Q-omics provides the consensus-scored HRK profile across patient tissues and cancer cell-line models. HRK expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, HRK is differentially expressed in 11, with the highest sampling consensus in THCA. Additionally, HRK RNA expression shows 15,680 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight KIRC, THCA, and TGCT as cancer lineages where HRK 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 HRK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HRK survival associations across molecular data types. HRK RNA expression shows survival associations in the most cancer types (26), followed by 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 HRK RNA expression–survival associations across cancer types. High HRK expression shows unfavorable associations in KIRC, MESO, LUSC and COAD, but favorable associations in SCLC and KIRP. The KIRC 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 KIRC as the clearest survival context for HRK RNA expression.
This table summarizes HRK tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 4. The strongest signals are observed in THCA for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for HRK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HRK shows lower tumor expression in COAD, KIRC and BRCA and higher tumor expression in THCA, KIRP and KICH. The THCA box plot shows higher HRK RNA expression in tumor versus normal tissue (log2 FC = +1.684, t-test p < 0.001).
This table shows molecular features associated with HRK in patient tissues and cancer cell lines. In patient samples, HRK shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, HRK 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 BLOOD_Leukemia and BLOOD_Lymphoma.
