Q-omics provides the consensus-scored MAP6 profile across patient tissues and cancer cell-line models. MAP6 expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, MAP6 is differentially expressed in 16, with the highest sampling consensus in KIRC. Additionally, MAP6 protein abundance shows 26,918 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight UVM, KIRC, and GBM as cancer lineages where MAP6 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 MAP6 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MAP6 survival associations across molecular data types. MAP6 RNA expression shows survival associations in the most cancer types (20), followed by mutation status (2) 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 MAP6 RNA expression–survival associations across cancer types. High MAP6 expression shows unfavorable associations in LGG and COAD, but favorable associations in UVM, PAAD, KIRC and LUAD. The UVM Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .001). Together, the overview and detailed table identify UVM as the clearest survival context for MAP6 RNA expression.
This table summarizes MAP6 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for MAP6. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MAP6 shows lower tumor expression in KIRC, KICH, KIRP, THCA, LUAD and UCEC. The KIRC box plot shows higher MAP6 RNA expression in normal versus tumor tissue (log2 FC = −2.209, t-test p < 0.001).
This table shows molecular features associated with MAP6 in patient tissues and cancer cell lines. In patient samples, MAP6 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, MAP6 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in SKIN and LUNG_SCLC.
