Results 141 to 150 of about 5,918,554 (301)
We show that emergence of castration‐resistant prostate (CRPC) is associated with significant upregulation of cyclins that positively regulate cyclin‐dependent kinase 2 (CDK2) and concomitant downregulation of CDK4 cyclins. This renders CRPC cells dependent on the high activity of CDK2, and CDK2 inhibitors synergistically sensitize CRPC cells to both ...
Joyeeta Chatterjee +3 more
wiley +1 more source
Partial inhibition of focal adhesion kinase (FAK) can paradoxically promote tumor growth, rather than simply producing a weaker antitumor effect than that observed with strong FAK suppression. In breast cancer and melanoma models, targeting p110δ PI3K, particularly in macrophages, counteracted these tumor‐promoting effects, highlighting the importance ...
Lydia Xenou +4 more
wiley +1 more source
Unraveling the epigenetic code in cancer cell–tumor microenvironment crosstalk
Epigenetic regulation is a key driver of cancer development and progression. Diverse epigenetic alterations in cancer cells and components of the tumor microenvironment (TME) orchestrate their communication through multiple mechanisms. We discuss how the epigenetic code coordinates bidirectional cancer cell–TME crosstalk to promote cancer progression ...
Ji Hoon Park, Mi‐Young Kim
wiley +1 more source
Fiscal year ends June 30.; "November 20, 2007."Constitutes the annual report of the ...
Kansas. Legislative Post Audit Committee.
core +1 more source
Fiscal year ends June 30.; "November 1, 2005."Constitutes the annual report of the ...
Kansas. Legislative Post Audit Committee.
core +1 more source
Arginine methylation can be viewed as a persistence‐prone post‐translational modification regulated by a network of PRMTs. Competitive and compensatory interactions among PRMTs can redistribute methylation across substrate pools shaped by sequence, structural, spatial, and environmental layers, reinforcing RNA‐processing, chromatin, and signaling ...
So Hyun Kwon, Ji Min Lee
wiley +1 more source
Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim +7 more
wiley +1 more source
High‐risk bladder cancer is typically treated with Bacillus Calmette‐Guérin (BCG), but 30–40% of patients relapse. No FDA‐ or CE‐approved biomarkers currently predict or prognosticate BCG failure. We systematically reviewed the literature and identified 72 eligible studies, revealing several promising biomarkers associated with BCG treatment response ...
Rui Ribeiro‐Pereira +7 more
wiley +1 more source
Loss of NAPRT promotes lung tumor initiation and growth through a noncanonical mechanism, independent of its role in NAD+ biosynthesis. Mechanistically, NAPRT depletion activates the mTORC2‐driven AKT/β‐catenin signaling axis to enhance clonogenic and invasive phenotypes. Furthermore, lung‐specific Naprt deletion significantly increases tumor burden in
Myung Joon Oh +11 more
wiley +1 more source
In head and neck squamous cell carcinoma (HNSCC) p53 and p63 exert opposite roles on the transcription regulation of the lncRNA NEAT1. Under basal conditions, p53 levels are low and p63 represses NEAT1 expression. Upon genotoxic stress, p53 is rapidly induced, displacing p63 from the NEAT1 promoter leading to NEAT1 transcriptional activation and ...
Sara De Domenico +5 more
wiley +1 more source

