Q-omics provides the consensus-scored PDCL3 profile across patient tissues and cancer cell-line models. PDCL3 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, PDCL3 is differentially expressed in 12, with the highest sampling consensus in HNSC. Additionally, PDCL3 protein abundance shows 18,940 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight ACC, HNSC, and GBM as cancer lineages where PDCL3 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 PDCL3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PDCL3 survival associations across molecular data types. PDCL3 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (5) 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 PDCL3 RNA expression–survival associations across cancer types. High PDCL3 expression shows unfavorable associations in ACC, MESO, LIHC, KICH and KIRP, but favorable associations in BLCA. 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 PDCL3 RNA expression.
This table summarizes PDCL3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 5. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PDCL3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PDCL3 shows higher tumor expression in HNSC, KIRC, LUAD, LIHC, LUSC and BRCA. The HNSC box plot shows higher PDCL3 RNA expression in tumor versus normal tissue (log2 FC = +0.893, t-test p < 0.001).
This table shows molecular features associated with PDCL3 in patient tissues and cancer cell lines. In patient samples, PDCL3 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, PDCL3 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 BREAST and BLOOD_Lymphoma.
