Q-omics provides the consensus-scored CLRN3 profile across patient tissues and cancer cell-line models. CLRN3 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CLRN3 is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, CLRN3 RNA expression shows 14,953 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight KIRC, and TGCT as cancer lineages where CLRN3 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 CLRN3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CLRN3 survival associations across molecular data types. CLRN3 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CLRN3 RNA expression–survival associations across cancer types. High CLRN3 expression shows unfavorable associations in KICH and LUSC, but favorable associations in KIRC, STAD, MESO and BRCA. 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 CLRN3 RNA expression.
This table summarizes CLRN3 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 3. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for CLRN3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CLRN3 shows lower tumor expression in KICH, LIHC and LUSC and higher tumor expression in KIRC, STAD and THCA. The KIRC box plot shows higher CLRN3 RNA expression in tumor versus normal tissue (log2 FC = +2.983, t-test p < 0.001).
This table shows molecular features associated with CLRN3 in patient tissues and cancer cell lines. In patient samples, CLRN3 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, CLRN3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and LARGE_INTESTINE.
