Results 161 to 170 of about 2,892,311 (358)

Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine

open access: yesMolecular Oncology, EarlyView.
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

open access: yesMolecular Oncology, EarlyView.
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

The IFNγ‐CIITA‐MHC II axis modulates melanoma cell susceptibility to NK‐cell‐mediated cytotoxicity

open access: yesMolecular Oncology, EarlyView.
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

The neural crest‐associated gene ERRFI1 is involved in melanoma progression and resistance toward targeted therapy

open access: yesMolecular Oncology, EarlyView.
ERRFI1, a neural crest (NC)‐associated gene, was upregulated in melanoma and negatively correlated with the expression of melanocytic differentiation markers and the susceptibility of melanoma cells toward BRAF inhibitors (BRAFi). Knocking down ERRFI1 significantly increased the sensitivity of melanoma cells to BRAFi.
Nina Wang   +8 more
wiley   +1 more source

The nuclear envelope. The major site of insulin binding in rat liver nuclei.

open access: hybrid, 1978
Riccardo Vigneri   +4 more
openalex   +1 more source

Glycosylated LGALS3BP is highly secreted by bladder cancer cells and represents a novel urinary disease biomarker

open access: yesMolecular Oncology, EarlyView.
Urinary LGALS3BP is elevated in bladder cancer patients compared to healthy controls as detected by the 1959 antibody–based ELISA. The antibody shows enhanced reactivity to the high‐mannose glycosylated variant secreted by cancer cells treated with kifunensine (KIF).
Asia Pece   +18 more
wiley   +1 more source

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