KCTD15 is overexpressed in human childhood B-cell acute lymphoid leukemia(14 visite) Smaldone G, Beneduce G, Incoronato M, Pane K, Franzese M, Coppola L, Cordella A, Parasole R, Ripaldi M, Nassa G, Soricelli A, Vitagliano L, Mirabelli P, Salvatore M
Sci Rep (ISSN: 2045-2322linking), 2019 Dec 27; 9(1): 20108-20108.
Tipo di articolo: Journal Article
Impact factor: 4.122, Impact factor a 5 anni: 5.078
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Parole chiave: Non disponibili.
*** IBB - CNR *** IRCCS SDN, Via E. Gianturco 113, 80143, Napoli, Italy. Department of Pediatric Hematology-Oncology, Santobono-Pausilipon Hospital, Naples, Italy. Laboratory of Molecular Medicine and Genomics, Department of Medicine and Surgery, University of Salerno, Baronissi, Italy. Department of Sport Sciences & Healthiness, University of Naples 'Parthenope', 80131, Napoli, Italy. Institute of Biostructures and Bioimaging, C.N.R., 80134, Napoli, Italy. firstname.lastname@example.org.
Leukemic cells originate from the malignant transformation of undifferentiated myeloid/lymphoid hematopoietic progenitors normally residing in bone marrow. As the precise molecular mechanisms underlying this heterogeneous disease are yet to be disclosed, the identification and the validation of novel actors in leukemia is of extreme importance. Here, we show that KCTD15, a member of the emerging class of KCTD ((K)potassium Channel Tetramerization Domain containing) proteins, is strongly upregulated in patients affected by B-cell type acute lymphoblastic leukemia (B-ALL) and in continuous cell lines (RS4;11, REH, TOM-1, SEM) derived from this form of childhood leukemia. Interestingly, KCTD15 downregulation induces apoptosis and cell death suggesting that it has a role in cellular homeostasis and proliferation. In addition, stimulation of normal lymphocytes with the pokeweed mitogen leads to increased KCTD15 levels in a fashion comparable to those observed in proliferating leukemic cells. In this way, the role of KCTD15 is likely not confined to the B-ALL pathological state and extends to activation and proliferation of normal lymphocytes. Collectively, data here presented indicate that KCTD15 is an important and hitherto unidentified player in childhood lymphoid leukemia, and its study could open a new scenario for the identification of altered and still unknown molecular pathways in leukemia.<br>
Petraglia F, Singh AA, Carafa V, Nebbioso A, Conte M, Scisciola L, Valente S, Baldi A, Mandoli A, Petrizzi VB, Ingenito C, De Falco S, Cicatiello V, Apicella I, Janssen-megens EM, Kim B, Yi G, Logie C, Heath S, Ruvo M, Wierenga ATJ, Flicek P, Yaspo ML, Della Valle V, Bernard O, Tomassi S, Novellino E, Feoli A, Sbardella G, Gut I, Vellenga E, Stunnenberg HG, Mai A, Martens JHA, Altucci L * Combined HAT/EZH2 modulation leads to cancer-selective cell death(145 visite) Oncotarget (ISSN: 1949-2553electronic, 1949-2553linking), 2018 May 22; 9(39): 25630-25646. Impact Factor:5.008 DettagliEsporta in BibTeXEsporta in EndNote
46 Records (44 escludendo Abstract e Conferenze). Impact factor totale: 168.786 (162.354 escludendo Abstract e Conferenze). Impact factor a 5 anni totale: 180.404 (173.986 escludendo Abstract e Conferenze).