Q-omics provides the consensus-scored GPC6 profile across patient tissues and cancer cell-line models. GPC6 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, GPC6 is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, GPC6 protein abundance shows 25,451 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRC, and LUAD as cancer lineages where GPC6 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 GPC6 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GPC6 survival associations across molecular data types. GPC6 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (10) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible GPC6 RNA expression–survival associations across cancer types. High GPC6 expression shows unfavorable associations in MESO, UVM, BLCA and LUAD, but favorable associations in KIRC and DLBC. 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 GPC6 RNA expression.
This table summarizes GPC6 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for GPC6. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GPC6 shows lower tumor expression in COAD, BLCA and READ and higher tumor expression in KIRC, HNSC and LUAD. The KIRC box plot shows higher GPC6 RNA expression in tumor versus normal tissue (log2 FC = +1.257, t-test p < 0.001).
This table shows molecular features associated with GPC6 in patient tissues and cancer cell lines. In patient samples, GPC6 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, GPC6 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in CNS and SKIN.
