Q-omics provides the consensus-scored ITK profile across patient tissues and cancer cell-line models. ITK expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, ITK is differentially expressed in 9, with the highest sampling consensus in KIRC. Additionally, ITK protein abundance shows 24,725 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight HNSC, KIRC, and PDAC as cancer lineages where ITK 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 ITK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ITK survival associations across molecular data types. ITK RNA expression shows survival associations in the most cancer types (25), followed by mutation status (5) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ITK RNA expression–survival associations across cancer types. High ITK expression shows unfavorable associations in UVM, but favorable associations in HNSC, SKCM, BRCA, LUAD and CESC. 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 ITK RNA expression.
This table summarizes ITK tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for ITK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ITK shows lower tumor expression in LUSC, COAD, BLCA and THCA and higher tumor expression in KIRC and STAD. The KIRC box plot shows higher ITK RNA expression in tumor versus normal tissue (log2 FC = +1.361, t-test p < 0.001).
This table shows molecular features associated with ITK in patient tissues and cancer cell lines. In patient samples, ITK shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, ITK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and BLOOD_Leukemia.
