Xian, Jie
(2020)
From clinic to laboratory: Signal transduction analysis and future applications, [Dissertation thesis], Alma Mater Studiorum Università di Bologna.
Dottorato di ricerca in
Scienze biomediche e neuromotorie, 33 Ciclo. DOI 10.48676/unibo/amsdottorato/9535.
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Abstract
Results: Here we reported the first case of EH with multifocal metachronous bone lesions. This case shows the possible existence of multifocal metachronous EH without producing a fatal outcome. FOS gene rearrangement is critical to assistant the diagnosis of EH. On the other hand, we studied inositide signalling in AML, confirming the IC50 of MOLM-13, HL-60, THP-1 and U-937 hematopoietic cell lines when exposed to Azacitidine and Venetoclax. Moreover, Azacitidine and Venetoclax treatment could induce an increase of the Sub-G0/G1 phase, as well as a G0/G1 arrest in MOLM-13 cells and HL-60 cells. At the same time, it seems to prolong the S phase in U-937 cells. Furthermore, the combination therapy was also able to specifically induce myelopoiesis, as MOLM-13 and THP-1 cells showed an increased expression of CD14. Finally, the combined treatment triggers a higher expression of PLC-β1, which activates the signaling pathway to degrade PKCα.
Abstract
Results: Here we reported the first case of EH with multifocal metachronous bone lesions. This case shows the possible existence of multifocal metachronous EH without producing a fatal outcome. FOS gene rearrangement is critical to assistant the diagnosis of EH. On the other hand, we studied inositide signalling in AML, confirming the IC50 of MOLM-13, HL-60, THP-1 and U-937 hematopoietic cell lines when exposed to Azacitidine and Venetoclax. Moreover, Azacitidine and Venetoclax treatment could induce an increase of the Sub-G0/G1 phase, as well as a G0/G1 arrest in MOLM-13 cells and HL-60 cells. At the same time, it seems to prolong the S phase in U-937 cells. Furthermore, the combination therapy was also able to specifically induce myelopoiesis, as MOLM-13 and THP-1 cells showed an increased expression of CD14. Finally, the combined treatment triggers a higher expression of PLC-β1, which activates the signaling pathway to degrade PKCα.
Tipologia del documento
Tesi di dottorato
Autore
Xian, Jie
Supervisore
Dottorato di ricerca
Ciclo
33
Coordinatore
Settore disciplinare
Settore concorsuale
Parole chiave
Epithelioid hemangioma, Acute Myeloid Leukemia, nuclear inositide-dependent pathways, phosphoinositides, cell signalling
URN:NBN
DOI
10.48676/unibo/amsdottorato/9535
Data di discussione
4 Dicembre 2020
URI
Altri metadati
Tipologia del documento
Tesi di dottorato
Autore
Xian, Jie
Supervisore
Dottorato di ricerca
Ciclo
33
Coordinatore
Settore disciplinare
Settore concorsuale
Parole chiave
Epithelioid hemangioma, Acute Myeloid Leukemia, nuclear inositide-dependent pathways, phosphoinositides, cell signalling
URN:NBN
DOI
10.48676/unibo/amsdottorato/9535
Data di discussione
4 Dicembre 2020
URI
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