Q-omics provides the consensus-scored SRC profile across patient tissues and cancer cell-line models. SRC 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, SRC is differentially expressed in 15, with the highest sampling consensus in HNSC. Additionally, SRC RNA expression shows 19,251 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight KIRC, HNSC, and KIRP as cancer lineages where SRC 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 SRC — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SRC survival associations across molecular data types. SRC RNA expression shows survival associations in the most cancer types (22), followed by mutation status (4) 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 SRC RNA expression–survival associations across cancer types. High SRC expression shows unfavorable associations in KIRC, LIHC, LUSC and MESO, but favorable associations in BLCA and ACC. The KIRC 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 KIRC as the clearest survival context for SRC RNA expression.
This table summarizes SRC tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 5. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for SRC. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SRC shows higher tumor expression in HNSC, KIRP, STAD, BRCA, KIRC and COAD. The HNSC box plot shows higher SRC RNA expression in tumor versus normal tissue (log2 FC = +1.160, t-test p < 0.001).
This table shows molecular features associated with SRC in patient tissues and cancer cell lines. In patient samples, SRC shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, SRC 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 SOFT_TISSUE and UPPER_AERODIGESTIVE_TRACT.
