaluate impact cornerstone treatments into system shaping. A large series 976 bone marrow samples from 735 patients affected by PCD was studied flow analysis identify...

10.3389/fonc.2021.682658 article EN cc-by Frontiers in Oncology 2021-06-15
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