Q-omics provides the consensus-scored PCID2 profile across patient tissues and cancer cell-line models. PCID2 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, PCID2 is differentially expressed in 14, with the highest sampling consensus in COAD. Additionally, PCID2 protein abundance shows 20,791 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight ACC, COAD, and GBM as cancer lineages where PCID2 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 PCID2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PCID2 survival associations across molecular data types. PCID2 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (7) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PCID2 RNA expression–survival associations across cancer types. High PCID2 expression shows unfavorable associations in ACC, LIHC, HNSC, CESC and KICH, but favorable associations in SCLC. 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 PCID2 RNA expression.
This table summarizes PCID2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 6. The strongest signals are observed in COAD for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for PCID2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PCID2 shows lower tumor expression in THCA and KICH and higher tumor expression in COAD, LIHC, HNSC and READ. The COAD box plot shows higher PCID2 RNA expression in tumor versus normal tissue (log2 FC = +1.360, t-test p < 0.001).
This table shows molecular features associated with PCID2 in patient tissues and cancer cell lines. In patient samples, PCID2 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, PCID2 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 BONE and BLOOD_Leukemia.
