Q-omics provides the consensus-scored GCFC2 profile across patient tissues and cancer cell-line models. GCFC2 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, GCFC2 is differentially expressed in 14, with the highest sampling consensus in THCA. Additionally, GCFC2 RNA expression shows 21,166 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRP, THCA, and ACC as cancer lineages where GCFC2 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 GCFC2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GCFC2 survival associations across molecular data types. GCFC2 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (2) 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 GCFC2 RNA expression–survival associations across cancer types. High GCFC2 expression shows unfavorable associations in KIRP, UVM, ACC, LGG and UCEC, but favorable associations in KIRC. The KIRP 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 KIRP as the clearest survival context for GCFC2 RNA expression.
This table summarizes GCFC2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 6. The strongest signals are observed in THCA for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for GCFC2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GCFC2 shows lower tumor expression in THCA and KICH and higher tumor expression in HNSC, BLCA, LUSC and CHOL. The THCA box plot shows higher GCFC2 RNA expression in normal versus tumor tissue (log2 FC = −0.525, t-test p < 0.001).
This table shows molecular features associated with GCFC2 in patient tissues and cancer cell lines. In patient samples, GCFC2 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, GCFC2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUSC, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and LARGE_INTESTINE.
