Giovanna Cutrona

@ospedalesanmartino.it

UO Molecular Pathology
IRCCS Ospedale Policlinico San Martino

RESEARCH INTERESTS

Leukemia/Lymphoma
147

Scopus Publications

6326

Scholar Citations

42

Scholar h-index

111

Scholar i10-index

Scopus Publications

  • Immunogenetic Architecture of Chronic Lymphocytic Leukemia at Early Stage: Insights from the O-CLL1 Cohort
    Davide Bagnara, Andrea Nicola Mazzarello, Monica Colombo, Ennio Nano, Niccolò Cardente, et al.
    Antibodies, 2026
    Background/Objectives: The immunoglobulin heavy-chain variable (IGHV) gene repertoire represents a characteristic feature of chronic lymphocytic leukemia (CLL), although its configuration is not well defined at the early disease stages. The IGHV repertoire of a cohort of early CLL patients was analyzed and compared to that of a “real-world” reference cohort. Methods: Patients from the O-CLL1 observational protocol, which enrolled only Binet stage A cases within twelve months from diagnosis, were studied. IGHV/IGHJ rearrangements were sequenced and annotated following ERIC recommendations, and stereotyped subsets were assigned using ARResT/AssignSubsets. The repertoire features were compared with the dataset of a real-world cohort of patients with heterogeneous staging (CTR cohort) and with published early-diagnosis series. Results: IGHV and IGHJ gene distributions and HCDR3-length profiles in O-CLL1 closely mirrored those of CTR, indicating that the BcR IG repertoire at diagnosis is already defined rather than being selected during disease progression. Mutated IGHV (M-CLL) predominated, with a frequency of stereotyped BcR IG comparable to that of other early-diagnosis cohorts. However, within this conserved framework, subset #4 was over-represented among M-CLL from O-CLL without an increased overall IGHV4-34 gene usage, suggestive of a selective expansion rather than a recombinational bias. Subset #4 cases retained canonical HCDR3 motifs and showed time-to-first-treatment like other M-CLL, likely reflecting the younger age structure of O-CLL1. Conclusions: Early-diagnosis CLL displays a biased IGHV repertoire with stereotyped configurations characteristic of CLL, including subsets that are rare in the normal B-cell repertoire. These findings support a central role for antigen-driven selection in shaping CLL evolution.
  • Intraclonal Enrichment of IL-23 Receptor Complex Expression in the Proliferative Fraction of Chronic Lymphocytic Leukemia
    Martina Cardillo, Fabiana Ferrero, Nadia Bertola, Ennio Nano, Rosanna Massara, et al.
    International Journal of Molecular Sciences, 2026
    Chronic lymphocytic leukemia (CLL) is a dynamic malignancy in which intraclonal subfractions differ in activation history and responsiveness to microenvironmental signals. Here, we investigated the expression and inducibility of IL-12 family receptor subunits (IL-23R, IL-12Rβ1, IL-12Rβ2) and the related receptor complexes in recirculating CLL cells, with a focus on CXCR4/CD5-defined fractions: the proliferative fraction (PF; CXCR4dim/CD5bright; most recently divided, tissue-emigrated cells) and the resting fraction (RF; CXCR4bright/CD5dim; older, quiescent cells). At baseline, IL-12Rβ1 was enriched in the PF and was associated with a higher proportion of cells expressing IL-23R and IL-12R receptor complexes. Concomitantly, RT-qPCR disclosed higher IL-12Rβ1 mRNA levels. Following antigen-independent activation with CpG or CpG + IL-15, there was a marked increase in IL-23R and IL-12Rβ1 but not in IL-12Rβ2 surface expression, resulting in preferential upregulation of the IL-23R complex over the IL-12R complex. Fraction-specific analyses showed stronger induction of IL-23R and IL-23R complex expression in PF compared with RF. These findings identify an intraclonal bias toward IL-23 responsiveness in the CLL cells with a phenotype of recently divided, tissue-emigrated cells and suggest the IL-23/IL-23R axis as a potential therapeutic target.
  • To Treat or Not to Treat: Navigating Early-Stage CLL in the Era of Targeted Therapy
    Enrica Antonia Martino, Santino Caserta, Ernesto Vigna, Giovanna Cutrona, Antonella Bruzzese, et al.
    European Journal of Haematology, 2026
    Chronic lymphocytic leukemia (CLL) is most frequently diagnosed at early, asymptomatic stages (Rai 0/Binet A), in which a watch‐and‐wait strategy remains the standard of care, based on historical trials demonstrating no overall survival benefit from early treatment. Over the past two decades, however, substantial advances in genomic profiling—including immunoglobulin heavy‐chain variable region (IGHV) mutational status, TP53 disruption, recurrent gene mutations, and complex karyotype—have uncovered marked biological heterogeneity among early‐stage patients and substantially improved prediction of disease progression. In parallel, targeted therapies such as Bruton tyrosine kinase (BTK) inhibitors and venetoclax‐based combinations have transformed the management of symptomatic CLL, raising renewed interest in whether early intervention might favorably alter the natural history of biologically high‐risk disease. In this review, we critically examine the evolution of prognostication in early‐stage CLL, integrate contemporary molecular and clinical risk models, and summarize evidence from both historical chemotherapy‐era studies and modern early‐intervention trials. We discuss key unresolved controversies, including reliance on surrogate endpoints, the risks of overtreatment, and the persistent absence of an overall survival benefit across all early‐treatment strategies. Finally, we outline future research priorities, including refined genomic stratification, minimal residual disease‐driven (MRD)‐driven approaches, and combination targeted therapies currently under investigation. Despite renewed interest in preemptive treatment, available evidence supports continued observation for asymptomatic patients outside clinical trials.
  • Targeting the p53/xCT/GSH Axis with PRIMA-1Met Combined with Sulfasalazine Shows Therapeutic Potential in Chronic Lymphocytic Leukemia
    Martina Pasino, Andrea Speciale, Silvia Ravera, Giovanna Cutrona, Rosanna Massara, et al.
    International Journal of Molecular Sciences, 2025
    In Chronic Lymphocytic Leukemia (CLL), mutations at the TP53 tumor suppressor gene are an important hallmark since they may strongly influence the therapeutic decision. PRIMA-1Met (also known as APR-246/Eprenetapopt) is a small molecule able to restore the wild-type (wt) p53 conformation to mutant p53 proteins and to stimulate apoptosis in tumor cells; in addition, it can deplete the glutathione reservoir, increasing reactive oxygen species (ROS) production. In this study, we investigated whether combining PRIMA-1Met with Sulfasalazine (SAS), a SLC7A11/xCT inhibitor, reduces CLL cell viability by targeting mutant p53 and the glutathione pathway. The results demonstrated that, in CLL cells, PRIMA-1Met did not restore the wt functions in the mutant p53 proteins, but it strongly reduced the antioxidant defense and induced cell death. PRIMA-1Met and SAS combination synergistically reduced cell survival regardless of p53 status and further impaired antioxidant capacity, especially in mutant p53 cells, linking their cytotoxic effect to redox imbalance. Thus, the association of PRIMA-1Met with drugs targeting the antioxidant response could represent a valid strategy to kill CLL cells carrying either wt or mutant p53.
  • MicroRNA Profiling as a Predictive Indicator for Time to First Treatment in Chronic Lymphocytic Leukemia: Insights from the O-CLL1 Prospective Study
    Ennio Nano, Francesco Reggiani, Adriana Agnese Amaro, Paola Monti, Monica Colombo, et al.
    Non Coding RNA, 2024
    A “watch and wait” strategy, delaying treatment until active disease manifests, is adopted for most CLL cases; however, prognostic models incorporating biomarkers have shown to be useful to predict treatment requirement. In our prospective O-CLL1 study including 224 patients, we investigated the predictive role of 513 microRNAs (miRNAs) on time to first treatment (TTFT). In the context of this study, six well-established variables (i.e., Rai stage, beta-2-microglobulin levels, IGVH mutational status, del11q, del17p, and NOTCH1 mutations) maintained significant associations with TTFT in a basic multivariable model, collectively yielding a Harrell’s C-index of 75% and explaining 45.4% of the variance in the prediction of TTFT. Concerning miRNAs, 73 out of 513 were significantly associated with TTFT in a univariable model; of these, 16 retained an independent relationship with the outcome in a multivariable analysis. For 8 of these (i.e., miR-582-3p, miR-33a-3p, miR-516a-5p, miR-99a-5p, and miR-296-3p, miR-502-5p, miR-625-5p, and miR-29c-3p), a lower expression correlated with a shorter TTFT, whereas in the remaining eight (i.e., miR-150-5p, miR-148a-3p, miR-28-5p, miR-144-5p, miR-671-5p, miR-1-3p, miR-193a-3p, and miR-124-3p), the higher expression was associated with shorter TTFT. Integrating these miRNAs into the basic model significantly enhanced predictive accuracy, raising the Harrell’s C-index to 81.1% and the explained variation in TTFT to 63.3%. Moreover, the inclusion of the miRNA scores enhanced the integrated discrimination improvement (IDI) and the net reclassification index (NRI), underscoring the potential of miRNAs to refine CLL prognostic models and providing insights for clinical decision-making. In silico analyses on the differently expressed miRNAs revealed their potential regulatory functions of several pathways, including those involved in the therapeutic responses. To add a biological context to the clinical evidence, an miRNA–mRNA correlation analysis revealed at least one significant negative correlation between 15 of the identified miRNAs and a set of 50 artificial intelligence (AI)-selected genes, previously identified by us as relevant for TTFT prediction in the same cohort of CLL patients. In conclusion, the identification of specific miRNAs as predictors of TTFT holds promise for enhancing risk stratification in CLL to predict therapeutic needs. However, further validation studies and in-depth functional analyses are required to confirm the robustness of these observations and to facilitate their translation into meaningful clinical utility.
  • Unexpected chronic lymphocytic leukemia B cell activation by bisphosphonates
    Andrea N. Mazzarello, Elena Gugiatti, Vanessa Cossu, Nadia Bertola, Davide Bagnara, et al.
    Cancer Immunology Immunotherapy, 2024
    Chronic lymphocytic leukemia (CLL) is a disease of the elderly, often presenting comorbidities like osteoporosis and requiring, in a relevant proportion of cases, treatment with bisphosphonates (BPs). This class of drugs was shown in preclinical investigations to also possess anticancer properties. We started an in vitro study of the effects of BPs on CLL B cells activated by microenvironment-mimicking stimuli and observed that, depending on drug concentration, hormetic effects were induced on the leukemic cells. Higher doses induced cytotoxicity whereas at lower concentrations, more likely occurring in vivo, the drugs generated a protective effect from spontaneous and chemotherapy-induced apoptosis, and augmented CLL B cell activation/proliferation. This CLL-activation effect promoted by the BPs was associated with markers of poor CLL prognosis and required the presence of bystander stromal cells. Functional experiments suggested that this phenomenon involves the release of soluble factors and is increased by cellular contact between stroma and CLL B cells. Since CLL patients often present comorbidities such as osteoporosis and considering the diverse outcomes in both CLL disease progression and CLL response to treatment among patients, illustrating this phenomenon holds potential significance in driving additional investigations.
  • Unraveling the Bone Tissue Microenvironment in Chronic Lymphocytic Leukemia
    Paolo Giannoni, Cecilia Marini, Giovanna Cutrona, Gian Mario Sambuceti, Franco Fais, et al.
    Cancers, 2023
    Chronic lymphocytic leukemia (CLL) is the most frequent leukemia in Western countries. Although characterized by the progressive expansion and accumulation of leukemic B cells in peripheral blood, CLL cells develop in protective niches mainly located within lymph nodes and bone marrow. Multiple interactions between CLL and microenvironmental cells may favor the expansion of a B cell clone, further driving immune cells toward an immunosuppressive phenotype. Here, we summarize the current understanding of bone tissue alterations in CLL patients, further addressing and suggesting how the multiple interactions between CLL cells and osteoblasts/osteoclasts can be involved in these processes. Recent findings proposing the disruption of the endosteal niche by the expansion of a leukemic B cell clone appear to be a novel field of research to be deeply investigated and potentially relevant to provide new therapeutic approaches.
  • The time to first treatment is an independent predictor of overall survival in chronic lymphocytic leukemia
    Fortunato Morabito, Giovanni Tripepi, Francesca Romana Mauro, Luca Laurenti, Gianluigi Reda, et al.
    American Journal of Hematology, 2023
  • Genes selection using deep learning and explainable artificial intelligence for chronic lymphocytic leukemia predicting the need and time to therapy
    Fortunato Morabito, Carlo Adornetto, Paola Monti, Adriana Amaro, Francesco Reggiani, et al.
    Frontiers in Oncology, 2023
    Analyzing gene expression profiles (GEP) through artificial intelligence provides meaningful insight into cancer disease. This study introduces DeepSHAP Autoencoder Filter for Genes Selection (DSAF-GS), a novel deep learning and explainable artificial intelligence-based approach for feature selection in genomics-scale data. DSAF-GS exploits the autoencoder’s reconstruction capabilities without changing the original feature space, enhancing the interpretation of the results. Explainable artificial intelligence is then used to select the informative genes for chronic lymphocytic leukemia prognosis of 217 cases from a GEP database comprising roughly 20,000 genes. The model for prognosis prediction achieved an accuracy of 86.4%, a sensitivity of 85.0%, and a specificity of 87.5%. According to the proposed approach, predictions were strongly influenced by CEACAM19 and PIGP, moderately influenced by MKL1 and GNE, and poorly influenced by other genes. The 10 most influential genes were selected for further analysis. Among them, FADD, FIBP, FIBP, GNE, IGF1R, MKL1, PIGP, and SLC39A6 were identified in the Reactome pathway database as involved in signal transduction, transcription, protein metabolism, immune system, cell cycle, and apoptosis. Moreover, according to the network model of the 3D protein-protein interaction (PPI) explored using the NetworkAnalyst tool, FADD, FIBP, IGF1R, QTRT1, GNE, SLC39A6, and MKL1 appear coupled into a complex network. Finally, all 10 selected genes showed a predictive power on time to first treatment (TTFT) in univariate analyses on a basic prognostic model including IGHV mutational status, del(11q) and del(17p), NOTCH1 mutations, β2-microglobulin, Rai stage, and B-lymphocytosis known to predict TTFT in CLL. However, only IGF1R [hazard ratio (HR) 1.41, 95% CI 1.08-1.84, P=0.013), COL28A1 (HR 0.32, 95% CI 0.10-0.97, P=0.045), and QTRT1 (HR 7.73, 95% CI 2.48-24.04, P<0.001) genes were significantly associated with TTFT in multivariable analyses when combined with the prognostic factors of the basic model, ultimately increasing the Harrell’s c-index and the explained variation to 78.6% (versus 76.5% of the basic prognostic model) and 52.6% (versus 42.2% of the basic prognostic model), respectively. Also, the goodness of model fit was enhanced (χ2 = 20.1, P=0.002), indicating its improved performance above the basic prognostic model. In conclusion, DSAF-GS identified a group of significant genes for CLL prognosis, suggesting future directions for bio-molecular research.
  • A High Percentage of CD16+ Monocytes Correlates with the Extent of Bone Erosion in Chronic Lymphocytic Leukemia Patients: The Impact of Leukemic B Cells in Monocyte Differentiation and Osteoclast Maturation
    Paolo Giannoni, Cecilia Marini, Giovanna Cutrona, Katia Todoerti, Antonino Neri, et al.
    Cancers, 2022
    Significant skeletal alterations are present in Chronic Lymphocytic Leukemia (CLL) patients; bone erosion, particularly evident in the long bone shaft, appeared increased in the progressive disease stage. Moreover, the partial colonization of the bone with reactive bone marrow we documented via PET-FDG imaging suggests that neoplastic cell overgrowth contributes to bone derangement. Indeed, cytokines released by leukemic B cells impair osteoblast differentiation and enhance osteoclast formation in vitro. CD16, Fcγ-RIIIa, has been previously indicated as a marker of osteoclast precursors. We demonstrate, here, that the percentage of circulating monocytes, CD16+, is significantly higher in CLL patients than in normal controls and directly correlated with the extent of bone erosion. When we assessed if healthy monocytes, treated with a CLL-conditioned medium, modulated RANK, RANKL and CD16, we observed that all these molecules were up-regulated and CD16 to a greater extent. Altogether, these findings suggest that leukemic cells facilitate osteoclast differentiation. Interestingly, the evidence that monocytes, polarized toward the M2 phenotype, were characterized by high CD16 expression and showed a striking propensity to differentiate toward osteoclasts may provide further explanations for the enhanced levels of bone erosion detected, in agreement with the high number of immunosuppressive-M2 cells present in these patients.
  • The spectrum of subclonal TP53 mutations in chronic lymphocytic leukemia: A next generation sequencing retrospective study
    Giuseppa De Luca, Giannamaria Cerruti, Sonia Lastraioli, Romana Conte, Adalberto Ibatici, et al.
    Hematological Oncology, 2022
  • Old and New Facts and Speculations on the Role of the B Cell Receptor in the Origin of Chronic Lymphocytic Leukemia
    Davide Bagnara, Andrea Nicola Mazzarello, Fabio Ghiotto, Monica Colombo, Giovanna Cutrona, et al.
    International Journal of Molecular Sciences, 2022
  • MiR-146b-5p regulates IL-23 receptor complex expression in chronic lymphocytic leukemia cells
    Serena Matis, Anna Grazia Recchia, Monica Colombo, Martina Cardillo, Marina Fabbi, et al.
    Blood Advances, 2022
  • Characterizing Features of Human Circulating B Cells Carrying CLL-Like Stereotyped Immunoglobulin Rearrangements
    Davide Bagnara, Monica Colombo, Daniele Reverberi, Serena Matis, Rosanna Massara, et al.
    Frontiers in Oncology, 2022
  • LINC00152 expression in normal and Chronic Lymphocytic Leukemia B cells
    Serena Matis, Martina Rossi, Lorenzo Brondolo, Martina Cardillo, Daniele Reverberi, et al.
    Hematological Oncology, 2022
  • Chronic lymphocytic leukemia cells impair osteoblastogenesis and promote osteoclastogenesis: Role of TNFα, IL-6 and IL-11 cytokines
    Paolo Giannoni, Cecilia Marini, Giovanna Cutrona, Serena Matis, Maria Cristina Capra, et al.
    Haematologica, 2021
  • Lymphocyte Doubling Time As A Key Prognostic Factor To Predict Time To First Treatment In Early-Stage Chronic Lymphocytic Leukemia
    Fortunato Morabito, Giovanni Tripepi, Riccardo Moia, Anna Grazia Recchia, Paola Boggione, et al.
    Frontiers in Oncology, 2021
  • Effectiveness of ibrutinib as first-line therapy for chronic lymphocytic leukemia patients and indirect comparison with rituximab-bendamustine: Results of study on 486 cases outside clinical trials
    Fortunato Morabito, Giovanni Tripepi, Giovanni Del Poeta, Francesca Romana Mauro, Gianluigi Reda, et al.
    American Journal of Hematology, 2021
  • TP53 disruption as a risk factor in the era of targeted therapies: A multicenter retrospective study of 525 chronic lymphocytic leukemia cases
    Fortunato Morabito, Giovanni Del Poeta, Francesca Romana Mauro, Gianluigi Reda, Paolo Sportoletti, et al.
    American Journal of Hematology, 2021
  • Validation of the Alternative International Prognostic Score-E (AIPS-E): Analysis of Binet stage A chronic lymphocytic leukemia patients enrolled into the O-CLL1-GISL protocol
    Fortunato Morabito, Giovanni Tripepi, Ernesto Vigna, Sabrina Bossio, Graziella D’Arrigo, et al.
    European Journal of Haematology, 2021
  • Assessment of the 4-factor score: Retrospective analysis of 586 CLL patients receiving ibrutinib. A campus CLL study
    Fortunato Morabito, Giovanni Tripepi, Giovanni Del Poeta, Francesca Romana Mauro, Gianluigi Reda, et al.
    American Journal of Hematology, 2021
  • Comparison of ibrutinib and idelalisib plus rituximab in real-life relapsed/resistant chronic lymphocytic leukemia cases
    Fortunato Morabito, Giovanni Tripepi, Giovanni Del Poeta, Francesca Romana Mauro, Gianluigi Reda, et al.
    European Journal of Haematology, 2021
  • Human pluripotent stem cells identify molecular targets of trisomy 12 in chronic lymphocytic leukemia patients
    Jennifer C. Reid, Diana Golubeva, Allison L. Boyd, Cameron G. Hollands, Charisa Henly, et al.
    Cell Reports, 2021
  • Spotlight on melphalan flufenamide: An up-and-coming therapy for the treatment of myeloma
    Fortunato Morabito, Giovanni Tripepi, Enrica Antonia Martino, Ernesto Vigna, Francesco Mendicino, et al.
    Drug Design Development and Therapy, 2021
  • Antitumor effects of PRIMA-1 and PRIMA-1met (APR246) in hematological malignancies: Still a mutant p53-dependent affair?
    Paola Menichini, Paola Monti, Andrea Speciale, Giovanna Cutrona, Serena Matis, et al.
    Cells, 2021

RECENT SCHOLAR PUBLICATIONS

  • Immunogenetic Architecture of Chronic Lymphocytic Leukemia at Early Stage: Insights from the O-CLL1 Cohort
    D Bagnara, AN Mazzarello, M Colombo, E Nano, N Cardente, F Ferrero, ...
    Antibodies 15 (2), 25 , 2026
    2026
  • Intraclonal Enrichment of IL-23 Receptor Complex Expression in the Proliferative Fraction of Chronic Lymphocytic Leukemia
    M Cardillo, F Ferrero, N Bertola, E Nano, R Massara, MC Capra, ...
    International Journal of Molecular Sciences 27 (3), 1202 , 2026
    2026
  • To Treat or Not to Treat: Navigating Early‐Stage CLL in the Era of Targeted Therapy
    EA Martino, S Caserta, E Vigna, G Cutrona, A Bruzzese, F Mendicino, ...
    European Journal of Haematology , 2026
    2026
  • Asymmetric induction of IL-23R by CpG and IL-15 in proliferative CLL fractions highlights intraclonal heterogeneity in chronic lymphocytic leukemia
    M Cardillo, N Bertola, F Ferrero, R Massara, MC Capra, D Reverberi, ...
    bioRxiv, 2025.08. 27.672649 , 2025
    2025
  • Targeting the p53/xCT/GSH Axis with PRIMA-1 Met Combined with Sulfasalazine Shows Therapeutic Potential in Chronic Lymphocytic Leukemia
    M Pasino, A Speciale, S Ravera, G Cutrona, R Massara, N Bertola, ...
    International Journal of Molecular Sciences 26 (12), 5559 , 2025
    2025
    Citations: 2
  • Regulation of mitochondrial metabolism by IL12-family cytokines in chronic lymphocytic leukemia: A novel perspective on therapeutic resistance
    N Bertola, F Ferrero, V Cossu, E Nano, M Colombo, R Massara, ...
    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION 55 , 2025
    2025
  • MicroRNA Profiling as a Predictive Indicator for Time to First Treatment in Chronic Lymphocytic Leukemia: Insights from the O-CLL1 Prospective Study
    E Nano, F Reggiani, AA Amaro, P Monti, M Colombo, N Bertola, F Ferrero, ...
    Non-coding RNA 10 (5), 46 , 2024
    2024
    Citations: 2
  • Unexpected chronic lymphocytic leukemia B cell activation by bisphosphonates
    AN Mazzarello, E Gugiatti, V Cossu, N Bertola, D Bagnara, S Carta, ...
    Cancer Immunology, Immunotherapy 73 (2), 27 , 2024
    2024
  • Unraveling the bone tissue microenvironment in chronic lymphocytic leukemia
    P Giannoni, C Marini, G Cutrona, GM Sambuceti, F Fais, D de Totero
    Cancers 15 (20), 5058 , 2023
    2023
    Citations: 12
  • Genes selection using deep learning and explainable artificial intelligence for chronic lymphocytic leukemia predicting the need and time to therapy
    F Morabito, C Adornetto, P Monti, A Amaro, F Reggiani, M Colombo, ...
    Frontiers in oncology 13, 1198992 , 2023
    2023
    Citations: 20
  • The time to first treatment is an independent predictor of overall survival in chronic lymphocytic leukemia
    F Morabito, G Tripepi, FR Mauro, L Laurenti, G Reda, R Moia, ...
    American Journal of Hematology 98 (7), E157-E160 , 2023
    2023
    Citations: 1
  • Genes selection using deep learning and explainable artificial intelligence for chronic lymphocytic leukemia predicting the need and time to therapy
    S Galimberti, A Neri, C Adornetto, F Morabito, C Adornetto, P Monti, ...
    2023
  • A high percentage of CD16+ monocytes correlates with the extent of bone erosion in chronic lymphocytic leukemia patients: The impact of leukemic B cells in monocyte …
    P Giannoni, C Marini, G Cutrona, K Todoerti, A Neri, A Ibatici, ...
    Cancers 14 (23), 5979 , 2022
    2022
    Citations: 8
  • The spectrum of subclonal TP53 mutations in chronic lymphocytic leukemia: A next generation sequencing retrospective study
    G De Luca, G Cerruti, S Lastraioli, R Conte, A Ibatici, N Di Felice, ...
    Hematological Oncology 40 (5), 962-975 , 2022
    2022
    Citations: 6
  • Old and new facts and speculations on the role of the B cell receptor in the origin of chronic lymphocytic leukemia
    D Bagnara, AN Mazzarello, F Ghiotto, M Colombo, G Cutrona, F Fais, ...
    International Journal of Molecular Sciences 23 (22), 14249 , 2022
    2022
    Citations: 24
  • MiR-146b-5p regulates IL-23 receptor complex expression in chronic lymphocytic leukemia cells
    S Matis, A Grazia Recchia, M Colombo, M Cardillo, M Fabbi, K Todoerti, ...
    Blood Advances 6 (20), 5593-5612 , 2022
    2022
    Citations: 17
  • Characterizing features of human circulating B cells carrying CLL-like stereotyped immunoglobulin rearrangements
    D Bagnara, M Colombo, D Reverberi, S Matis, R Massara, N Cardente, ...
    Frontiers in oncology 12, 894419 , 2022
    2022
    Citations: 13
  • LINC00152 expression in normal and Chronic Lymphocytic Leukemia B cells
    S Matis, M Rossi, L Brondolo, M Cardillo, D Reverberi, R Massara, ...
    Hematological Oncology 40 (1), 41-48 , 2022
    2022
    Citations: 10
  • Lymphocyte doubling time as a key prognostic factor to predict time to first treatment in early-stage chronic lymphocytic leukemia
    F Morabito, G Tripepi, R Moia, AG Recchia, P Boggione, FR Mauro, ...
    Frontiers in oncology 11, 684621 , 2021
    2021
    Citations: 17
  • TP53 disruption as a risk factor in the era of targeted therapies: A multicenter retrospective study of 525 chronic lymphocytic leukemia cases
    F Morabito, G Del Poeta, FR Mauro, G Reda, P Sportoletti, L Laurenti, ...
    American Journal of Hematology 96 (8), E306-E310 , 2021
    2021
    Citations: 20

MOST CITED SCHOLAR PUBLICATIONS

  • In vivo measurements document the dynamic cellular kinetics of chronic lymphocytic leukemia B cells
    BT Messmer, D Messmer, SL Allen, JE Kolitz, P Kudalkar, D Cesar, ...
    The Journal of clinical investigation 115 (3), 755-764 , 2005
    2005
    Citations: 879
  • CD38 and chronic lymphocytic leukemia: a decade later
    F Malavasi, S Deaglio, R Damle, G Cutrona, M Ferrarini, N Chiorazzi
    Blood, The Journal of the American Society of Hematology 118 (13), 3470-3478 , 2011
    2011
    Citations: 338
  • Effects in live cells of a c-myc anti-gene PNA linked to a nuclear localization signal
    G Cutrona, EM Carpaneto, M Ulivi, S Roncella, O Landt, M Ferrarini, ...
    Nature biotechnology 18 (3), 300-303 , 2000
    2000
    Citations: 322
  • International prognostic score for asymptomatic early-stage chronic lymphocytic leukemia
    A Condoluci, L Terzi di Bergamo, P Langerbeins, MA Hoechstetter, ...
    Blood, The Journal of the American Society of Hematology 135 (21), 1859-1869 , 2020
    2020
    Citations: 195
  • Selective expansion of cytotoxic T lymphocytes with a CD4 + CD56 + surface phenotype and a T helper type 1 profile of cytokine secretion in the liver of patients …
    V Barnaba, A Franco, M Paroli, R Benvenuto, G De Petrillo, VL Burgio, ...
    The Journal of Immunology 152 (6), 3074-3087 , 1994
    1994
    Citations: 181
  • Interleukin-21 receptor (IL-21R) is up-regulated by CD40 triggering and mediates proapoptotic signals in chronic lymphocytic leukemia B cells
    D de Totero, R Meazza, S Zupo, G Cutrona, S Matis, M Colombo, ...
    Blood 107 (9), 3708-3715 , 2006
    2006
    Citations: 170
  • The opposite effects of IL-15 and IL-21 on CLL B cells correlate with differential activation of the JAK/STAT and ERK1/2 pathways
    D de Totero, R Meazza, M Capaia, M Fabbi, B Azzarone, E Balleari, ...
    Blood, The Journal of the American Society of Hematology 111 (2), 517-524 , 2008
    2008
    Citations: 146
  • The chronic lymphocytic leukemia international prognostic index predicts time to first treatment in early CLL: Independent validation in a prospective cohort of early stage …
    S Molica, TD Shanafelt, D Giannarelli, M Gentile, R Mirabelli, G Cutrona, ...
    American journal of hematology 91 (11), 1090-1095 , 2016
    2016
    Citations: 126
  • Small nucleolar RNAs as new biomarkers in chronic lymphocytic leukemia
    D Ronchetti, L Mosca, G Cutrona, G Tuana, M Gentile, S Fabris, L Agnelli, ...
    BMC medical genomics 6 (1), 27 , 2013
    2013
    Citations: 114
  • Heterogeneity of TP53 Mutations and P53 Protein Residual Function in Cancer: Does It Matter?
    P Monti, P Menichini, A Speciale, G Cutrona, F Fais, E Taiana, A Neri, ...
    Frontiers in oncology 10, 593383 , 2020
    2020
    Citations: 113
  • Apoptotic cells overexpress vinculin and induce vinculin-specific cytotoxic T-cell cross-priming
    A Propato, G Cutrona, V Francavilla, M Ulivi, E Schiaffella, O Landt, ...
    Nature medicine 7 (7), 807-813 , 2001
    2001
    Citations: 104
  • Predictive value of β2-microglobulin (β2-m) levels in chronic lymphocytic leukemia since Binet A stages
    M Gentile, G Cutrona, A Neri, S Molica, M Ferrarini, F Morabito
    Haematologica 94 (6), 887 , 2009
    2009
    Citations: 102
  • Validation of the CLL-IPI and comparison with the MDACC prognostic index in newly diagnosed patients
    M Gentile, TD Shanafelt, D Rossi, L Laurenti, FR Mauro, S Molica, ...
    Blood, The Journal of the American Society of Hematology 128 (16), 2093-2095 , 2016
    2016
    Citations: 97
  • Clinical monoclonal B lymphocytosis versus Rai 0 chronic lymphocytic leukemia: a comparison of cellular, cytogenetic, molecular, and clinical features
    F Morabito, L Mosca, G Cutrona, L Agnelli, G Tuana, M Ferracin, B Zagatti, ...
    Clinical cancer research 19 (21), 5890-5900 , 2013
    2013
    Citations: 96
  • Expression of CD10 by human T cells that undergo apoptosis both in vitro and in vivo
    G Cutrona, N Leanza, M Ulivi, G Melioli, VL Burgio, G Mazzarello, ...
    Blood, The Journal of the American Society of Hematology 94 (9), 3067-3076 , 1999
    1999
    Citations: 94
  • Integrative genomics analyses reveal molecularly distinct subgroups of B-cell chronic lymphocytic leukemia patients with 13q14 deletion
    L Mosca, S Fabris, M Lionetti, K Todoerti, L Agnelli, F Morabito, G Cutrona, ...
    Clinical Cancer Research 16 (23), 5641-5653 , 2010
    2010
    Citations: 92
  • Molecular and transcriptional characterization of 17p loss in B‐cell chronic lymphocytic leukemia
    S Fabris, L Mosca, K Todoerti, G Cutrona, M Lionetti, D Intini, S Matis, ...
    Genes, Chromosomes and Cancer 47 (9), 781-793 , 2008
    2008
    Citations: 84
  • B lymphocytes in humans express ZAP‐70 when activated in vivo
    G Cutrona, M Colombo, S Matis, D Reverberi, M Dono, V Tarantino, ...
    European journal of immunology 36 (3), 558-569 , 2006
    2006
    Citations: 81
  • Biological and clinical relevance of quantitative global methylation of repetitive DNA sequences in chronic lymphocytic leukemia
    S Fabris, V Bollati, L Agnelli, F Morabito, V Motta, G Cutrona, S Matis, ...
    Epigenetics 6 (2), 188-194 , 2011
    2011
    Citations: 80
  • microRNAome expression in chronic lymphocytic leukemia: comparison with normal B-cell subsets and correlations with prognostic and clinical parameters
    M Negrini, G Cutrona, C Bassi, S Fabris, B Zagatti, M Colombo, ...
    Clinical Cancer Research 20 (15), 4141-4153 , 2014
    2014
    Citations: 75