Q-omics provides the consensus-scored SYMPK profile across patient tissues and cancer cell-line models. SYMPK expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, SYMPK is differentially expressed in 15, with the highest sampling consensus in HNSC. Additionally, SYMPK protein abundance shows 26,262 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight MESO, HNSC, and LSCC as cancer lineages where SYMPK 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 SYMPK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SYMPK survival associations across molecular data types. SYMPK RNA expression shows survival associations in the most cancer types (21), followed by mutation status (10) 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 SYMPK RNA expression–survival associations across cancer types. High SYMPK expression shows unfavorable associations in MESO, ACC, LIHC, KIRC and LUAD, but favorable associations in SCLC. The MESO 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 MESO as the clearest survival context for SYMPK RNA expression.
This table summarizes SYMPK 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 COAD for protein.
This table ranks reproducible tumor–normal expression differences for SYMPK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SYMPK shows higher tumor expression in HNSC, KIRP, COAD, LIHC, BLCA and KIRC. The HNSC box plot shows higher SYMPK RNA expression in tumor versus normal tissue (log2 FC = +0.798, t-test p < 0.001).
This table shows molecular features associated with SYMPK in patient tissues and cancer cell lines. In patient samples, SYMPK shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, SYMPK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and SOFT_TISSUE.
