Results 181 to 190 of about 8,240,920 (301)

Human Cardiac Organoids: Advances and Prospects from Construction to Preclinical Drug Evaluation. [PDF]

open access: yesCells
Chen M   +9 more
europepmc   +1 more source

Human Metastatic Cholangiocarcinoma Patient-Derived Xenografts and Tumoroids for Preclinical Drug Evaluation. [PDF]

open access: yesClin Cancer Res, 2023
Serra-Camprubí Q   +30 more
europepmc   +1 more source

Castration‐resistant prostate cancer cells are addicted to the high activity of cyclin‐dependent kinase 2

open access: yesMolecular Oncology, EarlyView.
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

Microbiota-gut-brain axis multi-organ chip construction and applications in drug evaluation. [PDF]

open access: yesIMetaOmics
Tang Y   +9 more
europepmc   +1 more source

Live-cell imaging-based dynamic vascular formation assay for antivascular drug evaluation and screening. [PDF]

open access: yesiScience, 2023
Li Z   +8 more
europepmc   +1 more source

Unraveling the epigenetic code in cancer cell–tumor microenvironment crosstalk

open access: yesMolecular Oncology, EarlyView.
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

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

open access: yesMolecular Oncology, EarlyView.
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

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