Q-omics provides the consensus-scored CSMD2 profile across patient tissues and cancer cell-line models. CSMD2 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, CSMD2 is differentially expressed in 15, with the highest sampling consensus in HNSC. Additionally, CSMD2 RNA expression shows 16,171 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRP, HNSC, and UVM as cancer lineages where CSMD2 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 CSMD2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CSMD2 survival associations across molecular data types. CSMD2 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (6) 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 CSMD2 RNA expression–survival associations across cancer types. High CSMD2 expression shows unfavorable associations in KIRP, UVM, LIHC, BLCA and BRCA, but favorable associations in ACC. The KIRP 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 KIRP as the clearest survival context for CSMD2 RNA expression.
This table summarizes CSMD2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 1. The strongest signals are observed in HNSC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for CSMD2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CSMD2 shows higher tumor expression in HNSC, COAD, BLCA, LUAD, LIHC and BRCA. The HNSC box plot shows higher CSMD2 RNA expression in tumor versus normal tissue (log2 FC = +0.951, t-test p < 0.001).
This table shows molecular features associated with CSMD2 in patient tissues and cancer cell lines. In patient samples, CSMD2 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, CSMD2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in BREAST and CNS.
