Q-omics provides the consensus-scored HIRIP3 profile across patient tissues and cancer cell-line models. HIRIP3 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, HIRIP3 is differentially expressed in 16, with the highest sampling consensus in THCA. Additionally, HIRIP3 protein abundance shows 25,032 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, THCA, and GBM as cancer lineages where HIRIP3 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 HIRIP3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HIRIP3 survival associations across molecular data types. HIRIP3 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (2) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible HIRIP3 RNA expression–survival associations across cancer types. High HIRIP3 expression shows unfavorable associations in COAD and LAML, but favorable associations in KIRC, SKCM, ACC and CESC. 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 HIRIP3 RNA expression.
This table summarizes HIRIP3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 5. The strongest signals are observed in THCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for HIRIP3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HIRIP3 shows lower tumor expression in THCA, LUAD and UCEC and higher tumor expression in LIHC, HNSC and KIRC. The THCA box plot shows higher HIRIP3 RNA expression in normal versus tumor tissue (log2 FC = −0.463, t-test p < 0.001).
This table shows molecular features associated with HIRIP3 in patient tissues and cancer cell lines. In patient samples, HIRIP3 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, HIRIP3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and BLOOD_Leukemia.
