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Results for “Chitinase-3-Like Protein 1”

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Integrated analysis of VEGFA rs833061 (- 460T > C) promoter polymorphism and serum YKL-40 levels in bladder cancer: evidence of a genotype-phenotype association.

BACKGROUND: Angiogenesis plays a central role in bladder cancer progression. VEGFA regulates angiogenesis, whereas YKL-40 is a pro-angiogenic biomarker. The relationship between VEGFA polymorphism and circulating YKL-40 remains unclear. METHODS AND RESULTS: A hospital-based case-control study involving 120 bladder cancer patients and 120 age- and sex-matched healthy controls was conducted. VEGFA rs833061 genotyping was performed using ARMS-PCR and confirmed by Sanger sequencing. Serum YKL-40 concentrations were measured by ELISA. Multivariable binary logistic regression analysis adjusted for age, sex, and smoking status demonstrated that the CT and TT genotypes remained independently associated with an increased risk of bladder cancer. Serum YKL-40 concentrations were significantly elevated in patients and increased progressively with tumor stage. TT genotype carriers exhibited the highest serum YKL-40 levels. CONCLUSIONS: After adjustment for age, sex, and smoking status, the VEGFA rs833061 polymorphism remained independently associated with bladder cancer susceptibility and circulating YKL-40 concentrations. These findings provide preliminary evidence of a genotype-phenotype relationship; however, validation in larger multicentre cohorts is required.

Humans

Distinct immune landscapes characterize highly versus minimally invasive brain metastases.

Brain metastases (BrMs) occur in approximately 30% of cancer patients, causing nearly one-fifth of cancer deaths. While immune checkpoint inhibitors (ICIs) benefit some BrM patients, responses remain highly variable. This variability partly reflects distinct histopathological growth patterns that include minimally invasive (MI) and highly invasive (HI) brain BrMs. Here we show that MI BrMs exhibit robust immune infiltration, whereas HI lesions are immunosuppressed. However, histological differentiation between MI and HI can be challenging because of subjective margin assessment. Here, using highly multiplexed spatial proteomics on 119 tumor sections from 46 patients with BrMs, we identify CHI3L1 as a key mediator of the immunosuppressive microenvironment in HI BrMs. In preclinical models, genetic deletion of CHI3L1 converts immune-cold metastases into lymphocyte-rich, ICI-responsive lesions infiltrated by granzyme B+ CD8+ T cells. In BrM patients treated with ICI, immunohistochemical quantification of CHI3L1 expression was a stronger predictor of ICI response than traditional MI/HI classification. Thus, CHI3L1 represents a promising biomarker and therapeutic target for BrMs.

Humans