Q-omics provides the consensus-scored CTXN2 profile across patient tissues and cancer cell-line models. CTXN2 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in THCA. Among the 18 cancer types available for tumor–normal comparison, CTXN2 is differentially expressed in 9, with the highest sampling consensus in COAD. Additionally, CTXN2 RNA expression shows 11,505 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight THCA, COAD, and KIRP as cancer lineages where CTXN2 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 CTXN2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CTXN2 survival associations across molecular data types. CTXN2 RNA expression shows survival associations in the most cancer types (21), 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 CTXN2 RNA expression–survival associations across cancer types. High CTXN2 expression shows unfavorable associations in THCA, READ, MESO and UCEC, but favorable associations in UCS and OV. The THCA Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .006). Together, the overview and detailed table identify THCA as the clearest survival context for CTXN2 RNA expression.
This table summarizes CTXN2 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 COAD for RNA.
This table ranks reproducible tumor–normal expression differences for CTXN2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CTXN2 shows lower tumor expression in COAD, KICH and KIRC and higher tumor expression in BRCA, LUAD and LIHC. The COAD box plot shows higher CTXN2 RNA expression in normal versus tumor tissue (log2 FC = −0.117, t-test p < 0.001).
This table shows molecular features associated with CTXN2 in patient tissues and cancer cell lines. In patient samples, CTXN2 shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, CTXN2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in KIDNEY and BLOOD_Leukemia.
