Q-omics provides the consensus-scored PDIK1L profile across patient tissues and cancer cell-line models. PDIK1L expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, PDIK1L is differentially expressed in 13, with the highest sampling consensus in BLCA. Additionally, PDIK1L RNA expression shows 22,180 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight LUAD, BLCA, and GBM as cancer lineages where PDIK1L 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 PDIK1L — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PDIK1L survival associations across molecular data types. PDIK1L RNA expression shows survival associations in the most cancer types (21), followed by mutation status (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PDIK1L RNA expression–survival associations across cancer types. High PDIK1L expression shows unfavorable associations in LGG, but favorable associations in LUAD, HNSC, KIRC, SKCM and COAD. The LUAD 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 LUAD as the clearest survival context for PDIK1L RNA expression.
This table summarizes PDIK1L tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13. The strongest signals are observed in BLCA for RNA.
This table ranks reproducible tumor–normal expression differences for PDIK1L. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PDIK1L shows higher tumor expression in BLCA, LUAD, BRCA, LIHC, STAD and LUSC. The BLCA box plot shows higher PDIK1L RNA expression in tumor versus normal tissue (log2 FC = +1.222, t-test p < 0.001).
This table shows molecular features associated with PDIK1L in patient tissues and cancer cell lines. In patient samples, PDIK1L 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, PDIK1L RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and BLOOD_Leukemia.
