Q-omics provides the consensus-scored CRACDL profile across patient tissues and cancer cell-line models. CRACDL expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CRACDL is differentially expressed in 11, with the highest sampling consensus in KICH. Additionally, CRACDL protein abundance shows 23,701 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, KICH, and GBM as cancer lineages where CRACDL 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 CRACDL — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CRACDL survival associations across molecular data types. CRACDL RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CRACDL RNA expression–survival associations across cancer types. High CRACDL expression shows unfavorable associations in LGG and ESCA, but favorable associations in KIRC, THCA, CESC and MESO. 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 CRACDL RNA expression.
This table summarizes CRACDL tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 5. The strongest signals are observed in KICH for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CRACDL. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CRACDL shows lower tumor expression in KICH, HNSC, LUSC and LUAD and higher tumor expression in LIHC and THCA. The KICH box plot shows higher CRACDL RNA expression in normal versus tumor tissue (log2 FC = −1.809, t-test p < 0.001).
This table shows molecular features associated with CRACDL in patient tissues and cancer cell lines. In patient samples, CRACDL 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, CRACDL RNA and mutation anchors are most strongly linked to RNA-expression features, especially in STOMACH, while CRISPR and shRNA rows add functional-dependency signals in BREAST and LUNG_SCLC.
