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10. 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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13. Somatic mutational landscape of hereditary hematopoietic malignancies caused by germline variants in RUNX1, GATA2, and DDX41

Author

Homan, Claire C., Drazer, Michael W., Yu, Kai, Lawrence, David M., Feng, Jinghua, Arriola-Martinez, Luis, Pozsgai, Matthew J., McNeely, Kelsey E., Ha, Thuong, Venugopal, Parvathy, Arts, Peer, King-Smith, Sarah L., Cheah, Jesse, Armstrong, Mark, Wang, Paul, Bödör, Csaba, Cantor, Alan B., Cazzola, Mario, Degelman, Erin, DiNardo, Courtney D., Duployez, Nicolas, Favier, Remi, Fröhling, Stefan, Rio-Machin, Ana, Klco, Jeffery M., Krämer, Alwin, Kurokawa, Mineo, Lee, Joanne, Malcovati, Luca, Morgan, Neil V., Natsoulis, Georges, Owen, Carolyn, Patel, Keyur P., Preudhomme, Claude, Raslova, Hana, Rienhoff, Hugh, Ripperger, Tim, Schulte, Rachael, Tawana, Kiran, Velloso, Elvira, Yan, Benedict, Kim, Erika, Sood, Raman, Hsu, Amy P., Holland, Steven M., Phillips, Kerry, Poplawski, Nicola K., Babic, Milena, Wei, Andrew H., Forsyth, Cecily, Mar Fan, Helen, Lewis, Ian D., Cooney, Julian, Susman, Rachel, Fox, Lucy C., Blombery, Piers, Singhal, Deepak, Hiwase, Devendra, Phipson, Belinda, Schreiber, Andreas W., Hahn, Christopher N., Scott, Hamish S., Liu, Paul, Godley, Lucy A., and Brown, Anna L.

Published
2023
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15. 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

16. Secreted mutant calreticulins as rogue cytokines in myeloproliferative neoplasms

Author

Pecquet, Christian, Papadopoulos, Nicolas, Balligand, Thomas, Chachoua, Ilyas, Tisserand, Amandine, Vertenoeil, Gaëlle, Nédélec, Audrey, Vertommen, Didier, Roy, Anita, Marty, Caroline, Nivarthi, Harini, Defour, Jean-Philippe, El-Khoury, Mira, Hug, Eva, Majoros, Andrea, Xu, Erica, Zagrijtschuk, Oleh, Fertig, Tudor E., Marta, Daciana S., Gisslinger, Heinz, Gisslinger, Bettina, Schalling, Martin, Casetti, Ilaria, Rumi, Elisa, Pietra, Daniela, Cavalloni, Chiara, Arcaini, Luca, Cazzola, Mario, Komatsu, Norio, Kihara, Yoshihiko, Sunami, Yoshitaka, Edahiro, Yoko, Araki, Marito, Lesyk, Roman, Buxhofer-Ausch, Veronika, Heibl, Sonja, Pasquier, Florence, Havelange, Violaine, Plo, Isabelle, Vainchenker, William, Kralovics, Robert, and Constantinescu, Stefan N.

Published
2023
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19. 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. TP53 mutation status divides myelodysplastic syndromes with complex karyotypes into distinct prognostic subgroups.

Author

Haase, Detlef, Stevenson, Kristen E, Neuberg, Donna, Maciejewski, Jaroslaw P, Nazha, Aziz, Sekeres, Mikkael A, Ebert, Benjamin L, Garcia-Manero, Guillermo, Haferlach, Claudia, Haferlach, Torsten, Kern, Wolfgang, Ogawa, Seishi, Nagata, Yasunobu, Yoshida, Kenichi, Graubert, Timothy A, Walter, Matthew J, List, Alan F, Komrokji, Rami S, Padron, Eric, Sallman, David, Papaemmanuil, Elli, Campbell, Peter J, Savona, Michael R, Seegmiller, Adam, Adès, Lionel, Fenaux, Pierre, Shih, Lee-Yung, Bowen, David, Groves, Michael J, Tauro, Sudhir, Fontenay, Michaela, Kosmider, Olivier, Bar-Natan, Michal, Steensma, David, Stone, Richard, Heuser, Michael, Thol, Felicitas, Cazzola, Mario, Malcovati, Luca, Karsan, Aly, Ganster, Christina, Hellström-Lindberg, Eva, Boultwood, Jacqueline, Pellagatti, Andrea, Santini, Valeria, Quek, Lynn, Vyas, Paresh, Tüchler, Heinz, Greenberg, Peter L, Bejar, Rafael, and International Working Group for MDS Molecular Prognostic Committee

Subjects
International Working Group for MDS Molecular Prognostic Committee, Humans, Myelodysplastic Syndromes, Chromosome Aberrations, Prognosis, Combined Modality Therapy, Survival Rate, Follow-Up Studies, Karyotyping, Mutation, Aged, Aged, 80 and over, Middle Aged, Female, Male, Tumor Suppressor Protein p53, Biomarkers, Tumor, Hematology, Rare Diseases, Genetics, Clinical Sciences, Oncology and Carcinogenesis, Immunology
Abstract

Risk stratification is critical in the care of patients with myelodysplastic syndromes (MDS). Approximately 10% have a complex karyotype (CK), defined as more than two cytogenetic abnormalities, which is a highly adverse prognostic marker. However, CK-MDS can carry a wide range of chromosomal abnormalities and somatic mutations. To refine risk stratification of CK-MDS patients, we examined data from 359 CK-MDS patients shared by the International Working Group for MDS. Mutations were underrepresented with the exception of TP53 mutations, identified in 55% of patients. TP53 mutated patients had even fewer co-mutated genes but were enriched for the del(5q) chromosomal abnormality (p 10%), abnormal 3q, abnormal 9, and monosomy 7 as having the greatest survival risk. The poor risk associated with CK-MDS is driven by its association with prognostically adverse TP53 mutations and can be refined by considering clinical and karyotype features.

Published
2019

23. International Consensus Classification of Myeloid Neoplasms and Acute Leukemias: integrating morphologic, clinical, and genomic data

Author

Arber, Daniel A., Orazi, Attilio, Hasserjian, Robert P., Borowitz, Michael J., Calvo, Katherine R., Kvasnicka, Hans-Michael, Wang, Sa A., Bagg, Adam, Barbui, Tiziano, Branford, Susan, Bueso-Ramos, Carlos E., Cortes, Jorge E., Dal Cin, Paola, DiNardo, Courtney D., Dombret, Hervé, Duncavage, Eric J., Ebert, Benjamin L., Estey, Elihu H., Facchetti, Fabio, Foucar, Kathryn, Gangat, Naseema, Gianelli, Umberto, Godley, Lucy A., Gökbuget, Nicola, Gotlib, Jason, Hellström-Lindberg, Eva, Hobbs, Gabriela S., Hoffman, Ronald, Jabbour, Elias J., Kiladjian, Jean-Jacques, Larson, Richard A., Le Beau, Michelle M., Loh, Mignon L.-C., Löwenberg, Bob, Macintyre, Elizabeth, Malcovati, Luca, Mullighan, Charles G., Niemeyer, Charlotte, Odenike, Olatoyosi M., Ogawa, Seishi, Orfao, Alberto, Papaemmanuil, Elli, Passamonti, Francesco, Porkka, Kimmo, Pui, Ching-Hon, Radich, Jerald P., Reiter, Andreas, Rozman, Maria, Rudelius, Martina, Savona, Michael R., Schiffer, Charles A., Schmitt-Graeff, Annette, Shimamura, Akiko, Sierra, Jorge, Stock, Wendy A., Stone, Richard M., Tallman, Martin S., Thiele, Jürgen, Tien, Hwei-Fang, Tzankov, Alexandar, Vannucchi, Alessandro M., Vyas, Paresh, Wei, Andrew H., Weinberg, Olga K., Wierzbowska, Agnieszka, Cazzola, Mario, Döhner, Hartmut, and Tefferi, Ayalew

Published
2022
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26. Patient-specific MDS-RS iPSCs define the mis-spliced transcript repertoire and chromatin landscape of SF3B1-mutant HSPCs

Author

Asimomitis, Georgios, Deslauriers, André G., Kotini, Andriana G., Bernard, Elsa, Esposito, Davide, Olszewska, Malgorzata, Spyrou, Nikolaos, Arango Ossa, Juan, Mortera-Blanco, Teresa, Koche, Richard, Nannya, Yasuhito, Malcovati, Luca, Ogawa, Seishi, Cazzola, Mario, Aaronson, Stuart A., Hellström-Lindberg, Eva, Papaemmanuil, Elli, and Papapetrou, Eirini P.

Published
2022
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28. Pseudouridine-modified tRNA fragments repress aberrant protein synthesis and predict leukaemic progression in myelodysplastic syndrome

Author

Guzzi, Nicola, Muthukumar, Sowndarya, Cieśla, Maciej, Todisco, Gabriele, Ngoc, Phuong Cao Thi, Madej, Magdalena, Munita, Roberto, Fazio, Serena, Ekström, Simon, Mortera-Blanco, Teresa, Jansson, Monika, Nannya, Yasuhito, Cazzola, Mario, Ogawa, Seishi, Malcovati, Luca, Hellström-Lindberg, Eva, Dimitriou, Marios, and Bellodi, Cristian

Published
2022
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33. Germ line DDX41 mutations define a unique subtype of myeloid neoplasms

Author

Makishima, Hideki, Saiki, Ryunosuke, Nannya, Yasuhito, Korotev, Sophia, Gurnari, Carmelo, Takeda, June, Momozawa, Yukihide, Best, Steve, Krishnamurthy, Pramila, Yoshizato, Tetsuichi, Atsuta, Yoshiko, Shiozawa, Yusuke, Iijima-Yamashita, Yuka, Yoshida, Kenichi, Shiraishi, Yuichi, Nagata, Yasunobu, Kakiuchi, Nobuyuki, Onizuka, Makoto, Chiba, Kenichi, Tanaka, Hiroko, Kon, Ayana, Ochi, Yotaro, Nakagawa, Masahiro M., Okuda, Rurika, Mori, Takuto, Yoda, Akinori, Itonaga, Hidehiro, Miyazaki, Yasushi, Sanada, Masashi, Ishikawa, Takayuki, Chiba, Shigeru, Tsurumi, Hisashi, Kasahara, Senji, Muller-Tidow, Carsten, Takaori-Kondo, Akifumi, Ohyashiki, Kazuma, Kiguchi, Toru, Matsuda, Fumihiko, Jansen, Joop H., Polprasert, Chantana, Blombery, Piers, Kamatani, Yoichiro, Miyano, Satoru, Malcovati, Luca, Haferlach, Torsten, Kubo, Michiaki, Cazzola, Mario, Kulasekararaj, Austin G., Godley, Lucy A., Maciejewski, Jaroslaw P., and Ogawa, Seishi

Published
2022
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34. Biologics for asthma and risk of pneumonia.

Author

Matera, Maria Gabriella, Ora, Josuel, Calzetta, Luigino, Rogliani, Paola, and Cazzola, Mario

Abstract

Objective: Modification of the immune system with biologics raises theoretical concerns about the risk of infections but it is still unclear whether currently routinely used biologics in severe asthma may facilitate the development of pneumonia. Therefore, we aimed to determine whether omalizumab, mepolizumab, benralizumab, and dupilumab are associated with pneumonia in a real-world setting. Methods: A retrospective disproportionality analysis was performed using adverse event (AE) reports submitted to FAERS from January 2020 to September 30, 2023. MedDRA was used to identify infections and infestations and then pneumonia cases. ROR and PRR were used to measure disproportionality. Results: The percentage of reported cases of pneumonia compared to infections and infestations was highest for mepolizumab (36.8%), followed by omalizumab (32.6%), benralizumab (19.2%) and dupilumab (5.7%). We found a moderate or strong signal for increased risk of pneumonia with mepolizumab (ROR = 3.74, 95%CI 3.50–4.00), omalizumab (ROR = 3.26, 95%CI 3.06–3.49) and benralizumab (ROR = 2.65, 95%CI 2.49–2.83). Conclusions: Mepolizumab, omalizumab and benralizumab, but not dupilumab, were associated with high odds of reporting pneumonia. Our results represent only potential associations between these biologics and pneumonia but not causality. The nature of the FAERS database is such that the cause of the reported events is uncertain. Therefore, we can only roughly estimate the incidence of AEs by the signal strength (ROR value). Nevertheless, although causality could not be assessed, the signal from our study is interesting. We believe it deserves to be further substantiated by real-world studies with robust designs. [ABSTRACT FROM AUTHOR]

Published
2024
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37. Genomic Profiling for Predictive Treatment Strategies in Fibrotic Interstitial Lung Disease.

Author

Perrotta, Fabio, Sanduzzi Zamparelli, Stefano, D'Agnano, Vito, Montella, Antonia, Fomez, Ramona, Pagliaro, Raffaella, Schiattarella, Angela, Cazzola, Mario, Bianco, Andrea, and Mariniello, Domenica Francesca

Subjects
PULMONARY fibrosis, IDIOPATHIC pulmonary fibrosis, INTERSTITIAL lung diseases, HYPERSENSITIVITY pneumonitis, AUTOIMMUNE diseases
Abstract

Idiopathic pulmonary fibrosis (IPF) has traditionally been considered the archetype of progressive fibrotic interstitial lung diseases (f-ILDs), but several other f-ILDs can also manifest a progressive phenotype. Integrating genomic signatures into clinical practice for f-ILD patients may help to identify patients predisposed to a progressive phenotype. In addition to the risk of progressive pulmonary fibrosis, there is a growing body of literature examining how pharmacogenomics influences treatment response, particularly regarding the efficacy and safety profiles of antifibrotic and immunomodulatory agents. In this narrative review, we discuss current studies in IPF and other forms of pulmonary fibrosis, including systemic autoimmune disorders associated ILDs, sarcoidosis and hypersensitivity pneumonitis. We also provide insights into the future direction of research in this complex field. [ABSTRACT FROM AUTHOR]

Published
2024
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46. Use of Thiols in the Treatment of COVID-19: Current Evidence

Author

Cazzola, Mario, Rogliani, Paola, Salvi, Sundeep Santosh, Ora, Josuel, and Matera, Maria Gabriella

Subjects
Cytokines -- Health aspects, Free radicals (Chemistry) -- Health aspects, Acetylcysteine -- Health aspects, Blood clot -- Health aspects, Antioxidants -- Health aspects, Thrombosis -- Health aspects, Enzymes -- Health aspects, Thiols -- Health aspects, Coronaviruses -- Health aspects, Virus diseases -- Health aspects, Health
Abstract

There is a possible role for oxidative stress, a state characterized by an altered balance between the production of free radicals or reactive oxygen species (ROS) and antioxidant defences, in coronavirus disease 2019 (COVID-19), the genesis of which is quite complex. Excessive oxidative stress could be responsible for the alveolar damage, thrombosis, and red blood cell dysregulation observed in COVID-19. Apparently, deficiency of glutathione (GSH), a low-molecular-weight thiol that is the most important non-enzymatic antioxidant molecule and has the potential to keep the cytokine storm in check, is a plausible explanation for the severe manifestations and death in COVID-19 patients. Thiol drugs, which are considered mucolytic, also possess potent antioxidant and anti-inflammatory properties. They exhibit antibacterial activity against a variety of medically important bacteria and may be an effective strategy against influenza virus infection. The importance of oxidative stress during COVID-19 and the various pharmacological characteristics of thiol-based drugs suggest a possible role of thiols in the treatment of COVID-19. Oral and intravenous GSH, as well as GSH precursors such as N-acetylcysteine (NAC), or drugs containing the thiol moiety (erdosteine) may represent a novel therapeutic approach to block NF-kB and address the cytokine storm syndrome and respiratory distress observed in COVID-19 pneumonia patients, Author(s): Mario Cazzola [sup.1], Paola Rogliani [sup.1], Sundeep Santosh Salvi [sup.2], Josuel Ora [sup.1], Maria Gabriella Matera [sup.3] Author Affiliations: (1) grid.6530.0, 0000 0001 2300 0941, Unit of Respiratory Medicine, [...]

Published
2021
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48. Co-mutation pattern, clonal hierarchy, and clone size concur to determine disease phenotype of SRSF2P95-mutated neoplasms

Author

Todisco, Gabriele, Creignou, Maria, Gallì, Anna, Guglielmelli, Paola, Rumi, Elisa, Roncador, Marco, Rizzo, Ettore, Nannya, Yasuhito, Pietra, Daniela, Elena, Chiara, Bono, Elisa, Molteni, Elisabetta, Rosti, Vittorio, Catricalá, Silvia, Sarchi, Martina, Dimitriou, Marios, Ungerstedt, Johanna, Vannucchi, Alessandro Maria, Hellström-Lindberg, Eva, Ogawa, Seishi, Cazzola, Mario, and Malcovati, Luca

Published
2021
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