Results 321 to 330 of about 22,436,913 (372)

MTCH2 Deficiency Promotes E2F4/TFRC‐Mediated Ferroptosis and Sensitizes Colorectal Cancer Liver Metastasis to Sorafenib

open access: yesAdvanced Science, EarlyView.
This study identifies MTCH2 as a crucial regulator of ferroptosis in colorectal cancer (CRC) progression. High expression of MTCH2 is correlated with poor prognosis in CRC patients. Furthermore, MTCH2 depletion induces ferroptosis to suppress CRC liver metastasis via the E2F4/TFRC axis and sensitizes tumors to sorafenib treatment, supporting MTCH2 as a
Pu Xing   +18 more
wiley   +1 more source

Computational fluid dynamic modeling of the lymphatic system: a review of existing models and future directions. [PDF]

open access: yesBiomech Model Mechanobiol
Jayathungage Don TD   +5 more
europepmc   +1 more source

The Evolutionary Trajectory and Prognostic Value of GITR+ Tregs Reprogramed by Tumor‐Intrinsic PD‐1/c‐MET Signaling in Pancreatic Cancer

open access: yesAdvanced Science, EarlyView.
In pancreatic ductal adenocarcinoma (PDAC), tumor‐intrinsic PD‐1 signaling activates the MET pathway, leading to the establishment of an immunosuppressive tumor microenvironment (TME). This MET‐driven signaling cascade promotes the selective accumulation of GITR+ regulatory T cells (Tregs), a highly immunosuppressive subset.
Jiande Han   +16 more
wiley   +1 more source

The GGH/HuR Complex Binds and Stabilizes mRNAs to Maintain Tumor Cell Cycle and DNA Replication

open access: yesAdvanced Science, EarlyView.
Despite its canonical role in inhibiting DNA synthesis, GGH promotes tumor growth as a novel RNA‐binding protein. GGH binds GC‐rich 5′UTRs (e.g., CDC6/CCND1), recruits HuR to form a ternary complex that stabilizes mRNA via circular conformation, fueling DNA replication and the cell cycle. Targeting this axis suppresses NSCLC progression.
Yu Li   +9 more
wiley   +1 more source

5’‐Methylthioadenosine Metabolic Reprogramming Drives H3K79 Monomethylation‐Mediated PAK2 Upregulation to Promote Cadmium‐Induced Breast Cancer Progression by Impairing Autophagic Flux

open access: yesAdvanced Science, EarlyView.
Cadmium, a carcinogenic heavy metal, drives breast cancer progression via metabolic reprogramming and autophagic flux disruption. Multi‐omics revealed cadmium‐induced 5'‐methylthioadenosine depletion activates DOT1L‐mediated H3K79me1 at PAK2 promoter, upregulating PAK2 to block autophagy and driving malignancy. Clinically, 5'‐methylthioadenosine levels
Jingdian Li   +24 more
wiley   +1 more source

Connecting the Dots: The Cerebral Lymphatic System as a Bridge Between the Central Nervous System and Peripheral System in Health and Disease. [PDF]

open access: yesAging Dis
Zhao H   +20 more
europepmc   +1 more source

Type I Interferon Signaling Augments Autoimmunity in Neuromyelitis Optica Spectrum Disorder

open access: yesAdvanced Science, EarlyView.
The cGAS‐STING innate immune pathway is excessively activated both in peripheral monocytes and CNS microglia in patients with NMOSD, leading to an overproduction of IFN‐I. IFN‐I subsequently acts on AQP4‐specific autoreactive T cells. Blocking this pathway may offer novel therapeutic options for individuals with NMOSD.
Tian‐Xiang Zhang   +13 more
wiley   +1 more source

Advanced Microfluidics for Single Cell‐Based Cancer Research

open access: yesAdvanced Science, EarlyView.
Cutting‐edge microfluidic platforms are transforming single‐cell cancer research. This review highlights advanced technologies, from droplet microfluidics to tumour‐chips, that enable functional and spatial single‐cell analyses. By integrating biosensing, immune components, and patient‐derived materials, these systems offer new insights into tumour ...
Adriana Carneiro   +10 more
wiley   +1 more source

Harnessing the Immunomodulation of UV‐Exposed Keratinocyte Extracellular Vesicles for Inflammatory Disorder Treatment

open access: yesAdvanced Science, EarlyView.
Adopting a paradigm shift that transforms a known health hazard as a potential therapeutic asset, a novel therapeutic strategy is set out to investigate for inflammatory conditions by leveraging immunosuppressive properties of UV‐irradiated keratinocytes.
Lu Liu   +16 more
wiley   +1 more source

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