MER proto-oncogene, tyrosine kinaseGenealiases: MER · RP38 · Tyro12 · c-Eyk · c-mer
Q-omics provides the consensus-scored MERTK profile across patient tissues and cancer cell-line models. MERTK 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, MERTK is differentially expressed in 8, with the highest sampling consensus in HNSC. Additionally, MERTK RNA expression shows 19,236 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight KIRC, HNSC, and THYM as cancer lineages where MERTK 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 MERTK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MERTK survival associations across molecular data types. MERTK RNA expression shows survival associations in the most cancer types (22), followed by mutation status (6) 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 MERTK RNA expression–survival associations across cancer types. High MERTK expression shows unfavorable associations in ACC, UVM and KICH, but favorable associations in KIRC, LUAD and HNSC. 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 MERTK RNA expression.
This table summarizes MERTK tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8, while mass-spec protein shows differences in 4. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for MERTK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MERTK shows lower tumor expression in KIRP, BRCA and PAAD and higher tumor expression in HNSC, UCEC and LUSC. The HNSC box plot shows higher MERTK RNA expression in tumor versus normal tissue (log2 FC = +0.645, t-test p = .012).
This table shows molecular features associated with MERTK in patient tissues and cancer cell lines. In patient samples, MERTK shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, MERTK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BONE.
