Q-omics provides the consensus-scored CLCN2 profile across patient tissues and cancer cell-line models. CLCN2 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, CLCN2 is differentially expressed in 17, with the highest sampling consensus in HNSC. Additionally, CLCN2 RNA expression shows 20,244 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight ACC, HNSC, and LSCC as cancer lineages where CLCN2 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 CLCN2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CLCN2 survival associations across molecular data types. CLCN2 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (7) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CLCN2 RNA expression–survival associations across cancer types. High CLCN2 expression shows unfavorable associations in ACC, LIHC, KICH, LGG and UCEC, but favorable associations in LUSC. The ACC 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 ACC as the clearest survival context for CLCN2 RNA expression.
This table summarizes CLCN2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 17, while mass-spec protein shows differences in 5. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for CLCN2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CLCN2 shows lower tumor expression in COAD and higher tumor expression in HNSC, BLCA, LIHC, LUAD and STAD. The HNSC box plot shows higher CLCN2 RNA expression in tumor versus normal tissue (log2 FC = +1.578, t-test p < 0.001).
This table shows molecular features associated with CLCN2 in patient tissues and cancer cell lines. In patient samples, CLCN2 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, CLCN2 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 SOFT_TISSUE and BLOOD_Leukemia.
