Q-omics provides the consensus-scored KIT profile across patient tissues and cancer cell-line models. KIT expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, KIT is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, KIT protein abundance shows 23,600 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRC, and PDAC as cancer lineages where KIT 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 KIT — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes KIT survival associations across molecular data types. KIT RNA expression shows survival associations in the most cancer types (23), followed by mutation status (11) 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 KIT RNA expression–survival associations across cancer types. High KIT expression shows unfavorable associations in KIRP, UVM and SKCM, but favorable associations in KIRC, HNSC and LUAD. The KIRC 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 KIRC as the clearest survival context for KIT RNA expression.
This table summarizes KIT 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 6. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for KIT. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. KIT shows lower tumor expression in KIRC, COAD, THCA, KIRP, STAD and BLCA. The KIRC box plot shows higher KIT RNA expression in normal versus tumor tissue (log2 FC = −2.115, t-test p < 0.001).
This table shows molecular features associated with KIT in patient tissues and cancer cell lines. In patient samples, KIT 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, KIT RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and BONE.
