Q-omics provides the consensus-scored NCAM2 profile across patient tissues and cancer cell-line models. NCAM2 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, NCAM2 is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, NCAM2 protein abundance shows 24,272 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight ACC, KIRC, and GBM as cancer lineages where NCAM2 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 NCAM2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NCAM2 survival associations across molecular data types. NCAM2 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (6) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible NCAM2 RNA expression–survival associations across cancer types. High NCAM2 expression shows unfavorable associations in ACC, KIRC, BLCA, STAD and LUSC, but favorable associations in LGG. The ACC 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 ACC as the clearest survival context for NCAM2 RNA expression.
This table summarizes NCAM2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 4. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for NCAM2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NCAM2 shows lower tumor expression in KIRC, UCEC, LIHC, LUSC and COAD and higher tumor expression in BRCA. The KIRC box plot shows higher NCAM2 RNA expression in normal versus tumor tissue (log2 FC = −0.457, t-test p < 0.001).
This table shows molecular features associated with NCAM2 in patient tissues and cancer cell lines. In patient samples, NCAM2 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, NCAM2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and BREAST.
