Q-omics provides the consensus-scored G6PC profile across patient tissues and cancer cell-line models. G6PC expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, G6PC is differentially expressed in 10, with the highest sampling consensus in KIRP. Additionally, G6PC protein abundance shows 14,395 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, KIRP, and GBM as cancer lineages where G6PC 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 G6PC — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes G6PC survival associations across molecular data types. G6PC RNA expression shows survival associations in the most cancer types (25), followed by mutation status (6) 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 G6PC RNA expression–survival associations across cancer types. High G6PC expression shows unfavorable associations in CESC, ACC and SCLC, but favorable associations in KIRC, KIRP and LIHC. 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 G6PC RNA expression.
This table summarizes G6PC tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 1. The strongest signals are observed in KIRP for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for G6PC. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. G6PC shows lower tumor expression in KIRP, COAD, KIRC, KICH, THCA and CHOL. The KIRP box plot shows higher G6PC RNA expression in normal versus tumor tissue (log2 FC = −5.738, t-test p < 0.001).
This table shows molecular features associated with G6PC in patient tissues and cancer cell lines. In patient samples, G6PC 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, G6PC RNA and mutation anchors are most strongly linked to RNA-expression features, especially in STOMACH, while CRISPR and shRNA rows add functional-dependency signals in OESOPHAGUS and CNS.
