Q-omics provides the consensus-scored HOOK2 profile across patient tissues and cancer cell-line models. HOOK2 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, HOOK2 is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, HOOK2 protein abundance shows 20,042 significant protein co-abundance associations, with the highest sampling consensus in UCEC. Together, these results highlight HNSC, KIRC, and UCEC as cancer lineages where HOOK2 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 HOOK2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HOOK2 survival associations across molecular data types. HOOK2 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (6) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible HOOK2 RNA expression–survival associations across cancer types. High HOOK2 expression shows unfavorable associations in ACC, COAD and PRAD, but favorable associations in HNSC, KIRP and STAD. 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 HOOK2 RNA expression.
This table summarizes HOOK2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 9. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for HOOK2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HOOK2 shows lower tumor expression in KIRC, KIRP and THCA and higher tumor expression in COAD, UCEC and BLCA. The KIRC box plot shows higher HOOK2 RNA expression in normal versus tumor tissue (log2 FC = −0.694, t-test p < 0.001).
This table shows molecular features associated with HOOK2 in patient tissues and cancer cell lines. In patient samples, HOOK2 shows the broadest associations at the RNA and protein expression levels, with UCEC recurring as the lineage with the largest associated feature set. In cancer cell lines, HOOK2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Myeloma and LARGE_INTESTINE.
