Q-omics provides the consensus-scored CLPTM1L profile across patient tissues and cancer cell-line models. CLPTM1L expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CLPTM1L is differentially expressed in 17, with the highest sampling consensus in HNSC. Additionally, CLPTM1L protein abundance shows 32,676 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRC, HNSC, and PDAC as cancer lineages where CLPTM1L 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 CLPTM1L — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CLPTM1L survival associations across molecular data types. CLPTM1L RNA expression shows survival associations in the most cancer types (25), followed by mutation status (7) and mass-spec protein abundance (12). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CLPTM1L RNA expression–survival associations across cancer types. High CLPTM1L expression shows unfavorable associations in ACC, KIRP, LGG and BRCA, but favorable associations in KIRC and LUAD. 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 CLPTM1L RNA expression.
This table summarizes CLPTM1L 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 11. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for CLPTM1L. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CLPTM1L shows higher tumor expression in HNSC, KIRC, COAD, LUAD, STAD and LIHC. The HNSC box plot shows higher CLPTM1L RNA expression in tumor versus normal tissue (log2 FC = +1.382, t-test p < 0.001).
This table shows molecular features associated with CLPTM1L in patient tissues and cancer cell lines. In patient samples, CLPTM1L shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, CLPTM1L RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LARGE_INTESTINE.
