Gfi-1 inhibits proliferation and colony formation of p210BCR/ABL-expressing cells via transcriptional repression of STAT 5 and Mcl-1.
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Ursolic acid-mediated apoptosis of K562 cells involves Stat5/Akt pathway inhibition through the induction of Gfi-1Selecting the best frontline treatment in chronic myeloid leukemiaClitocine targets Mcl-1 to induce drug-resistant human cancer cell apoptosis in vitro and tumor growth inhibition in vivo.Anti-rheumatic agent auranofin induced apoptosis in chronic myeloid leukemia cells resistant to imatinib through both Bcr/Abl-dependent and -independent mechanismsGFI1 is repressed by p53 and inhibits DNA damage-induced apoptosis.Structure-Based Screen Identifies a Potent Small Molecule Inhibitor of Stat5a/b with Therapeutic Potential for Prostate Cancer and Chronic Myeloid Leukemia.Expression of p89(c-Mybex9b), an alternatively spliced form of c-Myb, is required for proliferation and survival of p210BCR/ABL-expressing cellsLymphoid progenitor cells from childhood acute lymphoblastic leukemia are functionally deficient and express high levels of the transcriptional repressor Gfi-1Bcl-xL anti-apoptotic network is dispensable for development and maintenance of CML but is required for disease progression where it represents a new therapeutic target.Nickel pyrithione induces apoptosis in chronic myeloid leukemia cells resistant to imatinib via both Bcr/Abl-dependent and Bcr/Abl-independent mechanisms.TIDEL-II: first-line use of imatinib in CML with early switch to nilotinib for failure to achieve time-dependent molecular targetsGambogic acid induces apoptosis in imatinib-resistant chronic myeloid leukemia cells via inducing proteasome inhibition and caspase-dependent Bcr-Abl downregulation.Low GFI1 expression in white blood cells of CP-CML patients at diagnosis is strongly associated with subsequent blastic transformation.The coffee diterpene kahweol enhances sensitivity to sorafenib in human renal carcinoma Caki cells through down-regulation of Mcl-1 and c-FLIP expression.A pharmacodynamic model of Bcr-Abl signalling in chronic myeloid leukaemia.Sustained inhibition of STAT5, but not JAK2, is essential for TKI-induced cell death in chronic myeloid leukemia.Non ABL-directed inhibitors as alternative treatment strategies for chronic myeloid leukemia.Growth factor independence 1 expression in myeloma cells enhances their growth, survival, and osteoclastogenesismiR-193b and miR-30c-1 inhibit, whereas miR-576-5p enhances melanoma cell invasion
P2860
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P2860
Gfi-1 inhibits proliferation and colony formation of p210BCR/ABL-expressing cells via transcriptional repression of STAT 5 and Mcl-1.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年学术文章
@wuu
2012年学术文章
@zh-cn
2012年学术文章
@zh-hans
2012年学术文章
@zh-my
2012年学术文章
@zh-sg
2012年學術文章
@yue
2012年學術文章
@zh
2012年學術文章
@zh-hant
name
Gfi-1 inhibits proliferation a ...... epression of STAT 5 and Mcl-1.
@en
type
label
Gfi-1 inhibits proliferation a ...... epression of STAT 5 and Mcl-1.
@en
prefLabel
Gfi-1 inhibits proliferation a ...... epression of STAT 5 and Mcl-1.
@en
P2093
P2860
P50
P356
P1433
P1476
Gfi-1 inhibits proliferation a ...... repression of STAT 5 and Mcl-1
@en
P2093
A R Soliera
B Calabretta
G Ferrari-Amorotti
L Peterson
M R Lidonnici
S A Mariani
S Cattelani
P2860
P2888
P304
P356
10.1038/LEU.2012.19
P577
2012-01-30T00:00:00Z
P6179
1023386972