Q-omics provides the consensus-scored CLDND1 profile across patient tissues and cancer cell-line models. CLDND1 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, CLDND1 is differentially expressed in 13, with the highest sampling consensus in HNSC. Additionally, CLDND1 protein abundance shows 28,655 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, HNSC, and GBM as cancer lineages where CLDND1 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 CLDND1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CLDND1 survival associations across molecular data types. CLDND1 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (2) and mass-spec protein abundance (10). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CLDND1 RNA expression–survival associations across cancer types. High CLDND1 expression shows unfavorable associations in KIRP, ACC, LIHC, MESO, DLBC and STAD. 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 CLDND1 RNA expression.
This table summarizes CLDND1 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 9. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CLDND1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CLDND1 shows lower tumor expression in THCA and higher tumor expression in HNSC, KIRC, LIHC, LUSC and CHOL. The HNSC box plot shows higher CLDND1 RNA expression in tumor versus normal tissue (log2 FC = +0.808, t-test p < 0.001).
This table shows molecular features associated with CLDND1 in patient tissues and cancer cell lines. In patient samples, CLDND1 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, CLDND1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and LARGE_INTESTINE.
