CRK like proto-oncogene, adaptor proteinGenealiases: []
Q-omics provides the consensus-scored CRKL profile across patient tissues and cancer cell-line models. CRKL expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, CRKL is differentially expressed in 13, with the highest sampling consensus in HNSC. Additionally, CRKL protein abundance shows 23,197 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRP, HNSC, and PDAC as cancer lineages where CRKL 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 CRKL — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CRKL survival associations across molecular data types. CRKL RNA expression shows survival associations in the most cancer types (22), followed by mutation status (3) 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 CRKL RNA expression–survival associations across cancer types. High CRKL expression shows unfavorable associations in KIRP, ACC and LIHC, but favorable associations in SCLC, KIRC and READ. The KIRP 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 KIRP as the clearest survival context for CRKL RNA expression.
This table summarizes CRKL tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CRKL. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CRKL shows lower tumor expression in THCA and higher tumor expression in HNSC, KIRC, LIHC, LUSC and BLCA. The HNSC box plot shows higher CRKL RNA expression in tumor versus normal tissue (log2 FC = +1.330, t-test p < 0.001).
This table shows molecular features associated with CRKL in patient tissues and cancer cell lines. In patient samples, CRKL shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, CRKL RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and LARGE_INTESTINE.
