Q-omics provides the consensus-scored NKAIN3 profile across patient tissues and cancer cell-line models. NKAIN3 expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, NKAIN3 is differentially expressed in 11, with the highest sampling consensus in HNSC. Additionally, NKAIN3 RNA expression shows 13,813 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight KIRP, HNSC, and THYM as cancer lineages where NKAIN3 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 NKAIN3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NKAIN3 survival associations across molecular data types. NKAIN3 RNA expression shows survival associations in the most cancer types (20), followed by 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 NKAIN3 RNA expression–survival associations across cancer types. High NKAIN3 expression shows unfavorable associations in OV, CESC and LUAD, but favorable associations in KIRP, ESCA and LGG. The KIRP Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRP as the clearest survival context for NKAIN3 RNA expression.
This table summarizes NKAIN3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11. The strongest signals are observed in HNSC for RNA.
This table ranks reproducible tumor–normal expression differences for NKAIN3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NKAIN3 shows lower tumor expression in HNSC, KIRC and KICH and higher tumor expression in LUAD, LUSC and PAAD. The HNSC box plot shows higher NKAIN3 RNA expression in normal versus tumor tissue (log2 FC = −0.139, t-test p < 0.001).
This table shows molecular features associated with NKAIN3 in patient tissues and cancer cell lines. In patient samples, NKAIN3 shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, NKAIN3 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 CNS and UPPER_AERODIGESTIVE_TRACT.
