Results 171 to 180 of about 1,937,940 (311)

PBRM1 Deficiency Reshapes an Immune Suppressive Microenvironment Through Epigenetic Tuning of PBRM1‐KDM5C‐IL6 Axis in ccRCC

open access: yesAdvanced Science, EarlyView.
PBRM1 ranks as the second most commonly mutated gene in ccRCC. This study reveals that PBRM1 loss promotes an immunosuppressive microenvironment by elevating M2 TAMs via the KDM5C–IL‐6 axis. These M2 TAMs, along with CAFs, form a barrier that excludes CD8+ T cells. Targeting IL‐6 synergizes with anti‐PD1 therapy, offering a promising strategy for PBRM1‐
Wenjiao Xia   +14 more
wiley   +1 more source

Hepatocyte Mettl3 Deficiency Drives Primary Sclerosing Cholangitis and Liver Fibrosis via Cholangiocyte‐Macrophage Crosstalk

open access: yesAdvanced Science, EarlyView.
Schematic illustration demonstrating that hepatic Mettl3 depletion significantly elevates the secretion of Mif and Csf1. This elevation facilitates Trem2+ macrophage infiltration and triggers cholangiocyte remodeling through the Spp1‐Cd44 interaction, resulting in spontaneous PSC development in vivo.
Wenting Pan   +19 more
wiley   +1 more source

Targeting the Notch1‐YY1‐ICAM1 Signaling Axis Enhances the Efficacy of Immunotherapy in HCC by Activating CD8+ T‐Cell‐Driven Cancer Cell Pyroptosis

open access: yesAdvanced Science, EarlyView.
In hepatocellular carcinoma (HCC), aberrantly activated Notch1 signaling induces its target gene YY1, which impairs immunotherapy efficacy by suppressing tumor cell‐ICAM1‐driven T cell activation and the mediated pyroptosis of T cells against tumor cells.
Ke Zhu   +10 more
wiley   +1 more source

Disrupting the Formation of YAP Condensates Promotes the Activation of AMPKα to Inhibit the Progression of Primary Liver Cancer

open access: yesAdvanced Science, EarlyView.
This study systematically investigates the function and molecular mechanisms of YAP phase separation in multiple primary liver cancers. These findings provide novel insights into phase separation‐mediated primary liver cancer development and validate targeted disruption of this process as an effective therapeutic strategy for primary liver cancer ...
Shuang‐Zhou Peng   +7 more
wiley   +1 more source

TriCON: A Carbon‐Based Triple‐Modal Nanoplatform for Pancreatic Cancer Therapy

open access: yesAdvanced Science, EarlyView.
We developed TriCON, a triple‐modality nanotherapeutic platform, to treat pancreatic ductal adenocarcinoma (PDAC) by synergizing gene editing, chemotherapy, and immunotherapy. TriCON utilizes CRISPR/Cas9 to target the poliovirus receptor (PVR), combined with nano‐encapsulated doxorubicin and checkpoint blockade. This approach achieved significant tumor
Xinyu Peng   +9 more
wiley   +1 more source

Cleavage‐Resistant CYLD Protects Against Autoimmune Hepatitis

open access: yesAdvanced Science, EarlyView.
Proteolytic cleavage of the deubiquitinase CYLD emerges as a critical driver of autoimmune hepatitis. TNFα‐induced CYLD loss in macrophages amplifies S100A9‐triggered MAPK activation, leading to excessive chemokine production and hepatic inflammation. Pharmacological inhibition of MEK signaling effectively attenuates experimental disease, highlighting ...
Han Liu   +13 more
wiley   +1 more source

Proteogenomic Characterization Reveals Subtype‐Specific Therapeutic Potential for HER2‐Low Breast Cancer

open access: yesAdvanced Science, EarlyView.
Multiomic profiling of HER2‐low breast cancer identifies three proteomic subtypes with distinct therapeutic strategies: endocrine, antiangiogenic, and anti‐HER2 therapies. Genomic and lactate modification landscapes are detailed, providing insights for precise management.
Shouping Xu   +20 more
wiley   +1 more source

GLUL Confers Perivascular Cancer‐Associated Fibroblasts With Pro‐Angiogenic Capacity to Promote Glioma Progression

open access: yesAdvanced Science, EarlyView.
Schematic illustration of the proposed model. Primary CAFs are isolated from fresh human GBM specimens according to established protocols. GLUL is essential for pro‐angiogenic capacity of CAFs through its impact on the PI3K/AKT pathway. GLUL enhances the pro‐angiogenic capacity of CAFs, driving aberrant tumor vasculature that fuels tumor growth ...
Qing Zhang   +4 more
wiley   +1 more source

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