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6 in total

1. MZH29 is a novel potent inhibitor that overcomes drug resistance FLT3 mutations in acute myeloid leukemia.

Authors: B Xu; Y Zhao; X Wang; P Gong; W Ge
Journal: Leukemia Date: 2016-10-24 Impact factor: 11.528

2. The sorafenib plus nutlin-3 combination promotes synergistic cytotoxicity in acute myeloid leukemic cells irrespectively of FLT3 and p53 status.

Authors: Giorgio Zauli; Claudio Celeghini; Elisabetta Melloni; Rebecca Voltan; Manuele Ongari; Mario Tiribelli; Maria Grazia di Iasio; Francesco Lanza; Paola Secchiero
Journal: Haematologica Date: 2012-06-11 Impact factor: 9.941

3. Expression differences of miR-142-5p between treatment-naïve chronic myeloid leukemia patients responding and non-responding to imatinib therapy suggest a link to oncogenic ABL2, SRI, cKIT and MCL1 signaling pathways critical for development of therapy resistance.

Authors: Theresa Klümper; Henrike Bruckmueller; Tobias Diewock; Meike Kaehler; Sierk Haenisch; Christiane Pott; Oliver Bruhn; Ingolf Cascorbi
Journal: Exp Hematol Oncol Date: 2020-09-26

MCL1 down-regulation plays a critical role in mediating the higher anti-leukaemic activity of the multi-kinase inhibitor Sorafenib with respect to Dasatinib.

1. MZH29 is a novel potent inhibitor that overcomes drug resistance FLT3 mutations in acute myeloid leukemia.

2. The sorafenib plus nutlin-3 combination promotes synergistic cytotoxicity in acute myeloid leukemic cells irrespectively of FLT3 and p53 status.

3. Expression differences of miR-142-5p between treatment-naïve chronic myeloid leukemia patients responding and non-responding to imatinib therapy suggest a link to oncogenic ABL2, SRI, cKIT and MCL1 signaling pathways critical for development of therapy resistance.

4. Sorafenib selectively depletes human glioblastoma tumor-initiating cells from primary cultures.

5. Sorafenib inhibits in vitro osteoclastogenesis by down-modulating Mcl-1.

6. Sorafenib Inhibition of Mcl-1 Accelerates ATRA-Induced Apoptosis in Differentiation-Responsive AML Cells.