C1QB (Complement C1q B Chain)

Immunohistochemistry demonstrated higher CD74 and C1QB expression in jaw osteosarcoma compared to long bone osteosarcoma in both rats and humans (P < 0.05). The expression levels of CD74 and C1QB were significantly higher in jaw osteosarcoma than in long bone osteosarcoma, suggesting that this differential expression may have clinical relevance for patient survival and warrants further investigation.

Based on human HCC data, SPP1, NQO1, RRM2, APOA1, APOC3, ALDOB, and IGF1 were identified as prognosticators indicating poor overall survival. This study presents the first cross-species transcriptomic analysis of canine HCC, revealing significant molecular resemblances to human HCC, indicating it may be a promising comparative model for studying tumor biology, drug responses, and novel therapeutic interventions.

In nasopharyngeal carcinoma it identifies tiny tertiary lymphoid structures, and in breast cancer it uncovers inflammatory M1-like macrophages near ductal carcinoma in situ and links them to pro-metastatic signaling. An interpretation module pinpoints key immune signatures, and GARDEN extends to spatial chromatin accessibility, providing insight into epigenetic regulation and informing diagnostics and therapeutic targeting.

This study identifies complement activation as a potential key contributor to thrombosis in JAK2V617F MPN patients, particularly those with SVT. The interplay between complement, coagulation, and endothelial dysfunction suggests potential therapeutic targets for reducing thrombotic complications in this high-risk population.

scRNA-seq identified the intricate tumor immune microenvironment, highlighting the pivotal roles of TAMs and mast cells in gastric cancer peritoneal metastasis. The CCL5-CCR1 pathway emerged as a potential immune checkpoint, offering novel insights for future immunotherapeutic and targeted therapeutic strategies in the treatment of gastric cancer peritoneal metastasis.

Mice were sham-irradiated or irradiated with 50 cGy prior to being orthotopically transplanted with syngeneic Trp53 null mammary epithelium and half were treated for 6 months with anti-inflammatory low-dose aspirin...Complement components C1qA, C1qB, and C1qC were significantly increased in tumor-bearing mice that had been irradiated, whereas similarly aged mice without tumors displayed a decline in complement system activity. The specific changes in the complement system, which mediates adaptive immune function, following radiation exposure may contribute to cancer progression as a function of age.

Moreover, imaging mass cytometry analysis indicated an anti-inflammatory phenotype differentiation of monocytes seeded on SVZ and WM. Thus, the established model is suitable for investigation of ECM properties and assessment of cell-matrix interactions.

These findings provide evidence for macrophage- and fibroblast-derived C1q in the progression of cSCC. They also suggest stromal C1q as a marker for cSCC metastasis and poor prognosis.

CXCL2, ANKRD22, SPP1, and C1QB showed strong prognostic characteristics in CESC and significant predictive capabilities for patient outcomes. The study also emphasized the critical role of T cells in CESC progression.

Our epigenetics-based model demonstrates excellent prognostic accuracy (AUC>0.997 in internal validation, 0.832-0.929 in external cohorts) and provides a practical tool for treatment stratification. These findings establish a clinically applicable framework for personalized therapy selection in OS patients.

Validation in additional datasets confirmed the MR analysis results and upstream regulatory factors were identified using NetworkAnalyst. Our findings offer fresh perspectives on the molecular underpinnings of glioma and highlight potential targets for therapeutic interventions.

The cell type and tumor-specific histone modifications and chromatin accessibility patterns underscore the dynamic nature of epigenetic regulation of C1Q, providing crucial insights into the intricate mechanisms governing the expression of these immunologically significant genes. The findings provide a foundation for future investigations into targeted epigenetic modulation, offering insights into potential therapeutic avenues for immune-related disorders and cancer mediated via C1q.