Q-omics provides the consensus-scored INTS5 profile across patient tissues and cancer cell-line models. INTS5 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, INTS5 is differentially expressed in 13, with the highest sampling consensus in HNSC. Additionally, INTS5 protein abundance shows 20,262 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, HNSC, and GBM as cancer lineages where INTS5 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 INTS5 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes INTS5 survival associations across molecular data types. INTS5 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (6) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible INTS5 RNA expression–survival associations across cancer types. High INTS5 expression shows unfavorable associations in KICH, BLCA, ACC and LIHC, but favorable associations in KIRC and UCEC. 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 INTS5 RNA expression.
This table summarizes INTS5 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 5. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for INTS5. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. INTS5 shows lower tumor expression in THCA and higher tumor expression in HNSC, LIHC, COAD, BRCA and STAD. The HNSC box plot shows higher INTS5 RNA expression in tumor versus normal tissue (log2 FC = +0.620, t-test p < 0.001).
This table shows molecular features associated with INTS5 in patient tissues and cancer cell lines. In patient samples, INTS5 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, INTS5 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BLOOD_Lymphoma.