Q-omics provides the consensus-scored LTK profile across patient tissues and cancer cell-line models. LTK expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, LTK is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, LTK RNA expression shows 15,277 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight HNSC, KIRC, and THYM as cancer lineages where LTK 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 LTK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LTK survival associations across molecular data types. LTK RNA expression shows survival associations in the most cancer types (26), followed by mutation status (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LTK RNA expression–survival associations across cancer types. High LTK expression shows unfavorable associations in ACC, UVM and SKCM, but favorable associations in HNSC, LUAD and PAAD. The HNSC 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 HNSC as the clearest survival context for LTK RNA expression.
This table summarizes LTK 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 1. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for LTK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LTK shows lower tumor expression in KIRC, COAD, LUSC, KIRP and LIHC and higher tumor expression in UCEC. The KIRC box plot shows higher LTK RNA expression in normal versus tumor tissue (log2 FC = −1.050, t-test p < 0.001).
This table shows molecular features associated with LTK in patient tissues and cancer cell lines. In patient samples, LTK 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, LTK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and BLOOD_Lymphoma.
