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3. Molecular taxonomy of myelodysplastic syndromes and its clinical implications

Author

Bernard, Elsa, Hasserjian, Robert P., Greenberg, Peter L., Arango Ossa, Juan E., Creignou, Maria, Tuechler, Heinz, Gutierrez-Abril, Jesus, Domenico, Dylan, Medina-Martinez, Juan S., Levine, Max, Liosis, Konstantinos, Farnoud, Noushin, Sirenko, Maria, Jädersten, Martin, Germing, Ulrich, Sanz, Guillermo, van de Loosdrecht, Arjan A., Nannya, Yasuhito, Kosmider, Olivier, Follo, Matilde Y., Thol, Felicitas, Zamora, Lurdes, Pinheiro, Ronald F., Pellagatti, Andrea, Elias, Harold K., Haase, Detlef, Ganster, Christina, Ades, Lionel, Tobiasson, Magnus, Palomo, Laura, Della Porta, Matteo Giovanni, Fenaux, Pierre, Belickova, Monika, Savona, Michael R., Klimek, Virginia M., Santos, Fabio P. S., Boultwood, Jacqueline, Kotsianidis, Ioannis, Santini, Valeria, Solé, Francesc, Platzbecker, Uwe, Heuser, Michael, Valent, Peter, Finelli, Carlo, Voso, Maria Teresa, Shih, Lee-Yung, Fontenay, Michaela, Jansen, Joop H., Cervera, José, Gattermann, Norbert, Ebert, Benjamin L., Bejar, Rafael, Malcovati, Luca, Ogawa, Seishi, Cazzola, Mario, Hellström-Lindberg, Eva, and Papaemmanuil, Elli

Published
2024
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4. Detection of Cancer Stem Cells in Normal and Dysplastic/Leukemic Human Blood

Author

De Stefano, Alessia, primary, Cappellini, Alessandra, additional, Casalin, Irene, additional, Paolini, Stefania, additional, Parisi, Sarah, additional, Marvi, Maria Vittoria, additional, Fazio, Antonietta, additional, Neri, Irene, additional, Koufi, Foteini-Dionysia, additional, Ratti, Stefano, additional, Finelli, Carlo, additional, Curti, Antonio, additional, Manzoli, Lucia, additional, Cocco, Lucio, additional, and Follo, Matilde Y., additional

Published
2024
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6. A miRNA screening identifies miR-192-5p as associated with response to azacitidine and lenalidomide therapy in myelodysplastic syndromes

Author

Mongiorgi, Sara, De Stefano, Alessia, Ratti, Stefano, Indio, Valentina, Astolfi, Annalisa, Casalin, Irene, Pellagatti, Andrea, Paolini, Stefania, Parisi, Sarah, Cavo, Michele, Pession, Andrea, McCubrey, James A., Suh, Pann-Ghill, Manzoli, Lucia, Boultwood, Jacqueline, Finelli, Carlo, Cocco, Lucio, and Follo, Matilde Y.

Published
2023
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7. Deciphering signaling pathways in hematopoietic stem cells: the molecular complexity of Myelodysplastic Syndromes (MDS) and leukemic progression

Author

Casalin, Irene, De Stefano, Alessia, Ceneri, Eleonora, Cappellini, Alessandra, Finelli, Carlo, Curti, Antonio, Paolini, Stefania, Parisi, Sarah, Zannoni, Letizia, Boultwood, Jacqueline, McCubrey, James A., Suh, Pann-Ghill, Ramazzotti, Giulia, Fiume, Roberta, Ratti, Stefano, Manzoli, Lucia, Cocco, Lucio, and Follo, Matilde Y.

Published
2024
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8. Implications of TP53 allelic state for genome stability, clinical presentation and outcomes in myelodysplastic syndromes

Author

Bernard, Elsa, Nannya, Yasuhito, Hasserjian, Robert P, Devlin, Sean M, Tuechler, Heinz, Medina-Martinez, Juan S, Yoshizato, Tetsuichi, Shiozawa, Yusuke, Saiki, Ryunosuke, Malcovati, Luca, Levine, Max F, Arango, Juan E, Zhou, Yangyu, Solé, Francesc, Cargo, Catherine A, Haase, Detlef, Creignou, Maria, Germing, Ulrich, Zhang, Yanming, Gundem, Gunes, Sarian, Araxe, van de Loosdrecht, Arjan A, Jädersten, Martin, Tobiasson, Magnus, Kosmider, Olivier, Follo, Matilde Y, Thol, Felicitas, Pinheiro, Ronald F, Santini, Valeria, Kotsianidis, Ioannis, Boultwood, Jacqueline, Santos, Fabio PS, Schanz, Julie, Kasahara, Senji, Ishikawa, Takayuki, Tsurumi, Hisashi, Takaori-Kondo, Akifumi, Kiguchi, Toru, Polprasert, Chantana, Bennett, John M, Klimek, Virginia M, Savona, Michael R, Belickova, Monika, Ganster, Christina, Palomo, Laura, Sanz, Guillermo, Ades, Lionel, Della Porta, Matteo Giovanni, Elias, Harold K, Smith, Alexandra G, Werner, Yesenia, Patel, Minal, Viale, Agnès, Vanness, Katelynd, Neuberg, Donna S, Stevenson, Kristen E, Menghrajani, Kamal, Bolton, Kelly L, Fenaux, Pierre, Pellagatti, Andrea, Platzbecker, Uwe, Heuser, Michael, Valent, Peter, Chiba, Shigeru, Miyazaki, Yasushi, Finelli, Carlo, Voso, Maria Teresa, Shih, Lee-Yung, Fontenay, Michaela, Jansen, Joop H, Cervera, José, Atsuta, Yoshiko, Gattermann, Norbert, Ebert, Benjamin L, Bejar, Rafael, Greenberg, Peter L, Cazzola, Mario, Hellström-Lindberg, Eva, Ogawa, Seishi, and Papaemmanuil, Elli

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Hematology, Stem Cell Research, Cancer, Clinical Research, Rare Diseases, Genetics, 2.1 Biological and endogenous factors, Aetiology, Alleles, Cohort Studies, DNA Copy Number Variations, DNA Mutational Analysis, Female, Gene Frequency, Genomic Instability, Humans, Loss of Heterozygosity, Male, Mutation, Myelodysplastic Syndromes, Phenotype, Prognosis, Survival Analysis, Treatment Outcome, Tumor Suppressor Protein p53, Medical and Health Sciences, Immunology, Biomedical and clinical sciences, Health sciences
Abstract

Tumor protein p53 (TP53) is the most frequently mutated gene in cancer1,2. In patients with myelodysplastic syndromes (MDS), TP53 mutations are associated with high-risk disease3,4, rapid transformation to acute myeloid leukemia (AML)5, resistance to conventional therapies6-8 and dismal outcomes9. Consistent with the tumor-suppressive role of TP53, patients harbor both mono- and biallelic mutations10. However, the biological and clinical implications of TP53 allelic state have not been fully investigated in MDS or any other cancer type. We analyzed 3,324 patients with MDS for TP53 mutations and allelic imbalances and delineated two subsets of patients with distinct phenotypes and outcomes. One-third of TP53-mutated patients had monoallelic mutations whereas two-thirds had multiple hits (multi-hit) consistent with biallelic targeting. Established associations with complex karyotype, few co-occurring mutations, high-risk presentation and poor outcomes were specific to multi-hit patients only. TP53 multi-hit state predicted risk of death and leukemic transformation independently of the Revised International Prognostic Scoring System (IPSS-R)11. Surprisingly, monoallelic patients did not differ from TP53 wild-type patients in outcomes and response to therapy. This study shows that consideration of TP53 allelic state is critical for diagnostic and prognostic precision in MDS as well as in future correlative studies of treatment response.

Published
2020

11. Evaluation of the Anti-Cancer Potential of Extracellular Vesicles Derived from Human Amniotic Fluid Stem Cells: Focus on Effective miRNAs in the Treatment of Melanoma Progression.

Author

Gatti, Martina, Beretti, Francesca, Ravegnini, Gloria, Gorini, Francesca, Ceneri, Eleonora, Bertucci, Emma, Follo, Matilde Y., and Maraldi, Tullia

Subjects
GENE expression, EXTRACELLULAR vesicles, STEM cells, ANTINEOPLASTIC agents, CANCER cells, AMNIOTIC liquid
Abstract

Mesenchymal stromal cells (MSCs) and their secretome show intrinsic antitumor properties, however, the anti-cancer effects of MSCs remain debated and depend on the cancer type or model. MSCs derived from discarded samples, such as human amniotic fluid (hAFSC), have been introduced as an attractive and potent stem cell source for clinical applications due to their collection procedures, which minimize ethical issues. Until now, various studies have obtained controversial results and poor understanding of the mechanisms behind the effects of perinatal cells on cancer cells. To better clarify this aspect, protein and miRNA expression profiling isolated from Extracellular vesicles (EVs) secreted by hAFSCs, obtained in the II or III trimester, were evaluated. Bioinformatic analysis was performed aiming at evaluating differential expression, pathway enrichment, and miRNA-mRNA networks. We highlighted that most of the highest expressed proteins and miRNAs are mainly involved in antioxidant and anti-cancer effects. Indeed, in the presence of hAFSC-EVs, a reduction of the G2/M phase was observed on melanoma cell lines, an activation of the apoptotic pathway occurred and the migration and invasion ability reduced. Our data demonstrated that II or III trimester hAFSCs can release bioactive factors into EVs, causing an efficient anti-cancer effect inhibiting melanoma progression. [ABSTRACT FROM AUTHOR]

Published
2024
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15. Inositide-Dependent Nuclear Signalling in Health and Disease

Author

Follo, Matilde Y., Ratti, Stefano, Manzoli, Lucia, Ramazzotti, Giulia, Faenza, Irene, Fiume, Roberta, Mongiorgi, Sara, Suh, Pann Ghill, McCubrey, James A., Cocco, Lucio, Barrett, James E., Editor-in-Chief, Flockerzi, Veit, Editorial Board Member, Frohman, Michael A., Editorial Board Member, Geppetti, Pierangelo, Editorial Board Member, Hofmann, Franz B., Editorial Board Member, Michel, Martin C., Editorial Board Member, Page, Clive P., Editorial Board Member, Wang, KeWei, Editorial Board Member, and Gomez-Cambronero, Julian, editor

Published
2020
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16. Myoblast-Derived Galectin 3 Impairs the Early Phases of Osteogenesis Affecting Notch and Akt Activity.

Author

Amore, Emanuela, Cenni, Vittoria, Piazzi, Manuela, Signore, Michele, Orlandi, Giulia, Neri, Simona, Biressi, Stefano, Barone, Rosario, Di Felice, Valentina, Follo, Matilde Y., Bertacchini, Jessika, and Palumbo, Carla

Subjects
CELL differentiation, PEPTIDES, BONE growth, BONE remodeling, EXTRACELLULAR matrix
Abstract

Galectin-3 (Gal-3) is a pleiotropic lectin produced by most cell types, which regulates multiple cellular processes in various tissues. In bone, depending on its cellular localization, Gal-3 has a dual and opposite role. If, on the one hand, intracellular Gal-3 promotes bone formation, on the other, its circulating form affects bone remodeling, antagonizing osteoblast differentiation and increasing osteoclast activity. From an analysis of the secretome of cultured differentiating myoblasts, we interestingly found the presence of Gal-3. After that, we confirmed that Gal-3 was expressed and released in the extracellular environment from myoblast cells during their differentiation into myotubes, as well as after mechanical strain. An in vivo analysis revealed that Gal-3 was triggered by trained exercise and was specifically produced by fast muscle fibers. Speculating a role for this peptide in the muscle-to-bone cross talk, a direct co-culture in vitro system, simultaneously combining media that were obtained from differentiated myoblasts and osteoblast cells, confirmed that Gal-3 is a mediator of osteoblast differentiation. Molecular and proteomic analyses revealed that the secreted Gal-3 modulated the biochemical processes occurring in the early phases of bone formation, in particular impairing the activity of the STAT3 and PDK1/Akt signaling pathways and, at the same time, triggering that one of Notch. Circulating Gal-3 also affected the expression of the most common factors involved in osteogenetic processes, including BMP-2, -6, and -7. Intriguingly, Gal-3 was able to interfere with the ability of differentiating osteoblasts to interact with the components of the extracellular bone matrix, a crucial condition required for a proper osteoblast differentiation. All in all, our evidence lays the foundation for further studies to present this lectin as a novel myokine involved in muscle-to-bone crosstalk. [ABSTRACT FROM AUTHOR]

Published
2024
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18. Cancer therapy and treatments during COVID-19 era

Author

Akula, Shaw M., Abrams, Stephen L., Steelman, Linda S., Candido, Saverio, Libra, Massimo, Lerpiriyapong, Kvin, Cocco, Lucio, Ramazzotti, Giulia, Ratti, Stefano, Follo, Matilde Y., Martelli, Alberto M., Blalock, William L., Piazzi, Manuela, Montalto, Giuseppe, Cervello, Melchiorre, Notarbartolo, Monica, Basecke, Jorg, and McCubrey, James A.

Published
2020
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20. Molecular and clinical presentation of UBA1-mutated myelodysplastic syndromes

Author

Sirenko, Maria, primary, Bernard, Elsa, additional, Creignou, Maria, additional, Domenico, Dylan, additional, Farina, Andrea, additional, Arango Ossa, Juan Esteban, additional, Kosmider, Olivier, additional, Hasserjian, Robert P, additional, Jädersten, Martin, additional, Germing, Ulrich, additional, Sanz, Guillermo F., additional, van de Loosdrecht, Arjan A., additional, Gurnari, Carmelo, additional, Follo, Matilde Y, additional, Thol, Felicitas R., additional, Zamora, Lurdes, additional, Pellagatti, Andrea, additional, Elias, Harold Kunal, additional, Haase, Detlef Thomas, additional, Sander, Birgitta, additional, Orna, Elisa, additional, Zoldan, Katharina, additional, Eder, Lea Naomi, additional, Sperr, Wolfgang R, additional, Thalhammer, Renate, additional, Ganster, Christina, additional, Adès, Lionel, additional, Tobiasson, Magnus, additional, Palomo, Laura, additional, Della Porta, Matteo Giovanni, additional, Huberman, Kety H, additional, Fenaux, Pierre, additional, Belickova, Monika, additional, Savona, Michael R., additional, Klimek, Virginia, additional, Santos, Fabio P S, additional, Boultwood, Jacqueline, additional, Kotsianidis, Ioannis, additional, Santini, Valeria, additional, Sole, Francesc, additional, Platzbecker, Uwe, additional, Heuser, Michael, additional, Valent, Peter, additional, Finelli, Carlo, additional, Voso, Maria Teresa, additional, Shih, Lee Yung, additional, Ogawa, Seishi, additional, Fontenay, Michaela, additional, Jansen, Joop H, additional, Cervera, José, additional, Ebert, Benjamin L, additional, Bejar, Rafael, additional, Greenberg, Peter L., additional, Gattermann, Norbert, additional, Malcovati, Luca, additional, Cazzola, Mario, additional, Beck, David B., additional, Hellstrom-Lindberg, Eva S, additional, Papaemmanuil, Elli, additional, and Pinheiro, Ronald Feitosa, additional

Published
2024
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22. DNA methylation profiling of myelodysplastic syndromes and clinical response to azacitidine: A multicentre retrospective study

Author

Noguera‐Castells, Aleix, primary, Campillo‐Marcos, Ignacio, additional, Davalos, Veronica, additional, García‐Prieto, Carlos A., additional, Valcárcel, David, additional, Molero, Antonieta, additional, Palomo, Laura, additional, Gattermann, Norbert, additional, Wulfert, Michael, additional, Chaparro‐González, Lorea, additional, Solé, Francesc, additional, Cabezón, Marta, additional, Jiménez‐Lorenzo, María J., additional, Xicoy, Blanca, additional, Zamora, Lurdes, additional, De Stefano, Alessia, additional, Casalin, Irene, additional, Finelli, Carlo, additional, Follo, Matilde Y., additional, and Esteller, Manel, additional

Published
2024
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24. Abilities of β-Estradiol to interact with chemotherapeutic drugs, signal transduction inhibitors and nutraceuticals and alter the proliferation of pancreatic cancer cells

Author

Akula, Shaw M., Candido, Saverio, Abrams, Stephen L., Steelman, Linda S., Lertpiriyapong, Kvin, Cocco, Lucio, Ramazzotti, Giulia, Ratti, Stefano, Follo, Matilde Y., Martelli, Alberto M., Murata, Ramiro M., Rosalen, Pedro L., Bueno-Silva, Bruno, Matias de Alencar, Severino, Falasca, Marco, Montalto, Giuseppe, Cervello, Melchiorre, Notarbartolo, Monica, Gizak, Agnieszka, Rakus, Dariusz, Libra, Massimo, and McCubrey, James A.

Published
2020
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25. Dual investigation of Myeloid and Lymphoid compartments: role of miRNAs in MDS and HOXA9 in B-ALL

Author

Follo, Matilde Yung, De Stefano, Alessia <1991>, Follo, Matilde Yung, and De Stefano, Alessia <1991>

Abstract

Here we report an exploration of uncommonly investigated molecules in these diseases, microRNA in MDS, and HoxA9 in B-ALL. miRNAs are small non-coding RNAs that regulate gene expression and are linked to cancer development and progression. MDS with an increased risk of AML progression are managed using hypomethylating agents(azacytidine), alone or in conjunction with other drugs. miRNA expression of 26 high-risk MDS-patients treated with azacytidine and lenalidomide, at baseline and during therapy, were analyzed. miR-192-5p was discovered as differentially expressed during therapy response. Patients were clustered in responder, non-responder, and early losing-response and showed a different expression of this miRNA, as well as of its target BCL2. This investigation also revealed a significant association between miR-192-5p levels during the therapy and extended Overall Survival (OS) and Leukemia-Free Survival (LFS) in responder patients. On the ALL side, HoxA9 is a member of the Hox-gene family. Dysregulated expression of HoxA9 has been associated with leukemia, where is commonly upregulated. A recent publication revealed a significant downregulation of HoxA9 mRNA levels in leukemic murine samples when compared with normal B-cell precursors. This was highly surprising, because HoxA9 is an oncogene involved in AML, T-ALL, and B-ALL with MLL rearrangement, and led to speculate on tumor suppressive role of this gene in IL7R mutant B-ALL. Proliferation on human cell lines was then assessed and the result was a proliferative disadvantage associated with HoxA9 overexpression. The downregulation mechanism was then investigated, evaluating on mice-derived leukemic cells the effect of SAHA. The aim of this dual investigation of miRNA in MDS and HoxA9 in B-ALL is to increase the understanding of the intricate web of molecular events that drive these hematological malignancies, ultimately striving for improved patient management and outcome.

Published
2024

26. Abilities of berberine and chemically modified berberines to interact with metformin and inhibit proliferation of pancreatic cancer cells

Author

Akula, Shaw M., Candido, Saverio, Libra, Massimo, Abrams, Stephen L., Steelman, Linda S., Lertpiriyapong, Kvin, Ramazzotti, Giulia, Ratti, Stefano, Follo, Matilde Y., Martelli, Alberto M., Murata, Ramiro M., Rosalen, Pedro L., Bueno-Silva, Bruno, Matias de Alencar, Severino, Montalto, Giuseppe, Cervello, Melchiorre, Gizak, Agnieszka, Rakus, Dariusz, Mao, Weifeng, Lin, Heng-Liang, Lombardi, Paolo, and McCubrey, James A.

Published
2019
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27. Effects of the MDM-2 inhibitor Nutlin-3a on PDAC cells containing and lacking WT-TP53 on sensitivity to chemotherapy, signal transduction inhibitors and nutraceuticals

Author

Candido, Saverio, Abrams, Stephen L., Steelman, Linda S., Lertpiriyapong, Kvin, Martelli, Alberto M., Cocco, Lucio, Ratti, Stefano, Follo, Matilde Y., Murata, Ramiro M., Rosalen, Pedro L., Bueno-Silva, Bruno, de Alencar, Severino Matias, Lombardi, Paolo, Mao, Weifeng, Montalto, Giuseppe, Cervello, Melchiorre, Rakus, Dariusz, Gizak, Agnieska, Lin, Heng-Liang, Libra, Massimo, Akula, Shaw M., and McCubrey, James A.

Published
2019
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31. Response of high-risk MDS to azacitidine and lenalidomide is impacted by baseline and acquired mutations in a cluster of three inositide-specific genes

Author

Follo, Matilde Y., Pellagatti, Andrea, Armstrong, Richard N., Ratti, Stefano, Mongiorgi, Sara, De Fanti, Sara, Bochicchio, Maria Teresa, Russo, Domenico, Gobbi, Marco, Miglino, Maurizio, Parisi, Sarah, Martinelli, Giovanni, Cavo, Michele, Luiselli, Donata, McCubrey, James A., Suh, Pann-Ghill, Manzoli, Lucia, Boultwood, Jacqueline, Finelli, Carlo, and Cocco, Lucio

Published
2019
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32. Nuclear Phospholipids and Signaling: An Update of the Story.

Author

Casalin, Irene, Ceneri, Eleonora, Ratti, Stefano, Manzoli, Lucia, Cocco, Lucio, and Follo, Matilde Y.

Subjects
CELL communication, INOSITOL, PHOSPHOINOSITIDES, PHOSPHOLIPIDS, LIPIDS
Abstract

In the last three decades, the presence of phospholipids in the nucleus has been shown and thoroughly investigated. A considerable amount of interest has been raised about nuclear inositol lipids, mainly because of their role in signaling acting. Here, we review the main issues of nuclear phospholipid localization and the role of nuclear inositol lipids and their related enzymes in cellular signaling, both in physiological and pathological conditions. [ABSTRACT FROM AUTHOR]

Published
2024
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33. Nuclear Phosphoinositides as Key Determinants of Nuclear Functions

Author

Vidalle, Magdalena C., primary, Sheth, Bhavwanti, additional, Fazio, Antonietta, additional, Marvi, Maria Vittoria, additional, Leto, Stefano, additional, Koufi, Foteini-Dionysia, additional, Neri, Irene, additional, Casalin, Irene, additional, Ramazzotti, Giulia, additional, Follo, Matilde Y., additional, Ratti, Stefano, additional, Manzoli, Lucia, additional, Gehlot, Sonakshi, additional, Divecha, Nullin, additional, and Fiume, Roberta, additional

Published
2023
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34. Inositide-Dependent Nuclear Signalling in Health and Disease

Author

Follo, Matilde Y., primary, Ratti, Stefano, additional, Manzoli, Lucia, additional, Ramazzotti, Giulia, additional, Faenza, Irene, additional, Fiume, Roberta, additional, Mongiorgi, Sara, additional, Suh, Pann Ghill, additional, McCubrey, James A., additional, and Cocco, Lucio, additional

Published
2019
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35. TiMMing: developing an innovative suite of bioinformatic tools to harmonize and track the origin of copy number alterations in the evolutive history of multiple myeloma

Author

Follo, Matilde Yung, Poletti, Andrea <1991>, Follo, Matilde Yung, and Poletti, Andrea <1991>

Abstract

Multiple Myeloma (MM) is a hematologic cancer with heterogeneous and complex genomic landscape, where Copy Number Alterations (CNAs) play a key role in the disease's pathogenesis and prognosis. It is of biological and clinical interest to study the temporal occurrence of early alterations, as they play a disease "driver" function by deregulating key tumor pathways. This study presents an innovative bioinformatic tools suite created for harmonizing and tracing the origin of CNAs throughout the evolutionary history of MM. To this aim, large cohorts of newly-diagnosed MM (NDMM, N=1582) and Smoldering-MM (SMM, N=282) were aggregated. The tools developed in this study enable the harmonization of CNAs as obtained from different genomic platforms in such a way that a high statistical power can be obtained. By doing so, the high numerosity of those cohorts was harnessed for the identification of novel genes characterized as "driver" (NFKB2, NOTCH2, MAX, EVI5 and MYC-ME2-enhancer), and the generation of an innovative timing model, implemented with a statistical method to introduce confidence intervals in the CNAs-calls. By applying this model on both NDMM and SMM cohorts, it was possible to identify specific CNAs (1q(CKS1B)amp, 13q(RB1)del, 11q(CCND1)amp and 14q(MAX)del) and categorize them as "early"/ "driver" events. A high level of precision was guaranteed by the narrow confidence intervals in the timing estimates. These CNAs were proposed as critical MM alterations, which play a foundational role in the evolutionary history of both SMM and NDMM. Finally, a multivariate survival model was able to identify the independent genomic alterations with the greatest effect on patients’ survival, including RB1-del, CKS1B-amp, MYC-amp, NOTCH2-amp and TRAF3-del/mut. In conclusion, the alterations that were identified as both "early-drivers” and correlated with patients’ survival were proposed as biomarkers that, if included in wider survival models, could provide a better disease st

Published
2023

36. Nuclear shape instability caused by lamin A deregulation promotes invasiveness in pediatric bone sarcomas: from nucleo-cytoskeleton dynamics to novel therapeutic opportunities

Author

Follo, Matilde Yung, Paganelli, Francesca <1994>, Follo, Matilde Yung, and Paganelli, Francesca <1994>

Abstract

Osteosarcoma (OS) and Ewing sarcoma (EWS) are the two most frequent primary bone tumors, in which metastases remain the most relevant adverse prognostic factor. Lamin A is the main constituent of the nuclear lamina, with a fundamental role in maintaining the connection between nucleus and cytoskeleton (through LINC complex proteins interactions), and its alterations can be implicated in tumor progression. We investigated how nucleo-cytoskeleton dynamics is influenced by lamin A modulation in OS and EWS, demonstrating that both these cancer models had low levels of lamin A, which are linked to a significantly more marked nuclear misshaping. In our in vitro studies, reduced levels of lamin A promoted migratory abilities in these tumors. Moreover, these findings were corroborated by gene expression analyses on EWS patient samples, showing that LMNA levels were significantly lower in metastatic lesions compared to primary tumors and that patients with low LMNA had a significant worse overall survival. We also found that LMNA expression significantly impaired EWS metastases formation in vivo. We demonstrated that low lamin A expression was linked to a severe mislocalization of LINC complex proteins, thus disrupting nucleo-cytoskeleton interactions, with a corresponding gain in malignant properties, which resulted in increased invasiveness. Lamin A overexpression or its accumulation by a statin-based pharmacological treatment allowed us to reconstitute a functional nucleo-cytoskeleton interplay, which resulted in significant downmodulation of ROCK2 and YAP, two crucial drivers of EWS aggressiveness. Our study demonstrated that lamin A is a favorable mediator of nuclear shape stability in bone sarcomas, and its modulation rescues LINC complex protein localization and regulates mechano-signaling pathways, thus promoting a less aggressive cancer phenotype. We also identified statins, already employed in clinical practice, as a tool capable to increase lamin A levels, and to

Published
2023

37. Abstract 6168: Implementation and adoption of a web tool to support precision diagnostic and treatment decisions for patient with myelodysplastic syndromes

Author

Bernard, Elsa, primary, Ossa, Juan E. Arango, additional, Tuechler, Heinz, additional, Greenberg, Peter L., additional, Hasserjian, Robert P., additional, Nannya, Yasuhito, additional, Devlin, Sean M., additional, Creignou, Maria, additional, Pinel, Philippe, additional, Monier, Lily, additional, Medina-Martinez, Juan S., additional, Domenico, Dylan, additional, Jädersten, Martin, additional, Germing, Ulrich, additional, Sanz, Guillermo, additional, van de Loosdrecht, Arjan A., additional, Kosmider, Olivier, additional, Follo, Matilde Y., additional, Thol, Felicitas, additional, Zamora, Lurdes, additional, Pinheiro, Ronald F., additional, Pellagatti, Andrea, additional, Haase, Detlef, additional, Fenaux, Pierre, additional, Belickova, Monika, additional, Savona, Michael R., additional, Klimek, Virginia M., additional, Santos, Fabio P., additional, Boultwood, Jacqueline, additional, Kotsianidis, Ioannis, additional, Santini, Valeria, additional, Solé, Francesc, additional, Platzbecker, Uwe, additional, Heuser, Michael, additional, Valent, Peter, additional, Ohyashiki, Kazuma, additional, Finelli, Carlo, additional, Voso, Maria Teresa, additional, Shih, Lee-Yung, additional, Fontenay, Michaela, additional, Jansen, Joop H., additional, Cervera, José, additional, Gattermann, Norbert, additional, Ebert, Benjamin L., additional, Bejar, Rafael, additional, Malcovati, Luca, additional, Cazzola, Mario, additional, Ogawa, Seishi, additional, Hellström-Lindberg, Eva, additional, and Papaemmanuil, Elli, additional

Published
2023
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38. Supplementary Table S1 from Prospective Phase II Study on 5-Days Azacitidine for Treatment of Symptomatic and/or Erythropoietin Unresponsive Patients with Low/INT-1–Risk Myelodysplastic Syndromes

Author

Filì, Carla, primary, Malagola, Michele, primary, Follo, Matilde Y., primary, Finelli, Carlo, primary, Iacobucci, Ilaria, primary, Martinelli, Giovanni, primary, Cattina, Federica, primary, Clissa, Cristina, primary, Candoni, Anna, primary, Fanin, Renato, primary, Gobbi, Marco, primary, Bocchia, Monica, primary, Defina, Marzia, primary, Spedini, Pierangelo, primary, Skert, Cristina, primary, Manzoli, Lucia, primary, Cocco, Lucio, primary, and Russo, Domenico, primary

Published
2023
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39. Supplementary Figure S2 from Prospective Phase II Study on 5-Days Azacitidine for Treatment of Symptomatic and/or Erythropoietin Unresponsive Patients with Low/INT-1–Risk Myelodysplastic Syndromes

Author

Filì, Carla, primary, Malagola, Michele, primary, Follo, Matilde Y., primary, Finelli, Carlo, primary, Iacobucci, Ilaria, primary, Martinelli, Giovanni, primary, Cattina, Federica, primary, Clissa, Cristina, primary, Candoni, Anna, primary, Fanin, Renato, primary, Gobbi, Marco, primary, Bocchia, Monica, primary, Defina, Marzia, primary, Spedini, Pierangelo, primary, Skert, Cristina, primary, Manzoli, Lucia, primary, Cocco, Lucio, primary, and Russo, Domenico, primary

Published
2023
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41. Author Correction: Implications of TP53 allelic state for genome stability, clinical presentation and outcomes in myelodysplastic syndromes

Author

Bernard, Elsa, Nannya, Yasuhito, Hasserjian, Robert P., Devlin, Sean M., Tuechler, Heinz, Medina-Martinez, Juan S., Yoshizato, Tetsuichi, Shiozawa, Yusuke, Saiki, Ryunosuke, Malcovati, Luca, Levine, Max F., Arango, Juan E., Zhou, Yangyu, Solé, Francesc, Cargo, Catherine A., Haase, Detlef, Creignou, Maria, Germing, Ulrich, Zhang, Yanming, Gundem, Gunes, Sarian, Araxe, van de Loosdrecht, Arjan A., Jädersten, Martin, Tobiasson, Magnus, Kosmider, Olivier, Follo, Matilde Y., Thol, Felicitas, Pinheiro, Ronald F., Santini, Valeria, Kotsianidis, Ioannis, Boultwood, Jacqueline, Santos, Fabio P. S., Schanz, Julie, Kasahara, Senji, Ishikawa, Takayuki, Tsurumi, Hisashi, Takaori-Kondo, Akifumi, Kiguchi, Toru, Polprasert, Chantana, Bennett, John M., Klimek, Virginia M., Savona, Michael R., Belickova, Monika, Ganster, Christina, Palomo, Laura, Sanz, Guillermo, Ades, Lionel, Della Porta, Matteo Giovanni, Elias, Harold K., Smith, Alexandra G., Werner, Yesenia, Patel, Minal, Viale, Agnès, Vanness, Katelynd, Neuberg, Donna S., Stevenson, Kristen E., Menghrajani, Kamal, Bolton, Kelly L., Fenaux, Pierre, Pellagatti, Andrea, Platzbecker, Uwe, Heuser, Michael, Valent, Peter, Chiba, Shigeru, Miyazaki, Yasushi, Finelli, Carlo, Voso, Maria Teresa, Shih, Lee-Yung, Fontenay, Michaela, Jansen, Joop H., Cervera, José, Atsuta, Yoshiko, Gattermann, Norbert, Ebert, Benjamin L., Bejar, Rafael, Greenberg, Peter L., Cazzola, Mario, Hellström-Lindberg, Eva, Ogawa, Seishi, and Papaemmanuil, Elli

Published
2021
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45. DNA Methylation Profiles Capture Clinical and Molecular Heterogeneity of MDS and Can be Harnessed for the Development of Robust Biomarkers Predictive of Response to Azacitidine

Author

Yang, Qin, primary, Brogi, Alice, additional, Griffiths, Elizabeth A., additional, Follo, Matilde Y, additional, Finelli, Carlo, additional, Radich, Jerald P., additional, Rauh, Michael J, additional, Sekeres, Mikkael A., additional, Bejar, Rafael, additional, Santini, Valeria, additional, and Figueroa, Maria Ken E., additional

Published
2022
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46. Incidence, Clinical Associations, and Co-Mutation Patterns of UBA1 Mutations in MDS

Author

Sirenko, Maria, primary, Bernard, Elsa, additional, Beck, David B., additional, Creignou, Maria, additional, Domenico, Dylan, additional, Farina, Andrea, additional, Arango, Juan E, additional, Kosmider, Olivier, additional, Hasserjian, Robert P., additional, Jadersten, Martin, additional, Germing, Ulrich, additional, Sanz, Guillermo, additional, van de Loosdrecht, Arjan A., additional, Follo, Matilde Y, additional, Thol, Felicitas R., additional, Zamora, Lurdes, additional, Pinheiro, Ronald Feitosa, additional, Pellagatti, Andrea, additional, Elias, Harold K., additional, Haase, Detlef, additional, Ganster, Christina, additional, Ades, Lionel, additional, Tobiasson, Magnus, additional, Palomo, Laura, additional, Della Porta, Matteo G., additional, Huberman, Kety, additional, Fenaux, Pierre, additional, Belickova, Monika, additional, Savona, Michael R., additional, Klimek, Virginia M., additional, Santos, Fabio Pires de Souza, additional, Boultwood, Jacqueline, additional, Kotsianidis, Ioannis, additional, Santini, Valeria, additional, Solé, Francesc, additional, Platzbecker, Uwe, additional, Heuser, Michael, additional, Valent, Peter, additional, Finelli, Carlo, additional, Voso, Maria Teresa, additional, Shih, Lee-Yung, additional, Ogawa, Seishi, additional, Fontenay, Michaela, additional, Jansen, Joop H., additional, Cervera, Jose, additional, Ebert, Benjamin L., additional, Bejar, Rafael, additional, Greenberg, Peter L, additional, Gattermann, Norbert, additional, Malcovati, Luca, additional, Cazzola, Mario, additional, Hellström-Lindberg, Eva, additional, and Papaemmanuil, Elli, additional

Published
2022
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47. Venetoclax Rapidly and Strongly Enhances the Phospholipase C Response to Azacitidine Therapy in Myelodysplastic Syndromes

Author

Follo, Matilde Y, primary, De Stefano, Alessia, additional, Mongiorgi, Sara, additional, Casalin, Irene, additional, Cappellini, Alessandra, additional, Ratti, Stefano, additional, Pellagatti, Andrea, additional, Fogli, Miriam, additional, Cavo, Michele, additional, Manzoli, Lucia, additional, Cocco, Lucio, additional, Boultwood, Jacqueline, additional, Parisi, Sarah, additional, Paolini, Stefania, additional, Curti, Antonio, additional, and Finelli, Carlo, additional

Published
2022
Full Text
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