chondroitin sulfate proteoglycan family member 4B, pseudogeneGenealiases: []
Q-omics provides the consensus-scored CSPG4BP profile across patient tissues and cancer cell-line models. CSPG4BP expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in STAD. Among the 18 cancer types available for tumor–normal comparison, CSPG4BP is differentially expressed in 9, with the highest sampling consensus in KIRP. Additionally, CSPG4BP RNA expression shows 11,686 significant gene co-expression associations, with the highest sampling consensus in LIHC. Together, these results highlight STAD, KIRP, and LIHC as cancer lineages where CSPG4BP shows reproducible signals across survival, tumor–normal expression, and patient cross-omics analyses.
Every result is evaluated using two consensus scores. Sampling consensus measures how consistently a finding is reproduced within a cancer lineage across different conditions. Lineage consensus measures how broadly the result is shared across cancer types, distinguishing pan-cancer signals from lineage-specific patterns.
Premium analyses for CSPG4BP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CSPG4BP survival associations across molecular data types. CSPG4BP RNA expression shows survival associations in the most cancer types (24). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CSPG4BP RNA expression–survival associations across cancer types. High CSPG4BP expression shows unfavorable associations in STAD, HNSC and KICH, but favorable associations in LUAD, ESCA and OV. The STAD Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .002). Together, the overview and detailed table identify STAD as the clearest survival context for CSPG4BP RNA expression.
This table summarizes CSPG4BP tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for CSPG4BP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CSPG4BP shows lower tumor expression in KIRP, KIRC, KICH and THCA and higher tumor expression in HNSC and UCEC. The KIRP box plot shows higher CSPG4BP RNA expression in normal versus tumor tissue (log2 FC = −0.824, t-test p < 0.001).
This table shows molecular features associated with CSPG4BP in patient tissues and cancer cell lines. In patient samples, CSPG4BP shows the broadest associations at the RNA and protein expression levels, with LIHC recurring as the lineage with the largest associated feature set.
