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3. Venetoclax: A Game Changer in the Treatment of Younger AML Patients?

Author

Molica, Matteo, Perrone, Salvatore, Federico, Vincenzo, Alati, Caterina, Molica, Stefano, and Rossi, Marco

Subjects
THERAPEUTIC use of antineoplastic agents, CANCER chemotherapy, BENCHMARKING (Management), AT-risk people, MOLECULAR structure, COMBINED modality therapy, DIFFUSION of innovations, DISEASE remission
Abstract

Simple Summary: In recent studies, the combination of venetoclax with intensive chemotherapy has demonstrated encouraging results in the treatment of fit patients with de novo and relapsed/refractory acute myeloid leukemia (AML). This review focuses on ongoing clinical trials that investigated the addition of venetoclax to frontline regimens in younger AML patients and specific molecularly defined subgroups. Results of these trials indicate the potential benefits of integrating venetoclax into intensive chemotherapy strategies across European Leukemia Net (ELN) risk subcategories, thus offering valuable guidance for developing future clinical trials. The combination approach based on venetoclax (VEN) with azacytidine (AZA) has significantly improved outcomes for elderly patients with acute myeloid leukemia (AML). This innovative approach has led to higher rates of overall response, measurable residual disease (MRD)-negative remissions, and overall survival compared with AZA monotherapy. As a result, this combination has emerged as the gold-standard treatment for elderly or unfit patients with AML who are not eligible for intensive therapy. In younger, fit patients with AML, intensive induction and consolidation chemotherapy is commonly used as a first-line approach; however, relapse continues to be the main reason for treatment failure in approximately 30–40% of patients. Efforts to improve MRD-negative response rates and to facilitate the transition to allogeneic hematopoietic stem cell transplantation, particularly in high-risk AML, have inspired trials exploring the combination of intensive chemotherapy with targeted agents. VEN, a first-in-class anti-BCL2 agent, combined with intensive chemotherapy regimens has shown deep MRD-negative remissions, producing prolonged event-free survival and enhancing the transition to allogeneic transplant in first-complete-remission patients. These benefits support the incremental advantages of adding VEN to intensive chemotherapy approaches across ELN risk subcategories, and provides a robust benchmark to design future trials. In this review, we will discuss current studies assessing the efficacy of frontline regimens integrating VEN into intensive chemotherapy in younger patients with AML and specific molecularly defined subgroups. [ABSTRACT FROM AUTHOR]

Published
2024
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4. A Novel Bispecific T-Cell Engager (CD1a x CD3ε) BTCE Is Effective against Cortical-Derived T Cell Acute Lymphoblastic Leukemia (T-ALL) Cells

Author

Riillo, Caterina, primary, Caracciolo, Daniele, additional, Grillone, Katia, additional, Polerà, Nicoletta, additional, Tuccillo, Franca Maria, additional, Bonelli, Patrizia, additional, Juli, Giada, additional, Ascrizzi, Serena, additional, Scionti, Francesca, additional, Arbitrio, Mariamena, additional, Lopreiato, Mariangela, additional, Siciliano, Maria Anna, additional, Sestito, Simona, additional, Talarico, Gabriella, additional, Galea, Eulalia, additional, Galati, Maria Concetta, additional, Pensabene, Licia, additional, Loprete, Giovanni, additional, Rossi, Marco, additional, Ballerini, Andrea, additional, Gentile, Massimo, additional, Britti, Domenico, additional, Di Martino, Maria Teresa, additional, Tagliaferri, Pierosandro, additional, and Tassone, Pierfrancesco, additional

Published
2022
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6. Glioblastoma Surgery Imaging–Reporting and Data System: Validation and Performance of the Automated Segmentation Task

Author

Bouget, David, primary, Eijgelaar, Roelant S., additional, Pedersen, André, additional, Kommers, Ivar, additional, Ardon, Hilko, additional, Barkhof, Frederik, additional, Bello, Lorenzo, additional, Berger, Mitchel S., additional, Nibali, Marco Conti, additional, Furtner, Julia, additional, Fyllingen, Even Hovig, additional, Hervey-Jumper, Shawn, additional, Idema, Albert J. S., additional, Kiesel, Barbara, additional, Kloet, Alfred, additional, Mandonnet, Emmanuel, additional, Müller, Domenique M. J., additional, Robe, Pierre A., additional, Rossi, Marco, additional, Sagberg, Lisa M., additional, Sciortino, Tommaso, additional, Van den Brink, Wimar A., additional, Wagemakers, Michiel, additional, Widhalm, Georg, additional, Witte, Marnix G., additional, Zwinderman, Aeilko H., additional, Reinertsen, Ingerid, additional, De Witt Hamer, Philip C., additional, and Solheim, Ole, additional

Published
2021
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7. Raman Spectroscopy and Machine Learning for IDH Genotyping of Unprocessed Glioma Biopsies

Author

Sciortino, Tommaso, primary, Secoli, Riccardo, additional, d’Amico, Ester, additional, Moccia, Sara, additional, Conti Nibali, Marco, additional, Gay, Lorenzo, additional, Rossi, Marco, additional, Pecco, Nicolò, additional, Castellano, Antonella, additional, De Momi, Elena, additional, Fernandes, Bethania, additional, Riva, Marco, additional, and Bello, Lorenzo, additional

Published
2021
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8. Targeting Primary Motor Cortex (M1) Functional Components in M1 Gliomas Enhances Safe Resection and Reveals M1 Plasticity Potentials

Author

Rossi, Marco, primary, Viganò, Luca, additional, Puglisi, Gugliemo, additional, Conti Nibali, Marco, additional, Leonetti, Antonella, additional, Gay, Lorenzo, additional, Sciortino, Tommaso, additional, Fornia, Luca, additional, Callipo, Vincenzo, additional, Lamperti, Marta, additional, Riva, Marco, additional, Cerri, Gabriella, additional, and Bello, Lorenzo, additional

Published
2021
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9. Glioblastoma Surgery Imaging—Reporting and Data System: Standardized Reporting of Tumor Volume, Location, and Resectability Based on Automated Segmentations

Author

Kommers, Ivar, primary, Bouget, David, additional, Pedersen, André, additional, Eijgelaar, Roelant S., additional, Ardon, Hilko, additional, Barkhof, Frederik, additional, Bello, Lorenzo, additional, Berger, Mitchel S., additional, Conti Nibali, Marco, additional, Furtner, Julia, additional, Fyllingen, Even H., additional, Hervey-Jumper, Shawn, additional, Idema, Albert J. S., additional, Kiesel, Barbara, additional, Kloet, Alfred, additional, Mandonnet, Emmanuel, additional, Müller, Domenique M. J., additional, Robe, Pierre A., additional, Rossi, Marco, additional, Sagberg, Lisa M., additional, Sciortino, Tommaso, additional, van den Brink, Wimar A., additional, Wagemakers, Michiel, additional, Widhalm, Georg, additional, Witte, Marnix G., additional, Zwinderman, Aeilko H., additional, Reinertsen, Ingerid, additional, Solheim, Ole, additional, and De Witt Hamer, Philip C., additional

Published
2021
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11. The Non-Coding RNA Landscape of Plasma Cell Dyscrasias

Author

Morelli, Eugenio, primary, Gullà, Annamaria, additional, Rocca, Roberta, additional, Federico, Cinzia, additional, Raimondi, Lavinia, additional, Malvestiti, Stefano, additional, Agosti, Valter, additional, Rossi, Marco, additional, Costa, Giosuè, additional, Giavaresi, Gianluca, additional, Azab, Abdel Kareem, additional, Cagnetta, Antonia, additional, Cea, Michele, additional, Tagliaferri, Pierosandro, additional, Neri, Antonino, additional, Munshi, Nikhil C., additional, Viglietto, Giuseppe, additional, Tassone, Pierfrancesco, additional, and Amodio, Nicola, additional

Published
2020
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12. Anti-tumor Activity and Epigenetic Impact of the Polyphenol Oleacein in Multiple Myeloma

Author

Juli, Giada, primary, Oliverio, Manuela, additional, Bellizzi, Dina, additional, Gallo Cantafio, Maria Eugenia, additional, Grillone, Katia, additional, Passarino, Giuseppe, additional, Colica, Carmela, additional, Nardi, Monica, additional, Rossi, Marco, additional, Procopio, Antonio, additional, Tagliaferri, Pierosandro, additional, Tassone, Pierfrancesco, additional, and Amodio, Nicola, additional

Published
2019
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13. Replacement of miR-155 Elicits Tumor Suppressive Activity and Antagonizes Bortezomib Resistance in Multiple Myeloma

Author

Amodio, Nicola, primary, Gallo Cantafio, Maria, additional, Botta, Cirino, additional, Agosti, Valter, additional, Federico, Cinzia, additional, Caracciolo, Daniele, additional, Ronchetti, Domenica, additional, Rossi, Marco, additional, Driessen, Christoph, additional, Neri, Antonino, additional, Tagliaferri, Pierosandro, additional, and Tassone, Pierfrancesco, additional

Published
2019
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14. Colorectal Cancer and Alcohol Consumption--Populations to Molecules.

Author

Rossi, Marco, Jahanzaib Anwar, Muhammad, Usman, Ahmad, Keshavarzian, Ali, and Bishehsari, Faraz

Subjects
*CARCINOGENESIS, *PEOPLE with alcoholism, *ALDEHYDES, *COLON (Anatomy), *COLON tumors, *ALCOHOL drinking, *LIPID peroxidation (Biology), *OXIDATIVE stress, *CHRONOBIOLOGY disorders, *EPIGENOMICS, IMMUNE system physiology, RECTUM tumors
Abstract

Colorectal cancer (CRC) is a major cause of morbidity and mortality, being the third most common cancer diagnosed in both men and women in the world. Several environmental and habitual factors have been associated with the CRC risk. Alcohol intake, a common and rising habit of modern society, is one of the major risk factors for development of CRC. Here, we will summarize the evidence linking alcohol with colon carcinogenesis and possible underlying mechanisms. Some epidemiologic studies suggest that even moderate drinking increases the CRC risk. Metabolism of alcohol involves ethanol conversion to its metabolites that could exert carcinogenic effects in the colon. Production of ethanol metabolites can be affected by the colon microbiota, another recently recognized mediating factor to colon carcinogenesis. The generation of acetaldehyde and alcohol's other metabolites leads to activation of cancer promoting cascades, such as DNA-adduct formation, oxidative stress and lipid peroxidation, epigenetic alterations, epithelial barrier dysfunction, and immune modulatory effects. Not only does alcohol induce its toxic effect through carcinogenic metabolites, but alcoholics themselves are predisposed to a poor diet, low in folate and fiber, and circadian disruption, which could further augment alcohol-induced colon carcinogenesis. [ABSTRACT FROM AUTHOR]

Published
2018
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