Q-omics provides the consensus-scored ITPRIP profile across patient tissues and cancer cell-line models. ITPRIP expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, ITPRIP is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, ITPRIP RNA expression shows 19,272 significant gene co-expression associations, with the highest sampling consensus in DLBC. Together, these results highlight KIRC, and DLBC as cancer lineages where ITPRIP 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 ITPRIP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ITPRIP survival associations across molecular data types. ITPRIP RNA expression shows survival associations in the most cancer types (25), 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 ITPRIP RNA expression–survival associations across cancer types. High ITPRIP expression shows unfavorable associations in LGG, BLCA and STAD, but favorable associations in KIRC, UVM and SCLC. 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 ITPRIP RNA expression.
This table summarizes ITPRIP tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, 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 ITPRIP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ITPRIP shows lower tumor expression in LUAD, UCEC, BRCA and BLCA and higher tumor expression in KIRC and COAD. The KIRC box plot shows higher ITPRIP RNA expression in tumor versus normal tissue (log2 FC = +1.296, t-test p < 0.001).
This table shows molecular features associated with ITPRIP in patient tissues and cancer cell lines. In patient samples, ITPRIP shows the broadest associations at the RNA and protein expression levels, with DLBC recurring as the lineage with the largest associated feature set. In cancer cell lines, ITPRIP RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in BONE and CNS.
