Q-omics provides the consensus-scored VIPR1 profile across patient tissues and cancer cell-line models. VIPR1 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in LIHC. Among the 18 cancer types available for tumor–normal comparison, VIPR1 is differentially expressed in 14, with the highest sampling consensus in LUAD. Additionally, VIPR1 RNA expression shows 23,055 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight LIHC, LUAD, and GBM as cancer lineages where VIPR1 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 VIPR1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes VIPR1 survival associations across molecular data types. VIPR1 RNA expression shows survival associations in the most cancer types (23), 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 VIPR1 RNA expression–survival associations across cancer types. High VIPR1 expression shows favorable associations in LIHC, BLCA, KIRP, MESO, KIRC and COAD. The LIHC 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 LIHC as the clearest survival context for VIPR1 RNA expression.
This table summarizes VIPR1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 8. The strongest signals are observed in THCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for VIPR1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. VIPR1 shows lower tumor expression in LUAD, THCA, COAD, KIRP, LUSC and LIHC. The LUAD box plot shows higher VIPR1 RNA expression in normal versus tumor tissue (log2 FC = −3.378, t-test p < 0.001).
This table shows molecular features associated with VIPR1 in patient tissues and cancer cell lines. In patient samples, VIPR1 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, VIPR1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in BREAST and LARGE_INTESTINE.
