Q-omics provides the consensus-scored PCCB profile across patient tissues and cancer cell-line models. PCCB expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, PCCB is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, PCCB protein abundance shows 26,280 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight UVM, KIRC, and GBM as cancer lineages where PCCB 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 PCCB — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PCCB survival associations across molecular data types. PCCB RNA expression shows survival associations in the most cancer types (20), followed by mutation status (4) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PCCB RNA expression–survival associations across cancer types. High PCCB expression shows unfavorable associations in UVM, SKCM and MESO, but favorable associations in KIRP, BRCA 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 = .001). Together, the overview and detailed table identify UVM as the clearest survival context for PCCB RNA expression.
This table summarizes PCCB 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 PCCB. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PCCB shows lower tumor expression in KIRC and higher tumor expression in LUSC, HNSC, LUAD, BRCA and UCEC. The KIRC box plot shows higher PCCB RNA expression in normal versus tumor tissue (log2 FC = −1.632, t-test p < 0.001).
This table shows molecular features associated with PCCB in patient tissues and cancer cell lines. In patient samples, PCCB 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, PCCB RNA and mutation anchors are most strongly linked to RNA-expression features, especially in STOMACH, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and BONE.
