Bcl‐xL represents a therapeutic target in Philadelphia negative myeloproliferative neoplasms
Myeloproliferative neoplasms are divided into essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF). Although ruxolitinib was proven to be effective in reducing symptoms, patients rarely achieve complete molecular remission. Therefore, it is relevant to identify new...
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Published in | Journal of cellular and molecular medicine Vol. 24; no. 18; pp. 10978 - 10986 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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England
John Wiley & Sons, Inc
01.09.2020
John Wiley and Sons Inc |
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Abstract | Myeloproliferative neoplasms are divided into essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF). Although ruxolitinib was proven to be effective in reducing symptoms, patients rarely achieve complete molecular remission. Therefore, it is relevant to identify new therapeutic targets to improve the clinical outcome of patients. Bcl‐xL protein, the long isoform encoded by alternative splicing of the Bcl‐x gene, acts as an anti‐apoptotic regulator. Our study investigated the role of Bcl‐xL as a marker of severity of MPN and the possibility to target Bcl‐xL in patients. 129 MPN patients and 21 healthy patients were enrolled in the study. We analysed Bcl‐xL expression in leucocytes and in enriched CD34+ and CD235a+ cells. Furthermore, ABT‐737, a Bcl‐xL inhibitor, was tested in HEL cells and in leucocytes from MPN patients. Bcl‐xL was found progressively over‐expressed in cells from ET, PV and PMF patients, independently by JAK2 mutational status. Moreover, our data indicated that the combination of ABT‐737 and ruxolitinib resulted in a significantly higher apoptotic rate than the individual drug. Our study suggests that Bcl‐xL plays an important role in MPN independently from JAK2 V617F mutation. Furthermore, data demonstrate that targeting simultaneously JAK2 and Bcl‐xL might represent an interesting new approach. |
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AbstractList | Myeloproliferative neoplasms are divided into essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF). Although ruxolitinib was proven to be effective in reducing symptoms, patients rarely achieve complete molecular remission. Therefore, it is relevant to identify new therapeutic targets to improve the clinical outcome of patients. Bcl‐xL protein, the long isoform encoded by alternative splicing of the Bcl‐x gene, acts as an anti‐apoptotic regulator. Our study investigated the role of Bcl‐xL as a marker of severity of MPN and the possibility to target Bcl‐xL in patients. 129 MPN patients and 21 healthy patients were enrolled in the study. We analysed Bcl‐xL expression in leucocytes and in enriched CD34+ and CD235a+ cells. Furthermore, ABT‐737, a Bcl‐xL inhibitor, was tested in HEL cells and in leucocytes from MPN patients. Bcl‐xL was found progressively over‐expressed in cells from ET, PV and PMF patients, independently by JAK2 mutational status. Moreover, our data indicated that the combination of ABT‐737 and ruxolitinib resulted in a significantly higher apoptotic rate than the individual drug. Our study suggests that Bcl‐xL plays an important role in MPN independently from JAK2 V617F mutation. Furthermore, data demonstrate that targeting simultaneously JAK2 and Bcl‐xL might represent an interesting new approach. Myeloproliferative neoplasms are divided into essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF). Although ruxolitinib was proven to be effective in reducing symptoms, patients rarely achieve complete molecular remission. Therefore, it is relevant to identify new therapeutic targets to improve the clinical outcome of patients. Bcl‐xL protein, the long isoform encoded by alternative splicing of the Bcl‐x gene, acts as an anti‐apoptotic regulator. Our study investigated the role of Bcl‐xL as a marker of severity of MPN and the possibility to target Bcl‐xL in patients. 129 MPN patients and 21 healthy patients were enrolled in the study. We analysed Bcl‐xL expression in leucocytes and in enriched CD34+ and CD235a+ cells. Furthermore, ABT‐737, a Bcl‐xL inhibitor, was tested in HEL cells and in leucocytes from MPN patients. Bcl‐xL was found progressively over‐expressed in cells from ET, PV and PMF patients, independently by JAK2 mutational status. Moreover, our data indicated that the combination of ABT‐737 and ruxolitinib resulted in a significantly higher apoptotic rate than the individual drug. Our study suggests that Bcl‐xL plays an important role in MPN independently from JAK2 V617F mutation. Furthermore, data demonstrate that targeting simultaneously JAK2 and Bcl‐xL might represent an interesting new approach. Abstract Myeloproliferative neoplasms are divided into essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF). Although ruxolitinib was proven to be effective in reducing symptoms, patients rarely achieve complete molecular remission. Therefore, it is relevant to identify new therapeutic targets to improve the clinical outcome of patients. Bcl‐xL protein, the long isoform encoded by alternative splicing of the Bcl‐x gene, acts as an anti‐apoptotic regulator. Our study investigated the role of Bcl‐xL as a marker of severity of MPN and the possibility to target Bcl‐xL in patients. 129 MPN patients and 21 healthy patients were enrolled in the study. We analysed Bcl‐xL expression in leucocytes and in enriched CD34+ and CD235a+ cells. Furthermore, ABT‐737, a Bcl‐xL inhibitor, was tested in HEL cells and in leucocytes from MPN patients. Bcl‐xL was found progressively over‐expressed in cells from ET, PV and PMF patients, independently by JAK2 mutational status. Moreover, our data indicated that the combination of ABT‐737 and ruxolitinib resulted in a significantly higher apoptotic rate than the individual drug. Our study suggests that Bcl‐xL plays an important role in MPN independently from JAK2 V617F mutation. Furthermore, data demonstrate that targeting simultaneously JAK2 and Bcl‐xL might represent an interesting new approach. |
Author | Podestà, Marina Gobbi, Marco De Fava, Carmen Andreani, Giacomo Jovanovski, Aleksandar Lo Iacono, Marco Rosso, Valentina Frassoni, Francesco Lame, Dorela Saglio, Giuseppe Petiti, Jessica Cilloni, Daniela |
AuthorAffiliation | 1 Department of Clinical and Biological Sciences University of Turin Turin Italy 2 Department of Pediatric Hemato‐Oncology and Stem Cell and Cellular Therapy Laboratory Institute G. Gaslini Genova Italy |
AuthorAffiliation_xml | – name: 1 Department of Clinical and Biological Sciences University of Turin Turin Italy – name: 2 Department of Pediatric Hemato‐Oncology and Stem Cell and Cellular Therapy Laboratory Institute G. Gaslini Genova Italy |
Author_xml | – sequence: 1 givenname: Jessica orcidid: 0000-0001-8640-2462 surname: Petiti fullname: Petiti, Jessica email: jessica.petiti@unito.it organization: University of Turin – sequence: 2 givenname: Marco surname: Lo Iacono fullname: Lo Iacono, Marco organization: University of Turin – sequence: 3 givenname: Valentina surname: Rosso fullname: Rosso, Valentina organization: University of Turin – sequence: 4 givenname: Giacomo surname: Andreani fullname: Andreani, Giacomo organization: University of Turin – sequence: 5 givenname: Aleksandar surname: Jovanovski fullname: Jovanovski, Aleksandar organization: University of Turin – sequence: 6 givenname: Marina surname: Podestà fullname: Podestà, Marina organization: Institute G. Gaslini – sequence: 7 givenname: Dorela surname: Lame fullname: Lame, Dorela organization: University of Turin – sequence: 8 givenname: Marco De surname: Gobbi fullname: Gobbi, Marco De organization: University of Turin – sequence: 9 givenname: Carmen surname: Fava fullname: Fava, Carmen organization: University of Turin – sequence: 10 givenname: Giuseppe surname: Saglio fullname: Saglio, Giuseppe organization: University of Turin – sequence: 11 givenname: Francesco surname: Frassoni fullname: Frassoni, Francesco organization: University of Turin – sequence: 12 givenname: Daniela orcidid: 0000-0001-6346-4791 surname: Cilloni fullname: Cilloni, Daniela organization: University of Turin |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32790151$$D View this record in MEDLINE/PubMed |
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Keywords | myeloproliferative neoplasms ABT-737 Bcl-xL therapeutic target |
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Snippet | Myeloproliferative neoplasms are divided into essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF). Although ruxolitinib was... Abstract Myeloproliferative neoplasms are divided into essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF). Although... |
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SubjectTerms | ABT‐737 Alternative splicing Apoptosis Bcl-x protein Bcl‐xL Blood cancer CD34 antigen Gene expression Janus kinase 2 Kinases Leukocytes Lymphoma Medical prognosis Myelofibrosis myeloproliferative neoplasms Original Polycythemia Polycythemia vera Remission Software Therapeutic applications therapeutic target Therapeutic targets Tumors |
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Title | Bcl‐xL represents a therapeutic target in Philadelphia negative myeloproliferative neoplasms |
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