Results 61 to 70 of about 1,360,875 (361)
Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine
The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu +18 more
wiley +1 more source
A synthetic benzoxazine dimer derivative targets c‐Myc to inhibit colorectal cancer progression
Benzoxazine dimer derivatives bind to the bHLH‐LZ region of c‐Myc, disrupting c‐Myc/MAX complexes, which are evaluated from SAR analysis. This increases ubiquitination and reduces cellular c‐Myc. Impairing DNA repair mechanisms is shown through proteomic analysis.
Nicharat Sriratanasak +8 more
wiley +1 more source
This study characterizes the responses of primary acute myeloid leukemia (AML) patient samples to the MCL‐1 inhibitor MIK665. The results revealed that monocytic differentiation is associated with MIK665 sensitivity. Conversely, elevated ABCB1 expression is a potential biomarker of resistance to the treatment, which can be overcome by the combination ...
Joseph Saad +17 more
wiley +1 more source
P760: PATTERNS OF HYPOMETHYLATING AGENT FAILURE IN PATIENTS WITH MYELODYSPLASTIC SYNDROMES
K. Chien +16 more
doaj +1 more source
Optimizing survival outcomes with post-remission therapy in acute myeloid leukemia. [PDF]
Optimization of post-remission therapies to maintain complete remission and prevent relapse is a major challenge in treating patients with acute myeloid leukemia (AML).
Chan, Steven M +4 more
core +1 more source
Myeloid forms of leukemia would seem to be an ideal disease for investigators wishing to develop targeted immunotherapy because the leukemia is derived from antigen-presenting cells and because clinical data have demonstrated that there is potent T-cell immunity to chronic myeloid leukemia when donor lymphocyte infusions are used to treat relapse after
openaire +3 more sources
The IFNγ‐CIITA‐MHC II axis modulates melanoma cell susceptibility to NK‐cell‐mediated cytotoxicity
Natural killer (NK) cells play a central role in anti‐melanoma immunity. However, melanoma cells adapt during co‐culture by upregulating CIITA and MHC II in response to interferon gamma (IFNγ), thereby evading NK‐cell lysis. Blocking IFNγ signaling or treatment with dimethyl fumarate/simvastatin counteracts this immune escape and maintains NK‐cell ...
Lena C. M. Krause +6 more
wiley +1 more source

