Q-omics provides the consensus-scored MKKS profile across patient tissues and cancer cell-line models. MKKS expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in LIHC. Among the 18 cancer types available for tumor–normal comparison, MKKS is differentially expressed in 13, with the highest sampling consensus in HNSC. Additionally, MKKS RNA expression shows 18,385 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight LIHC, HNSC, and UVM as cancer lineages where MKKS 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 MKKS — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MKKS survival associations across molecular data types. MKKS RNA expression shows survival associations in the most cancer types (21), followed by mutation status (3) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MKKS RNA expression–survival associations across cancer types. High MKKS expression shows unfavorable associations in LIHC, UVM, MESO and LUAD, but favorable associations in KIRC and READ. The LIHC 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 LIHC as the clearest survival context for MKKS RNA expression.
This table summarizes MKKS 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 2. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for MKKS. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MKKS shows lower tumor expression in THCA and KIRC and higher tumor expression in HNSC, LIHC, STAD and LUSC. The HNSC box plot shows higher MKKS RNA expression in tumor versus normal tissue (log2 FC = +0.644, t-test p < 0.001).
This table shows molecular features associated with MKKS in patient tissues and cancer cell lines. In patient samples, MKKS shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, MKKS 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 BLOOD_Leukemia.
