Q-omics provides the consensus-scored CRTAP profile across patient tissues and cancer cell-line models. CRTAP expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, CRTAP is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, CRTAP protein abundance shows 28,418 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight ACC, KIRC, and GBM as cancer lineages where CRTAP 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 CRTAP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CRTAP survival associations across molecular data types. CRTAP RNA expression shows survival associations in the most cancer types (21), followed by mutation status (6) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CRTAP RNA expression–survival associations across cancer types. High CRTAP expression shows unfavorable associations in ACC, KICH, BLCA, MESO and STAD, but favorable associations in DLBC. The ACC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .002). Together, the overview and detailed table identify ACC as the clearest survival context for CRTAP RNA expression.
This table summarizes CRTAP 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 CRTAP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CRTAP shows lower tumor expression in BLCA, UCEC and LUAD and higher tumor expression in KIRC, LIHC and KIRP. The KIRC box plot shows higher CRTAP RNA expression in tumor versus normal tissue (log2 FC = +0.682, t-test p < 0.001).
This table shows molecular features associated with CRTAP in patient tissues and cancer cell lines. In patient samples, CRTAP 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, CRTAP RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BONE.
