Q-omics provides the consensus-scored CEACAM16 profile across patient tissues and cancer cell-line models. CEACAM16 expression is associated with patient survival in 19 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CEACAM16 is differentially expressed in 8, with the highest sampling consensus in THCA. Additionally, CEACAM16 RNA expression shows 8,917 significant gene co-expression associations, with the highest sampling consensus in ESCA. Together, these results highlight KIRC, THCA, and ESCA as cancer lineages where CEACAM16 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 CEACAM16 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CEACAM16 survival associations across molecular data types. CEACAM16 RNA expression shows survival associations in the most cancer types (19), followed by mutation status (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CEACAM16 RNA expression–survival associations across cancer types. High CEACAM16 expression shows unfavorable associations in KIRC, LGG, LIHC, KIRP and THYM, but favorable associations in HNSC. 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 CEACAM16 RNA expression.
This table summarizes CEACAM16 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8. The strongest signals are observed in THCA for RNA.
This table ranks reproducible tumor–normal expression differences for CEACAM16. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CEACAM16 shows lower tumor expression in THCA, COAD and LUSC and higher tumor expression in LIHC, STAD and PRAD. The THCA box plot shows higher CEACAM16 RNA expression in normal versus tumor tissue (log2 FC = −0.030, t-test p = .003).
This table shows molecular features associated with CEACAM16 in patient tissues and cancer cell lines. In patient samples, CEACAM16 shows the broadest associations at the RNA and protein expression levels, with ESCA recurring as the lineage with the largest associated feature set. In cancer cell lines, CEACAM16 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in OESOPHAGUS and LARGE_INTESTINE.
