Q-omics provides the consensus-scored HOOK3 profile across patient tissues and cancer cell-line models. HOOK3 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, HOOK3 is differentially expressed in 7, with the highest sampling consensus in KIRC. Additionally, HOOK3 RNA expression shows 20,447 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight HNSC, KIRC, and KIRP as cancer lineages where HOOK3 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 HOOK3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HOOK3 survival associations across molecular data types. HOOK3 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (4) 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 HOOK3 RNA expression–survival associations across cancer types. High HOOK3 expression shows unfavorable associations in KICH, MESO, UVM and ACC, but favorable associations in HNSC and KIRC. 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 HOOK3 RNA expression.
This table summarizes HOOK3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 7, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for HOOK3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HOOK3 shows lower tumor expression in BRCA and KICH and higher tumor expression in KIRC, CHOL, LIHC and COAD. The KIRC box plot shows higher HOOK3 RNA expression in tumor versus normal tissue (log2 FC = +0.365, t-test p < 0.001).
This table shows molecular features associated with HOOK3 in patient tissues and cancer cell lines. In patient samples, HOOK3 shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, HOOK3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in CNS and UPPER_AERODIGESTIVE_TRACT.
