Lorenzo Pignataro
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Lorenzo Pignataro has a total of 408 co-authors. Here are the top co-authors by number of shared publications:
- Sara Torretta
Fondazione Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Ca' Granda Ospedale Maggiore Policlinico, Department of Otorhinolaryngology, Italy
65 shared publications - Pasquale Capaccio
Department of Otorhinolaryngology & Head and Neck Surgery, Fatebenefratelli Hospital, ASST Fatebenefratelli Sacco, 20121 Milan, Italy
46 shared publications - Giancarlo Pruneri
Department of Diagnostic Innovation, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy
29 shared publications - Adrian Andronache
Experimental Therapeutics Program, IFOM ETS - The AIRC Institute of Molecular Oncology Milan, Italy
27 shared publications - Alessandra Tucci
Hematology Division, ERN/EuroloodNet, ASST Spedali Civili di Brescia, Brescia, Italy
27 shared publications - Andrés José Maria Ferreri
Strategic Program on Lymphomas IRCCS San Raffaele Scientific Institute, Milano and Vita‐Salute San Raffaele University Milan Italy
27 shared publications
Latest Publications
- Open Access
- 30 December 2025
- Published by MDPI AG in Biomedicines
- Vol. 14 (1) , 77
Nasal Cytology Is Useful for Evaluating and Monitoring the Therapeutic Response to Biologics in Chronic Rhinosinusitis with Nasal Polyposis
Background/Objectives: In recent years, the recognition that type 2 inflammation plays a leading role in CRSwNP has enabled the more tailored treatment of the disease through improved patient endotyping. We studied 45 patients with severe CRSwNP who were treated with dupilumab or mepolizumab. The aim was to evaluate the efficacy of these treatments on endoscopic, clinical and patient reported parameters, and to assess whether nasal cytology could be useful for identifying responsive patients and monitoring their response to biologic drugs. Methods: Follow-up visits were scheduled at baseline (T0), and at 3 (T3), 6 (T6), 12 (T12), and 24 months (T24). At each visit, patients underwent blood analysis, nasal endoscopy, and nasal scraping for cytology. They also completed the SNOT-22 questionnaire, a visual analog scale (VAS) for nasal obstruction and smell perception, and the Asthma Control Test (ACT) test in cases of concomitant asthma. Results: Biological therapy demonstrated broad efficacy in disease management, based on both clinical and cytological findings. The Nasal Polyp Score, SNOT-22 questionnaire, VAS scores for nasal obstruction and smell, and ACT score showed progressive improvement. Blood eosinophil counts and total IgE levels also decreased over time (T0 vs. T24: p = 0.008 and p < 0.001, respectively). At nasal cytology, a reduction in eosinophil cell count and in the mixed mast cell–eosinophil pattern during treatment with both biologics were observed (T0 vs. T24: p < 0.001). Positive effects were typically recorded within six months of treatment and were sustained after two years. Conclusions: Although the histological evaluation of infiltrated tissues remains the gold standard for assessing mucosal eosinophilia, nasal cytology appears to be a simpler, non-invasive, and repeatable method for evaluating local eosinophilia. Identifying endotypes and assessing the severity of inflammation are crucial for predicting the efficacy of different treatment options.
- 30 December 2025
- Published by MDPI AG in Biomedicines
- Vol. 14 (1) , 77
Open AccessNasal Cytology Is Useful for Evaluating and Monitoring the Therapeutic Response to Biologics in Chronic Rhinosinusitis with Nasal Polyposis
Background/Objectives: In recent years, the recognition that type 2 inflammation plays a leading role in CRSwNP has enabled the more tailored treatment of the disease through improved patient endotyping. We studied 45 patients with severe CRSwNP who were treated with dupilumab or mepolizumab. The aim was to evaluate the efficacy of these treatments on endoscopic, clinical and patient reported parameters, and to assess whether nasal cytology could be useful for identifying responsive patients and monitoring their response to biologic drugs. Methods: Follow-up visits were scheduled at baseline (T0), and at 3 (T3), 6 (T6), 12 (T12), and 24 months (T24). At each visit, patients underwent blood analysis, nasal endoscopy, and nasal scraping for cytology. They also completed the SNOT-22 questionnaire, a visual analog scale (VAS) for nasal obstruction and smell perception, and the Asthma Control Test (ACT) test in cases of concomitant asthma. Results: Biological therapy demonstrated broad efficacy in disease management, based on both clinical and cytological findings. The Nasal Polyp Score, SNOT-22 questionnaire, VAS scores for nasal obstruction and smell, and ACT score showed progressive improvement. Blood eosinophil counts and total IgE levels also decreased over time (T0 vs. T24: p = 0.008 and p < 0.001, respectively). At nasal cytology, a reduction in eosinophil cell count and in the mixed mast cell–eosinophil pattern during treatment with both biologics were observed (T0 vs. T24: p < 0.001). Positive effects were typically recorded within six months of treatment and were sustained after two years. Conclusions: Although the histological evaluation of infiltrated tissues remains the gold standard for assessing mucosal eosinophilia, nasal cytology appears to be a simpler, non-invasive, and repeatable method for evaluating local eosinophilia. Identifying endotypes and assessing the severity of inflammation are crucial for predicting the efficacy of different treatment options.
- Open Access
- 3 July 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table S4 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with MYC and BCL2 Rearrangements
IGH and CD79B expression and interaction in HGBCL-DH-BCL2(-BCL6), and relation to follicular lymphoma.
- 3 July 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S4 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with MYC and BCL2 Rearrangements
IGH and CD79B expression and interaction in HGBCL-DH-BCL2(-BCL6), and relation to follicular lymphoma.
- Open Access
- 3 July 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table S5 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with MYC and BCL2 Rearrangements
Configuration of IGH, MYC and BCL2 loci in HGBCL-DH-BCL2(-BCL6) and RAG1/2 involvement in t(8;22).
- 3 July 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S5 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with MYC and BCL2 Rearrangements
Configuration of IGH, MYC and BCL2 loci in HGBCL-DH-BCL2(-BCL6) and RAG1/2 involvement in t(8;22).
- Open Access
- 3 July 2025
- Published by American Association for Cancer Research (AACR)
Supplementary figure S6 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with MYC and BCL2 Rearrangements
Cytogenetic of COH-DHL1 and COH-THL1 HGBCL-DH-BCL2(-BCL6) cell line models (A-D); In vivo secondary Ighv gene rearrangements in BCR-less murine lambda-MYC lymphomas (E-J)
- 3 July 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary figure S6 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with MYC and BCL2 Rearrangements
Cytogenetic of COH-DHL1 and COH-THL1 HGBCL-DH-BCL2(-BCL6) cell line models (A-D); In vivo secondary Ighv gene rearrangements in BCR-less murine lambda-MYC lymphomas (E-J)
- Open Access
- 3 July 2025
- Published by American Association for Cancer Research (AACR)
Supplementary figure S4 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with MYC and BCL2 Rearrangements
IGH and CD79B expression, complex formation and IGH isotype choice in DLBCL and HGBCL-DH-BCL2
- 3 July 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary figure S4 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with MYC and BCL2 Rearrangements
IGH and CD79B expression, complex formation and IGH isotype choice in DLBCL and HGBCL-DH-BCL2
- Open Access
- 3 July 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table S1 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with MYC and BCL2 Rearrangements
DLBCL cases included in the study.
- 3 July 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S1 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with MYC and BCL2 Rearrangements
DLBCL cases included in the study.
- Open Access
- 3 July 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table S7 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with MYC and BCL2 Rearrangements
Supplementary Table S7 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with MYC and BCL2 Rearrangements
- 3 July 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S7 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with MYC and BCL2 Rearrangements
Supplementary Table S7 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with MYC and BCL2 Rearrangements
- Open Access
- 3 July 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table S2 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with MYC and BCL2 Rearrangements
Bulk and spatial gene expression data of MYC and BCL2 dual expressor DLBCL and HGBCL-DH-BCL2 (-BCL6).
- 3 July 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S2 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with MYC and BCL2 Rearrangements
Bulk and spatial gene expression data of MYC and BCL2 dual expressor DLBCL and HGBCL-DH-BCL2 (-BCL6).
- Open Access
- 3 July 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table S3 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with MYC and BCL2 Rearrangements
Non synonymus SNVs, IGHV gene rearrangements, AID expression status and N-glycosylation motifs in IGHV domains of HGBCL-DH-BCL2(-BCL6).
- 3 July 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S3 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with MYC and BCL2 Rearrangements
Non synonymus SNVs, IGHV gene rearrangements, AID expression status and N-glycosylation motifs in IGHV domains of HGBCL-DH-BCL2(-BCL6).