Q-omics provides the consensus-scored GIPR profile across patient tissues and cancer cell-line models. GIPR 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, GIPR is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, GIPR RNA expression shows 16,428 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, and UVM as cancer lineages where GIPR 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 GIPR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GIPR survival associations across molecular data types. GIPR RNA expression shows survival associations in the most cancer types (24), followed by mutation status (3) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible GIPR RNA expression–survival associations across cancer types. High GIPR expression shows unfavorable associations in KIRC and ACC, but favorable associations in BLCA, HNSC, SCLC and PAAD. The KIRC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for GIPR RNA expression.
This table summarizes GIPR 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 2. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for GIPR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GIPR shows lower tumor expression in KIRC, LUSC and READ and higher tumor expression in THCA, LIHC and CHOL. The KIRC box plot shows higher GIPR RNA expression in normal versus tumor tissue (log2 FC = −0.467, t-test p < 0.001).
This table shows molecular features associated with GIPR in patient tissues and cancer cell lines. In patient samples, GIPR shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, GIPR 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 URINARY_TRACT and SOFT_TISSUE.
