Q-omics provides the consensus-scored FCN2 profile across patient tissues and cancer cell-line models. FCN2 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in COAD. Among the 18 cancer types available for tumor–normal comparison, FCN2 is differentially expressed in 13, with the highest sampling consensus in THCA. Additionally, FCN2 protein abundance shows 16,026 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight COAD, THCA, and GBM as cancer lineages where FCN2 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 FCN2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FCN2 survival associations across molecular data types. FCN2 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (3) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible FCN2 RNA expression–survival associations across cancer types. High FCN2 expression shows unfavorable associations in COAD, LUSC and ESCA, but favorable associations in ACC, KIRC and THCA. The COAD 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 COAD as the clearest survival context for FCN2 RNA expression.
This table summarizes FCN2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 3. The strongest signals are observed in THCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for FCN2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FCN2 shows lower tumor expression in THCA, LIHC, BLCA, BRCA, KIRP and CHOL. The THCA box plot shows higher FCN2 RNA expression in normal versus tumor tissue (log2 FC = −0.573, t-test p < 0.001).
This table shows molecular features associated with FCN2 in patient tissues and cancer cell lines. In patient samples, FCN2 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, FCN2 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 OESOPHAGUS and LARGE_INTESTINE.
