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  1. Article: Lessons, Challenges and Future Therapeutic Opportunities for PI3K Inhibition in CLL.

    Guarente, Valerio / Sportoletti, Paolo

    Cancers

    2021  Volume 13, Issue 6

    Abstract: Chronic lymphocytic leukemia (CLL) shows constitutive phosphatidylinositol 3-kinase (PI3K) activation resulting from aberrant regulation of the B-cell receptor (BCR) signaling. PI3K inhibitors have been evaluated in CLL therapy, bringing a new treatment ... ...

    Abstract Chronic lymphocytic leukemia (CLL) shows constitutive phosphatidylinositol 3-kinase (PI3K) activation resulting from aberrant regulation of the B-cell receptor (BCR) signaling. PI3K inhibitors have been evaluated in CLL therapy, bringing a new treatment opportunity for patients with this disease. Despite the proven therapeutic efficacy, the use of approved PI3K inhibitors is limited by severe immune-mediated toxicities and given the availability of other more tolerable agents. This article reviews the relevance of PI3K signaling and pharmacologic inhibition in CLL. Data on efficacy and toxicity of PI3K inhibitors are also presented, as well as strategies for overcoming barriers for their clinical use in CLL treatment.
    Language English
    Publishing date 2021-03-13
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers13061280
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Synthesis and Characterization of ZIF-90 Nanoparticles as Potential Brain Cancer Therapy.

    Monarca, Lorenzo / Ragonese, Francesco / Sabbatini, Paola / Caglioti, Concetta / Stamegna, Matteo / Palazzetti, Federico / Sportoletti, Paolo / Costantino, Ferdinando / Fioretti, Bernard

    Pharmaceutics

    2024  Volume 16, Issue 3

    Abstract: Human glioblastoma is probably the most malignant and aggressive among cerebral tumors, of which it represents approximately 80% of the reported cases, with an overall survival rate that is quite low. Current therapies include surgery, chemotherapy, and ... ...

    Abstract Human glioblastoma is probably the most malignant and aggressive among cerebral tumors, of which it represents approximately 80% of the reported cases, with an overall survival rate that is quite low. Current therapies include surgery, chemotherapy, and radiotherapy, with associated consistent side effects and low efficacy. The hardness in reaching the site of action, and overcoming the blood-brain barrier, is a major limitation of pharmacological treatments. In this paper, we report the synthesis and characterization of ZIF-90 (ZIF, Zeolitic Imidazolate Framework) nanoparticles as putative carriers of anticancer drugs to the brain. In particular, we successfully evaluated the biocompatibility of these nanoparticles, their stability in body fluids, and their ability to uptake in U251 human glioblastoma cell lines. Furthermore, we managed to synthesize ZIF-90 particles loaded with berberine, an alkaloid reported as a possible effective adjuvant in the treatment of glioblastoma. These findings could suggest ZIF-90 as a possible new strategy for brain cancer therapy and to study the physiological processes present in the central nervous system.
    Language English
    Publishing date 2024-03-18
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527217-2
    ISSN 1999-4923
    ISSN 1999-4923
    DOI 10.3390/pharmaceutics16030414
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  3. Article ; Online: BCOR gene alterations in hematologic diseases.

    Sportoletti, Paolo / Sorcini, Daniele / Falini, Brunangelo

    Blood

    2021  Volume 138, Issue 24, Page(s) 2455–2468

    Abstract: The BCL6 corepressor (BCOR) is a transcription factor involved in the control of embryogenesis, mesenchymal stem cells function, hematopoiesis, and lymphoid development. Recurrent somatic clonal mutations of the BCOR gene and its homolog BCORL1 have been ...

    Abstract The BCL6 corepressor (BCOR) is a transcription factor involved in the control of embryogenesis, mesenchymal stem cells function, hematopoiesis, and lymphoid development. Recurrent somatic clonal mutations of the BCOR gene and its homolog BCORL1 have been detected in several hematologic malignancies and aplastic anemia. They are scattered across the whole gene length and mostly represent frameshifts (deletions, insertions), nonsense, and missence mutations. These disruptive events lead to the loss of full-length BCOR protein and to the lack or low expression of a truncated form of the protein, both consistent with the tumor suppressor role of BCOR.BCOR and BCORL1 mutations are similar to those causing 2 rare X-linked diseases: oculofaciocardiodental (OFCD) and Shukla-Vernon syndromes, respectively. Here, we focus on the structure and function of normal BCOR and BCORL1 in normal hematopoietic and lymphoid tissues and review the frequency and clinical significance of the mutations of these genes in malignant and nonmalignant hematologic diseases. Moreover, we discuss the importance of mouse models to better understand the role of Bcor loss, alone and combined with alterations of other genes (eg, Dnmt3a and Tet2), in promoting hematologic malignancies and in providing a useful platform for the development of new targeted therapies.
    MeSH term(s) Animals ; Gene Expression Regulation, Neoplastic ; Hematologic Diseases/genetics ; Hematologic Diseases/metabolism ; Hematologic Diseases/pathology ; Hematologic Neoplasms/genetics ; Hematologic Neoplasms/metabolism ; Hematologic Neoplasms/pathology ; Humans ; Mutation ; Proto-Oncogene Proteins/analysis ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Repressor Proteins/analysis ; Repressor Proteins/genetics ; Repressor Proteins/metabolism
    Chemical Substances BCOR protein, human ; BCORL1 protein, human ; Proto-Oncogene Proteins ; Repressor Proteins
    Language English
    Publishing date 2021-05-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2021010958
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: How does the NPM1 mutant induce leukemia?

    Sportoletti, Paolo

    Pediatric reports

    2011  Volume 3 Suppl 2, Page(s) e6

    Abstract: NPM1 is the most frequently mutated gene in AML and the role of the NPM1 mutant in acute myeloid leukemia along with its leukemogenic potential are still under investigation.NPM1 genetic alterations can contribute to leukemogenesis through the direct ... ...

    Abstract NPM1 is the most frequently mutated gene in AML and the role of the NPM1 mutant in acute myeloid leukemia along with its leukemogenic potential are still under investigation.NPM1 genetic alterations can contribute to leukemogenesis through the direct oncogenic effect of the mutant protein and the concomitant loss of one functional allele. Npm1 loss determines tumor development in the mouse while in human NPM1 maps in a chromosomal region frequently loss in myelodysplastic syndrome (MDS). The NPM1 mutant cytoplasmic delocalization in leukemic blasts alters multiple cellular pathways through either loss or gain of function effects on different protein partners.Here we discuss the most relevant studies on the role of the NPM1 molecule in hematological malignancies and both in vitro and in vivo studies that are trying to elucidate the way by which the NPM1 mutation induces leukemia.
    Language English
    Publishing date 2011-10-11
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2572005-3
    ISSN 2036-7503 ; 2036-7503
    ISSN (online) 2036-7503
    ISSN 2036-7503
    DOI 10.4081/pr.2011.s2.e6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: A scale of "bad" co-mutations in

    Falini, Brunangelo / Sportoletti, Paolo

    Blood

    2017  Volume 130, Issue 17, Page(s) 1877–1879

    MeSH term(s) Humans ; Leukemia, Myeloid, Acute/genetics ; Mutation ; Prognosis ; fms-Like Tyrosine Kinase 3/genetics
    Chemical Substances fms-Like Tyrosine Kinase 3 (EC 2.7.10.1)
    Language English
    Publishing date 2017-10-26
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2017-09-804062
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: NPM1-mutated acute myeloid leukemia: from bench to bedside.

    Falini, Brunangelo / Brunetti, Lorenzo / Sportoletti, Paolo / Martelli, Maria Paola

    Blood

    2020  Volume 136, Issue 15, Page(s) 1707–1721

    Abstract: The nucleophosmin (NPM1) gene encodes for a multifunctional protein with prominent nucleolar localization that shuttles between nucleus and cytoplasm. NPM1 mutations represent the most common genetic lesion in adult acute myeloid leukemia (AML; about one ...

    Abstract The nucleophosmin (NPM1) gene encodes for a multifunctional protein with prominent nucleolar localization that shuttles between nucleus and cytoplasm. NPM1 mutations represent the most common genetic lesion in adult acute myeloid leukemia (AML; about one third of cases), and they act deterministically to cause the aberrant cytoplasmic delocalization of NPM1 mutants. Because of its unique features, NPM1-mutated AML is recognized as a distinct entity in the 2017 World Health Organization (WHO) classification of hematopoietic neoplasms. Here, we focus on recently identified functions of wild-type NPM1 in the nucleolus and address new biological and clinical issues related to NPM1-mutated AML. The relevance of the cooperation between NPM1 and other mutations in driving AML with different outcomes is presented. We also discuss the importance of eradicating NPM1-mutated clones to achieve AML cure and the impact of preleukemic clonal hematopoiesis persistence in predisposing to second AML. The contribution of HOX genes' expression to the development of NPM1-mutated AML is also highlighted. Clinically, yet unsolved diagnostic issues in the 2017 WHO classification of myeloid neoplasms and the importance of NPM1 mutations in defining the framework of European LeukemiaNet genetic-based risk stratification are discussed. Finally, we address the value and limits of NPM1-based measurable residual disease assessment for treatment guidance and present the results of promising preclinical studies with XPO1 and menin-MLL inhibitors.
    MeSH term(s) Animals ; Cell Transformation, Neoplastic/genetics ; Clonal Hematopoiesis/genetics ; Disease Management ; Genetic Association Studies ; Genetic Predisposition to Disease ; Humans ; Leukemia, Myeloid, Acute/diagnosis ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/metabolism ; Leukemia, Myeloid, Acute/therapy ; Mutation ; Nuclear Proteins/genetics ; Precancerous Conditions/genetics ; Precancerous Conditions/metabolism ; Prognosis ; Translational Medical Research
    Chemical Substances Nuclear Proteins ; nucleophosmin (117896-08-9)
    Language English
    Publishing date 2020-07-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2019004226
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  7. Article: Venetoclax-Rituximab Treatment of Relapsed/Refractory CLL During the COVID-19 Pandemic: A Real-Life Experience in Selected Central-Southern Italian Regions.

    Molica, Stefano / Sportoletti, Paolo / Di Renzo, Nicola / Musto, Pellegrino / Pane, Fabrizio / Di Raimondo, Francesco

    Mediterranean journal of hematology and infectious diseases

    2021  Volume 13, Issue 1, Page(s) e2021042

    Language English
    Publishing date 2021-07-01
    Publishing country Italy
    Document type Journal Article
    ZDB-ID 2674750-9
    ISSN 2035-3006
    ISSN 2035-3006
    DOI 10.4084/MJHID.2021.042
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  8. Article ; Online: Uncommon lymphoplasmacytic lymphoma with IgA paraproteinemia: a challenging clinical diagnosis solved by MYD88 mutation analysis.

    Martino, Giovanni / Marra, Andrea / Ascani, Stefano / Sportoletti, Paolo

    Annals of hematology

    2018  Volume 98, Issue 6, Page(s) 1507–1508

    MeSH term(s) Aged ; B-Lymphocytes/immunology ; B-Lymphocytes/pathology ; Bone Marrow/pathology ; DNA Mutational Analysis ; Humans ; Immunoglobulin A/analysis ; Immunoglobulin kappa-Chains/analysis ; Male ; Mutation, Missense ; Myeloid Differentiation Factor 88/genetics ; Paraproteins/analysis ; Plasma Cells/immunology ; Plasma Cells/pathology ; Point Mutation ; Waldenstrom Macroglobulinemia/complications ; Waldenstrom Macroglobulinemia/diagnosis ; Waldenstrom Macroglobulinemia/genetics ; Waldenstrom Macroglobulinemia/immunology
    Chemical Substances Immunoglobulin A ; Immunoglobulin kappa-Chains ; MYD88 protein, human ; Myeloid Differentiation Factor 88 ; Paraproteins
    Language English
    Publishing date 2018-11-13
    Publishing country Germany
    Document type Case Reports ; Letter
    ZDB-ID 1064950-5
    ISSN 1432-0584 ; 0939-5555 ; 0945-8077
    ISSN (online) 1432-0584
    ISSN 0939-5555 ; 0945-8077
    DOI 10.1007/s00277-018-3545-9
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  9. Article ; Online: Polatuzumab-bendamustine-rituximab as bridge to CD19-directed CAR T cells in mantle cell lymphoma refractory to ibrutinib and venetoclax.

    Perriello, Vincenzo Maria / Falini, Lorenza / Ruggeri, Loredana / Sorcini, Daniele / Ballanti, Stelvio / Flenghi, Leonardo / Baffa, Nicodemo / Covarelli, Piero / Sportoletti, Paolo / Pierini, Antonio / Falini, Brunangelo

    EJHaem

    2023  Volume 4, Issue 2, Page(s) 559–562

    Language English
    Publishing date 2023-04-10
    Publishing country United States
    Document type Journal Article
    ISSN 2688-6146
    ISSN (online) 2688-6146
    DOI 10.1002/jha2.655
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  10. Article: A Curious Novel Combination of Nucleophosmin (NPM1) Gene Mutations Leading to Aberrant Cytoplasmic Dislocation of NPM1 in Acute Myeloid Leukemia (AML)

    Venanzi, Alessandra / Rossi, Roberta / Martino, Giovanni / Annibali, Ombretta / Avvisati, Giuseppe / Mameli, Maria Grazia / Sportoletti, Paolo / Tiacci, Enrico / Falini, Brunangelo / Martelli, Maria Paola

    Genes. 2021 Sept. 16, v. 12, no. 9

    2021  

    Abstract: Nucleophosmin (NPM1) mutations occurring in acute myeloid leukemia (AML) (about 50 so far identified) cluster almost exclusively in exon 12 and lead to common changes at the NPM1 mutants C-terminus, i.e., loss of tryptophans 288 and 290 (or 290 alone) ... ...

    Abstract Nucleophosmin (NPM1) mutations occurring in acute myeloid leukemia (AML) (about 50 so far identified) cluster almost exclusively in exon 12 and lead to common changes at the NPM1 mutants C-terminus, i.e., loss of tryptophans 288 and 290 (or 290 alone) and creation of a new nuclear export signal (NES), at the bases of exportin-1(XPO1)-mediated aberrant cytoplasmic NPM1. Immunohistochemistry (IHC) detects cytoplasmic NPM1 and is predictive of the molecular alteration. Besides IHC and molecular sequencing, Western blotting (WB) with anti-NPM1 mutant specific antibodies is another approach to identify NPM1-mutated AML. Here, we show that among 382 AML cases with NPM1 exon 12 mutations, one was not recognized by WB, and describe the discovery of a novel combination of two mutations involving exon 12. This appeared as a conventional mutation A with the known TCTG nucleotides insertion/duplication accompanied by a second event (i.e., an 8-nucleotide deletion occurring 15 nucleotides downstream of the TCTG insertion), resulting in a new C-terminal protein sequence. Strikingly, the sequence included a functional NES ensuring cytoplasmic relocation of the new mutant supporting the role of cytoplasmic NPM1 as critical in AML leukemogenesis.
    Keywords amino acid sequences ; exons ; immunohistochemistry ; mutants ; myeloid leukemia ; nucleotides ; protein transport
    Language English
    Dates of publication 2021-0916
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article
    ZDB-ID 2527218-4
    ISSN 2073-4425
    ISSN 2073-4425
    DOI 10.3390/genes12091426
    Database NAL-Catalogue (AGRICOLA)

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