Q-omics provides the consensus-scored CLDN10-AS1 profile across patient tissues and cancer cell-line models. CLDN10-AS1 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in PAAD. Among the 18 cancer types available for tumor–normal comparison, CLDN10-AS1 is differentially expressed in 8, with the highest sampling consensus in KIRC. Additionally, CLDN10-AS1 RNA expression shows 8,264 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight PAAD, KIRC, and KIRP as cancer lineages where CLDN10-AS1 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 CLDN10-AS1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CLDN10-AS1 survival associations across molecular data types. CLDN10-AS1 RNA expression shows survival associations in the most cancer types (24). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CLDN10-AS1 RNA expression–survival associations across cancer types. High CLDN10-AS1 expression shows unfavorable associations in PAAD, MESO and ESCA, but favorable associations in UVM, LAML and OV. The PAAD 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 PAAD as the clearest survival context for CLDN10-AS1 RNA expression.
This table summarizes CLDN10-AS1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for CLDN10-AS1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CLDN10-AS1 shows lower tumor expression in KIRC, KICH and KIRP and higher tumor expression in LUAD, COAD and THCA. The KIRC box plot shows higher CLDN10-AS1 RNA expression in normal versus tumor tissue (log2 FC = −1.760, t-test p < 0.001).
This table shows molecular features associated with CLDN10-AS1 in patient tissues and cancer cell lines. In patient samples, CLDN10-AS1 shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set.
