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1. Additional file 2 of Correction to: Focal adhesion kinase inhibitor TAE226 combined with Sorafenib slows down hepatocellular carcinoma by multiple epigenetic effects

Author

Romito, Ilaria, Porru, Manuela, Braghini, Maria Rita, Pompili, Luca, Panera, Nadia, Crudele, Annalisa, Gnani, Daniela, De Stefanis, Cristiano, Scarsella, Marco, Pomella, Silvia, Mortera, Stefano Levi, de Billy, Emmanuel, Conti, Adrian Libenzio, Marzano, Valeria, Putignani, Lorenza, Vinciguerra, Manlio, Balsano, Clara, Pastore, Anna, Rota, Rossella, Tartaglia, Marco, Leonetti, Carlo, and Alisi, Anna

Subjects
Data_FILES
Abstract

Additional file 7.

Published
2022
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2. Additional file 1 of Correction to: Focal adhesion kinase inhibitor TAE226 combined with Sorafenib slows down hepatocellular carcinoma by multiple epigenetic effects

Author

Romito, Ilaria, Porru, Manuela, Braghini, Maria Rita, Pompili, Luca, Panera, Nadia, Crudele, Annalisa, Gnani, Daniela, De Stefanis, Cristiano, Scarsella, Marco, Pomella, Silvia, Mortera, Stefano Levi, de Billy, Emmanuel, Conti, Adrian Libenzio, Marzano, Valeria, Putignani, Lorenza, Vinciguerra, Manlio, Balsano, Clara, Pastore, Anna, Rota, Rossella, Tartaglia, Marco, Leonetti, Carlo, and Alisi, Anna

Subjects
Data_FILES
Abstract

Additional file 6.

Published
2022
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3. Additional file 3 of Correction to: Focal adhesion kinase inhibitor TAE226 combined with Sorafenib slows down hepatocellular carcinoma by multiple epigenetic effects

Author

Romito, Ilaria, Porru, Manuela, Braghini, Maria Rita, Pompili, Luca, Panera, Nadia, Crudele, Annalisa, Gnani, Daniela, De Stefanis, Cristiano, Scarsella, Marco, Pomella, Silvia, Mortera, Stefano Levi, de Billy, Emmanuel, Conti, Adrian Libenzio, Marzano, Valeria, Putignani, Lorenza, Vinciguerra, Manlio, Balsano, Clara, Pastore, Anna, Rota, Rossella, Tartaglia, Marco, Leonetti, Carlo, and Alisi, Anna

Subjects
Data_FILES
Abstract

Additional file 8.

Published
2022
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4. Additional file 7 of Focal adhesion kinase inhibitor TAE226 combined with Sorafenib slows down hepatocellular carcinoma by multiple epigenetic effects

Author

Romito, Ilaria, Porru, Manuela, Braghini, Maria Rita, Pompili, Luca, Panera, Nadia, Crudele, Annalisa, Gnani, Daniela, De Stefanis, Cristiano, Scarsella, Marco, Pomella, Silvia, Levi Mortera, Stefano, de Billy, Emmanuel, Conti, Adrian Libenzio, Marzano, Valeria, Putignani, Lorenza, Vinciguerra, Manlio, Balsano, Clara, Pastore, Anna, Rota, Rossella, Tartaglia, Marco, Leonetti, Carlo, and Alisi, Anna

Subjects
digestive system diseases
Abstract

Additional file 7: Figure S2. Evaluation of the IC50 values of TAE226 and SOR on HCC cell viability after 2 and 5 days. Cell viability, measured by XTT assay, after 2 and 5 days from treatment with TAE226 or SOR, in HepG2 and Huh7 cells. Values are the mean OD �� SD of three independent experiments repeated at least in duplicate. Data were analysed by ANOVA. ***p

Published
2021
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5. Additional file 6 of Focal adhesion kinase inhibitor TAE226 combined with Sorafenib slows down hepatocellular carcinoma by multiple epigenetic effects

Author

Romito, Ilaria, Porru, Manuela, Braghini, Maria Rita, Pompili, Luca, Panera, Nadia, Crudele, Annalisa, Gnani, Daniela, De Stefanis, Cristiano, Scarsella, Marco, Pomella, Silvia, Levi Mortera, Stefano, de Billy, Emmanuel, Conti, Adrian Libenzio, Marzano, Valeria, Putignani, Lorenza, Vinciguerra, Manlio, Balsano, Clara, Pastore, Anna, Rota, Rossella, Tartaglia, Marco, Leonetti, Carlo, and Alisi, Anna

Subjects
digestive system diseases
Abstract

Additional file 6: Figure S1. FAK phosphorylation in HCC cells after IC50 values of treatments. Quantitative analysis of pTyr397FAK expression after 48 h of treatment with the different drugs, in HepG2 and Huh7 cells. Values are the mean arbitrary units �� SD of at least three independent experiments. Data were analysed by 2-tailed Student���s t test. *p

Published
2021
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6. Additional file 10 of Focal adhesion kinase inhibitor TAE226 combined with Sorafenib slows down hepatocellular carcinoma by multiple epigenetic effects

Author

Romito, Ilaria, Porru, Manuela, Braghini, Maria Rita, Pompili, Luca, Panera, Nadia, Crudele, Annalisa, Gnani, Daniela, De Stefanis, Cristiano, Scarsella, Marco, Pomella, Silvia, Levi Mortera, Stefano, de Billy, Emmanuel, Conti, Adrian Libenzio, Marzano, Valeria, Putignani, Lorenza, Vinciguerra, Manlio, Balsano, Clara, Pastore, Anna, Rota, Rossella, Tartaglia, Marco, Leonetti, Carlo, and Alisi, Anna

Abstract

Additional file 10: Figure S5. Analysis of FAK nuclear interaction with specific epigenetics regulators. (A) Coomassie-stained 1D SDS-PAGE gels used for the in-gel digestions of nuclear immunoprecipitates of FAK in HCC cells. The photographs showed gel lanes excision into 10 bands for mass spectrometry characterization of FAK nuclear interactors. (B) Pipeline employed for the analysis of proteomics data.

Published
2021
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7. Additional file 2 of Focal adhesion kinase inhibitor TAE226 combined with Sorafenib slows down hepatocellular carcinoma by multiple epigenetic effects

Author

Romito, Ilaria, Porru, Manuela, Braghini, Maria Rita, Pompili, Luca, Panera, Nadia, Crudele, Annalisa, Gnani, Daniela, De Stefanis, Cristiano, Scarsella, Marco, Pomella, Silvia, Levi Mortera, Stefano, de Billy, Emmanuel, Conti, Adrian Libenzio, Marzano, Valeria, Putignani, Lorenza, Vinciguerra, Manlio, Balsano, Clara, Pastore, Anna, Rota, Rossella, Tartaglia, Marco, Leonetti, Carlo, and Alisi, Anna

Abstract

Additional file 2: Table S2. In vivo antitumor efficacy of TAE226>SOR combination on orthotopic liver tumour.

Published
2021
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8. Additional file 9 of Focal adhesion kinase inhibitor TAE226 combined with Sorafenib slows down hepatocellular carcinoma by multiple epigenetic effects

Author

Romito, Ilaria, Porru, Manuela, Braghini, Maria Rita, Pompili, Luca, Panera, Nadia, Crudele, Annalisa, Gnani, Daniela, De Stefanis, Cristiano, Scarsella, Marco, Pomella, Silvia, Levi Mortera, Stefano, de Billy, Emmanuel, Conti, Adrian Libenzio, Marzano, Valeria, Putignani, Lorenza, Vinciguerra, Manlio, Balsano, Clara, Pastore, Anna, Rota, Rossella, Tartaglia, Marco, Leonetti, Carlo, and Alisi, Anna

Abstract

Additional file 9: Figure S4. Pilot study for quantitative setting of TAE226 concentration in a heterotopic HepG2 xenograft model of HCC. (A) Quantitative analysis of tumour weight at various time points in NT animals or after TAE226 treatments. P values were calculated at day 12 using an unpaired two-tailed t-test, between treated and untreated tumours. **** p

Published
2021
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9. Additional file 1 of Focal adhesion kinase inhibitor TAE226 combined with Sorafenib slows down hepatocellular carcinoma by multiple epigenetic effects

Author

Romito, Ilaria, Porru, Manuela, Braghini, Maria Rita, Pompili, Luca, Panera, Nadia, Crudele, Annalisa, Gnani, Daniela, De Stefanis, Cristiano, Scarsella, Marco, Pomella, Silvia, Levi Mortera, Stefano, de Billy, Emmanuel, Conti, Adrian Libenzio, Marzano, Valeria, Putignani, Lorenza, Vinciguerra, Manlio, Balsano, Clara, Pastore, Anna, Rota, Rossella, Tartaglia, Marco, Leonetti, Carlo, and Alisi, Anna

Abstract

Additional file 1: Table S1. List of antibodies.

Published
2021
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10. Additional file 11 of Focal adhesion kinase inhibitor TAE226 combined with Sorafenib slows down hepatocellular carcinoma by multiple epigenetic effects

Author

Romito, Ilaria, Porru, Manuela, Braghini, Maria Rita, Pompili, Luca, Panera, Nadia, Crudele, Annalisa, Gnani, Daniela, De Stefanis, Cristiano, Scarsella, Marco, Pomella, Silvia, Levi Mortera, Stefano, de Billy, Emmanuel, Conti, Adrian Libenzio, Marzano, Valeria, Putignani, Lorenza, Vinciguerra, Manlio, Balsano, Clara, Pastore, Anna, Rota, Rossella, Tartaglia, Marco, Leonetti, Carlo, and Alisi, Anna

Abstract

Additional file 11: Figure S6. pTyr397FAK nuclear interactors before and after treatment with TAE226 > SOR. Representative images of immunofluorescence for pTyr397FAK, ��-Catenin, HDAC1 and HDAC2 in HepG2 and Huh7 cells NT and after TAE226 > SOR treatment. 60X Magnification.

Published
2021
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11. Additional file 3 of Focal adhesion kinase inhibitor TAE226 combined with Sorafenib slows down hepatocellular carcinoma by multiple epigenetic effects

Author

Romito, Ilaria, Porru, Manuela, Braghini, Maria Rita, Pompili, Luca, Panera, Nadia, Crudele, Annalisa, Gnani, Daniela, De Stefanis, Cristiano, Scarsella, Marco, Pomella, Silvia, Levi Mortera, Stefano, de Billy, Emmanuel, Conti, Adrian Libenzio, Marzano, Valeria, Putignani, Lorenza, Vinciguerra, Manlio, Balsano, Clara, Pastore, Anna, Rota, Rossella, Tartaglia, Marco, Leonetti, Carlo, and Alisi, Anna

Abstract

Additional file 3: Table S3. Common up- and down-regulated genes.

Published
2021
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12. Additional file 5 of Focal adhesion kinase inhibitor TAE226 combined with Sorafenib slows down hepatocellular carcinoma by multiple epigenetic effects

Author

Romito, Ilaria, Porru, Manuela, Braghini, Maria Rita, Pompili, Luca, Panera, Nadia, Crudele, Annalisa, Gnani, Daniela, De Stefanis, Cristiano, Scarsella, Marco, Pomella, Silvia, Levi Mortera, Stefano, de Billy, Emmanuel, Conti, Adrian Libenzio, Marzano, Valeria, Putignani, Lorenza, Vinciguerra, Manlio, Balsano, Clara, Pastore, Anna, Rota, Rossella, Tartaglia, Marco, Leonetti, Carlo, and Alisi, Anna

Subjects
Data_FILES
Abstract

Additional file 5: Table S5. GO annotations.

Published
2021
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13. Additional file 8 of Focal adhesion kinase inhibitor TAE226 combined with Sorafenib slows down hepatocellular carcinoma by multiple epigenetic effects

Author

Romito, Ilaria, Porru, Manuela, Braghini, Maria Rita, Pompili, Luca, Panera, Nadia, Crudele, Annalisa, Gnani, Daniela, De Stefanis, Cristiano, Scarsella, Marco, Pomella, Silvia, Levi Mortera, Stefano, de Billy, Emmanuel, Conti, Adrian Libenzio, Marzano, Valeria, Putignani, Lorenza, Vinciguerra, Manlio, Balsano, Clara, Pastore, Anna, Rota, Rossella, Tartaglia, Marco, Leonetti, Carlo, and Alisi, Anna

Abstract

Additional file 8: Figure S3. IGF-1R in HCC cells after treatment with TAE226 > SOR compared to single treatments. Representative immunoblot and quantitative analysis of phosphorylated IGF-1R after 48 h from treatment with the different drugs, in HepG2 (A) and Huh7 cells (B). ��Tubulin served as loading control. Values are the mean arbitrary units �� SD of at least three independent experiments. Data were analysed by 2-tailed Student���s t test. **p

Published
2021
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14. Integrated Multiomic Profiling Identifies the Epigenetic Regulator PRC2 as a Therapeutic Target to Counteract Leukemia Immune Escape and Relapse

Author

Valentina Gambacorta, Stefano Beretta, Martina Ciccimarra, Laura Zito, Kety Giannetti, Angela Andrisani, Daniela Gnani, Lucia Zanotti, Giacomo Oliveira, Matteo Giovanni Carrabba, Davide Cittaro, Ivan Merelli, Fabio Ciceri, Raffaella Di Micco, Luca Vago, Gambacorta, Valentina, Beretta, Stefano, Ciccimarra, Martina, Zito, Laura, Giannetti, Kety, Andrisani, Angela, Gnani, Daniela, Zanotti, Lucia, Oliveira, Giacomo, Carrabba, Matteo Giovanni, Cittaro, Davide, Merelli, Ivan, Ciceri, Fabio, di Micco, Raffaella, and Vago, Luca

Subjects
Leukemia, Myeloid, Acute, Oncology, Recurrence, hemic and lymphatic diseases, Hematopoietic Stem Cell Transplantation, Histocompatibility Antigens Class II, Polycomb Repressive Complex 2, Humans, Tumor Escape, Chromatin, Epigenesis, Genetic
Abstract

Immune escape represents a major driver of acute myeloid leukemia (AML) reemergence after allogeneic hematopoietic cell transplantation (allo-HCT), with up to 40% of relapses prompted by nongenomic loss of HLA class II expression in leukemia cells. By integrative analysis of gene expression, DNA methylation, and chromatin accessibility in paired diagnosis/relapse primary samples and in the respective patient-derived xenografts (PDX), we identify the polycomb repressive complex 2 (PRC2) as a key epigenetic driver of this immune escape modality. We report that loss of expression of HLA class II molecules is accompanied by a PRC2-dependent reduction in chromatin accessibility. Pharmacologic inhibition of PRC2 subunits rescues HLA class II expression in AML relapses in vitro and in vivo, with consequent recovery of leukemia recognition by CD4+ T cells. Our results uncover a novel link between epigenetics and leukemia immune escape, which may rapidly translate into innovative strategies to cure or prevent AML posttransplantation relapse. Significance: Loss of HLA class II expression represents a frequent mechanism of leukemia posttransplantation relapse. Here we identify PRC2 as the main epigenetic driver of this immune escape modality and show that its chemical inhibition can reinstate a proficient graft-versus-leukemia effect, providing an innovative rationale for personalized epigenetic immunotherapies. See related commentary by Köhler and Zeiser, p. 1410. This article is highlighted in the In This Issue feature, p. 1397

Published
2022

15. Oncogene-induced maladaptive activation of trained immunity in the pathogenesis and treatment of Erdheim-Chester disease

Author

Mihai G. Netea, Riccardo Biavasco, Lorenzo Dagna, Simone Cenci, Travis Nemkov, Giulio Cavalli, Philippe Maksud, Claudio Doglioni, Gianfranco Distefano, Daniela Cesana, Charles A. Dinarello, Eleonora Cantoni, Anna Kajaste-Rudnitski, Corrado Campochiaro, Simone Cardaci, Daniela Gnani, Isak W. Tengesdal, Julien Haroche, Samuel Zambrano, Alessandro Tomelleri, Giacomo De Luca, Davide Stefanoni, Francesco Piras, Ivan Merelli, Angelo D'Alessandro, Maddalena Panigada, Davide Mazza, Rob J.W. Arts, Jorge Domínguez-Andrés, Alessia Loffreda, Laura Cassina, Raffaella Molteni, Eugenio Montini, Alessandra Boletta, Leo A. B. Joosten, Elisabetta Ferrero, Marina Ferrarini, Biavasco, Riccardo, Molteni, Raffaella, Stefanoni, Davide, Nemkov, Travi, Netea, Mihai G., Domínguez-Andrés, Jorge, Arts, Rob JW, Merelli, Ivan, Mazza, Davide, Zambrano, S, Panigada, Maddalena, Cantoni, Eleonora, Tengesdal, Isak, Maksud, Philippe, Piras, Francesco, De Luca, Giacomo, Cassina, Laura, Distefano, Gianfranco, Loffreda, Alessia, Gnani, Daniela, Doglioni, Claudio, Tomelleri, Alessandro, Campochiaro, Corrado, Joosten, Leo, Dinarello, Charles A, Kajaste-Rudnitski, Anna, Haroche, Julien, Cardaci, Simone, Cenci, Simone, Dagna, Lorenzo, Ferrarini, Marina, Ferrero, Elisabetta, Boletta, Alessandra, D'Alessandro, Angelo, Montini, Eugenio, and Cavalli, Giulio

Subjects
Proto-Oncogene Proteins B-raf, Erdheim-Chester Disease, Myeloid, medicine.medical_treatment, Immunology, lnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4], Inflammation, Biochemistry, Myeloid Neoplasm, Proinflammatory cytokine, Epigenesis, Genetic, Pathogenesis, medicine, Humans, Point Mutation, Protein kinase B, Cells, Cultured, business.industry, Monocyte, Macrophages, Immunity, Cell Biology, Hematology, Oncogenes, Cytokine, medicine.anatomical_structure, Cancer research, medicine.symptom, business
Abstract

Trained immunity (TI) is a proinflammatory program induced in monocyte/macrophages upon sensing of specific pathogens and is characterized by immunometabolic and epigenetic changes that enhance cytokine production. Maladaptive activation of TI (ie, in the absence of infection) may result in detrimental inflammation and development of disease; however, the exact role and extent of inappropriate activation of TI in the pathogenesis of human diseases is undetermined. In this study, we uncovered the oncogene-induced, maladaptive induction of TI in the pathogenesis of a human inflammatory myeloid neoplasm (Erdheim-Chester disease, [ECD]), characterized by the BRAFV600E oncogenic mutation in monocyte/macrophages and excess cytokine production. Mechanistically, myeloid cells expressing BRAFV600E exhibit all molecular features of TI: activation of the AKT/mammalian target of rapamycin signaling axis; increased glycolysis, glutaminolysis, and cholesterol synthesis; epigenetic changes on promoters of genes encoding cytokines; and enhanced cytokine production leading to hyperinflammatory responses. In patients with ECD, effective therapeutic strategies combat this maladaptive TI phenotype; in addition, pharmacologic inhibition of immunometabolic changes underlying TI (ie, glycolysis) effectively dampens cytokine production by myeloid cells. This study revealed the deleterious potential of inappropriate activation of TI in the pathogenesis of human inflammatory myeloid neoplasms and the opportunity for inhibition of TI in conditions characterized by maladaptive myeloid-driven inflammation.

Published
2021

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