Q-omics provides the consensus-scored PDCD6IP profile across patient tissues and cancer cell-line models. PDCD6IP expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PDCD6IP is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, PDCD6IP protein abundance shows 25,806 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRC, and PDAC as cancer lineages where PDCD6IP 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 PDCD6IP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PDCD6IP survival associations across molecular data types. PDCD6IP RNA expression shows survival associations in the most cancer types (25), followed by mutation status (8) 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 PDCD6IP RNA expression–survival associations across cancer types. High PDCD6IP expression shows unfavorable associations in LGG, LIHC, LUAD, LUSC and MESO, but favorable associations in KIRC. The KIRC 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 KIRC as the clearest survival context for PDCD6IP RNA expression.
This table summarizes PDCD6IP tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PDCD6IP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PDCD6IP shows lower tumor expression in KIRC, COAD, LUSC and THCA and higher tumor expression in LIHC and BLCA. The KIRC box plot shows higher PDCD6IP RNA expression in normal versus tumor tissue (log2 FC = −0.697, t-test p < 0.001).
This table shows molecular features associated with PDCD6IP in patient tissues and cancer cell lines. In patient samples, PDCD6IP shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, PDCD6IP RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and UPPER_AERODIGESTIVE_TRACT.
