Q-omics provides the consensus-scored CPVL profile across patient tissues and cancer cell-line models. CPVL expression is associated with patient survival in 29 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, CPVL is differentially expressed in 15, with the highest sampling consensus in KICH. Additionally, CPVL protein abundance shows 31,977 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight UVM, KICH, and LSCC as cancer lineages where CPVL 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 CPVL — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CPVL survival associations across molecular data types. CPVL RNA expression shows survival associations in the most cancer types (29), followed by mutation status (6) and mass-spec protein abundance (11). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CPVL RNA expression–survival associations across cancer types. High CPVL expression shows unfavorable associations in UVM, STAD, UCEC, BLCA, LGG and LIHC. The UVM 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 UVM as the clearest survival context for CPVL RNA expression.
This table summarizes CPVL tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for CPVL. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CPVL shows lower tumor expression in KICH, KIRC, LUAD, BLCA, UCEC and KIRP. The KICH box plot shows higher CPVL RNA expression in normal versus tumor tissue (log2 FC = −4.400, t-test p < 0.001).
This table shows molecular features associated with CPVL in patient tissues and cancer cell lines. In patient samples, CPVL 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, CPVL RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in BONE and SOFT_TISSUE.
