Q-omics provides the consensus-scored CTXN3 profile across patient tissues and cancer cell-line models. CTXN3 expression is associated with patient survival in 18 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CTXN3 is differentially expressed in 9, with the highest sampling consensus in KIRP. Additionally, CTXN3 RNA expression shows 11,029 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight KIRC, KIRP, and TGCT as cancer lineages where CTXN3 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 CTXN3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CTXN3 survival associations across molecular data types. CTXN3 RNA expression shows survival associations in the most cancer types (18), followed by mutation status (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CTXN3 RNA expression–survival associations across cancer types. High CTXN3 expression shows unfavorable associations in LIHC and THCA, but favorable associations in KIRC, HNSC, LGG and LUSC. 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 CTXN3 RNA expression.
This table summarizes CTXN3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9. The strongest signals are observed in KIRP for RNA.
This table ranks reproducible tumor–normal expression differences for CTXN3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CTXN3 shows lower tumor expression in KIRP, KIRC, KICH, COAD, BRCA and STAD. The KIRP box plot shows higher CTXN3 RNA expression in normal versus tumor tissue (log2 FC = −5.822, t-test p < 0.001).
This table shows molecular features associated with CTXN3 in patient tissues and cancer cell lines. In patient samples, CTXN3 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, CTXN3 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 SKIN.
