cannabinoid receptor interacting protein 1Genealiases: C2orf32 · CRIP-1 · CRIP1
Q-omics provides the consensus-scored CNRIP1 profile across patient tissues and cancer cell-line models. CNRIP1 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CNRIP1 is differentially expressed in 14, with the highest sampling consensus in BLCA. Additionally, CNRIP1 protein abundance shows 40,116 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, BLCA, and GBM as cancer lineages where CNRIP1 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 CNRIP1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CNRIP1 survival associations across molecular data types. CNRIP1 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (7) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CNRIP1 RNA expression–survival associations across cancer types. High CNRIP1 expression shows unfavorable associations in LUSC, KIRP and BLCA, but favorable associations in KIRC, LGG and LUAD. 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 CNRIP1 RNA expression.
This table summarizes CNRIP1 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 BLCA for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for CNRIP1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CNRIP1 shows lower tumor expression in BLCA, COAD, LUAD, LUSC and KICH and higher tumor expression in KIRC. The BLCA box plot shows higher CNRIP1 RNA expression in normal versus tumor tissue (log2 FC = −2.562, t-test p < 0.001).
This table shows molecular features associated with CNRIP1 in patient tissues and cancer cell lines. In patient samples, CNRIP1 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, CNRIP1 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 LIVER and BLOOD_Leukemia.
