Q-omics provides the consensus-scored KRT7 profile across patient tissues and cancer cell-line models. KRT7 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, KRT7 is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, KRT7 RNA expression shows 17,034 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight LUAD, KIRC, and LSCC as cancer lineages where KRT7 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 KRT7 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes KRT7 survival associations across molecular data types. KRT7 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (6) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible KRT7 RNA expression–survival associations across cancer types. High KRT7 expression shows unfavorable associations in LUAD, PAAD, UCEC, LGG and OV, but favorable associations in KIRP. The LUAD 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 LUAD as the clearest survival context for KRT7 RNA expression.
This table summarizes KRT7 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 5. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for KRT7. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. KRT7 shows lower tumor expression in KIRC, HNSC and LUSC and higher tumor expression in COAD, BLCA and STAD. The KIRC box plot shows higher KRT7 RNA expression in normal versus tumor tissue (log2 FC = −4.551, t-test p < 0.001).
This table shows molecular features associated with KRT7 in patient tissues and cancer cell lines. In patient samples, KRT7 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, KRT7 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and BONE.
