Q-omics provides the consensus-scored KTI12 profile across patient tissues and cancer cell-line models. KTI12 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in LIHC. Among the 18 cancer types available for tumor–normal comparison, KTI12 is differentially expressed in 15, with the highest sampling consensus in HNSC. Additionally, KTI12 RNA expression shows 18,905 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight LIHC, HNSC, and ACC as cancer lineages where KTI12 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 KTI12 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes KTI12 survival associations across molecular data types. KTI12 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (2) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible KTI12 RNA expression–survival associations across cancer types. High KTI12 expression shows unfavorable associations in LIHC, LGG, MESO, ACC and KICH, but favorable associations in SCLC. The LIHC 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 LIHC as the clearest survival context for KTI12 RNA expression.
This table summarizes KTI12 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 4. The strongest signals are observed in HNSC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for KTI12. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. KTI12 shows lower tumor expression in KICH and higher tumor expression in HNSC, LIHC, KIRP, LUAD and LUSC. The HNSC box plot shows higher KTI12 RNA expression in tumor versus normal tissue (log2 FC = +0.961, t-test p < 0.001).
This table shows molecular features associated with KTI12 in patient tissues and cancer cell lines. In patient samples, KTI12 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, KTI12 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 BREAST and BLOOD_Lymphoma.
