Q-omics provides the consensus-scored CSMD3 profile across patient tissues and cancer cell-line models. CSMD3 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CSMD3 is differentially expressed in 10, with the highest sampling consensus in HNSC. Additionally, CSMD3 RNA expression shows 12,111 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight KIRC, HNSC, and TGCT as cancer lineages where CSMD3 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 CSMD3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CSMD3 survival associations across molecular data types. CSMD3 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (11) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CSMD3 RNA expression–survival associations across cancer types. High CSMD3 expression shows unfavorable associations in KIRC, LUAD, KIRP, THCA and LUSC, but favorable associations in LGG. The KIRC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for CSMD3 RNA expression.
This table summarizes CSMD3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10. The strongest signals are observed in HNSC for RNA.
This table ranks reproducible tumor–normal expression differences for CSMD3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CSMD3 shows lower tumor expression in KIRC, KIRP and COAD and higher tumor expression in HNSC, BRCA and LIHC. The HNSC box plot shows higher CSMD3 RNA expression in tumor versus normal tissue (log2 FC = +0.116, t-test p < 0.001).
This table shows molecular features associated with CSMD3 in patient tissues and cancer cell lines. In patient samples, CSMD3 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, CSMD3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LARGE_INTESTINE.
