Results 151 to 160 of about 154,638 (269)

Icariin Enhances the Enzymatic Activity of N‐acetylgalactosaminidase to Augment Akkermansia Abundance in Gut Microbiota for Improved PD‐1 Blockade Efficacy in Tumor Suppression

open access: yesAdvanced Science, EarlyView.
Icariin promoted the growth of Akk by enhancing the activity of N‐acetylgalactosaminidase (Amuc_0920), which enhanced mucin utilization and provided a favorable nutrient environment for bacterial growth. This icariin‐mediated enrichment of Akk further reshaped the tumor microenvironment and promoted CD8+ T cell infiltration, ultimately synergizing with
Shuangying Qiao   +12 more
wiley   +1 more source

Socioeconomic Disparities in Cervical Cancer Patients Presenting to a Tertiary Care Facility [PDF]

open access: yesInternational Journal of Radiation Oncology*Biology*Physics, 2016
J.M. Beckta   +4 more
openaire   +1 more source

Tumor‐Derived LAMB3 Drives Immunosuppressive LRRC15+ Fibroblast Formation During Pancreatic Ductal Adenocarcinoma Development

open access: yesAdvanced Science, EarlyView.
A single‐cell atlas of pancreatic ductal adenocarcinoma development reveals progressive ductal‐fibroblast‐immune crosstalk. Tumor‐derived LAMB3 drives the formation of immunosuppressive LRRC15+ fibroblasts through the ITGB1/FAK/MAPK/FOSL2 signaling. Glycolytic reprogramming upregulates LAMB3 and correlates with LRRC15+ fibroblast enrichment.
Xuqing Shi   +23 more
wiley   +1 more source

IL‐7R‐Enriched Extracellular Vesicles From the Thymus Drive Colitis via Promoting Neutrophil Extracellular Trap Formation

open access: yesAdvanced Science, EarlyView.
Inflammatory bowel disease (IBD) pathogenesis remains unclear. This study reveals that thymus‐originated IL‐7R‐enriched extracellular vesicles exacerbate colitis by promoting neutrophil extracellular traps via a thymus‐gut axis, uncovering an inter‐organ communication mechanism in inflammatory bowel disease pathogenesis.
Yao Liao   +21 more
wiley   +1 more source

Enhancing CAR‐T Cell Efficacy in Solid Tumors by Inhibiting CCL5/VEGF‐Mediated Angiogenesis

open access: yesAdvanced Science, EarlyView.
This study reveals that CAR‐T cells in solid tumors produce CCL5, which paradoxically induces VEGF and angiogenesis to promote tumor growth. Blocking CCL5/VEGF signaling—through gene knockout, or the CCR5 inhibitor maraviroc—significantly enhances the antitumor efficacy of CAR‑T therapy (the diagram was created in Biorender).
Shishuo Sun   +15 more
wiley   +1 more source

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