Q-omics provides the consensus-scored GPM6B profile across patient tissues and cancer cell-line models. GPM6B expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, GPM6B is differentially expressed in 16, with the highest sampling consensus in KIRC. Additionally, GPM6B protein abundance shows 22,417 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight UVM, KIRC, and GBM as cancer lineages where GPM6B 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 GPM6B — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GPM6B survival associations across molecular data types. GPM6B RNA expression shows survival associations in the most cancer types (25), followed by mutation status (6) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible GPM6B RNA expression–survival associations across cancer types. High GPM6B expression shows unfavorable associations in UVM, UCEC and THCA, but favorable associations in LGG, LUAD and OV. The UVM 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 UVM as the clearest survival context for GPM6B RNA expression.
This table summarizes GPM6B 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 8. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for GPM6B. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GPM6B shows lower tumor expression in KIRC, KICH, COAD, THCA, BLCA and LUAD. The KIRC box plot shows higher GPM6B RNA expression in normal versus tumor tissue (log2 FC = −2.318, t-test p < 0.001).
This table shows molecular features associated with GPM6B in patient tissues and cancer cell lines. In patient samples, GPM6B 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, GPM6B RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in BREAST and UPPER_AERODIGESTIVE_TRACT.
