Q-omics provides the consensus-scored PIWIL1 profile across patient tissues and cancer cell-line models. PIWIL1 expression is associated with patient survival in 19 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, PIWIL1 is differentially expressed in 13, with the highest sampling consensus in COAD. Additionally, PIWIL1 protein abundance shows 12,811 significant protein co-abundance associations, with the highest sampling consensus in BRCA. Together, these results highlight KIRP, COAD, and BRCA as cancer lineages where PIWIL1 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 PIWIL1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PIWIL1 survival associations across molecular data types. PIWIL1 RNA expression shows survival associations in the most cancer types (19), followed by mutation status (8) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PIWIL1 RNA expression–survival associations across cancer types. High PIWIL1 expression shows unfavorable associations in KIRP, ACC, CESC, CHOL, LUSC and SARC. The KIRP 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 KIRP as the clearest survival context for PIWIL1 RNA expression.
This table summarizes PIWIL1 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 3. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for PIWIL1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PIWIL1 shows lower tumor expression in KIRC, KICH and KIRP and higher tumor expression in COAD, STAD and THCA. The COAD box plot shows higher PIWIL1 RNA expression in tumor versus normal tissue (log2 FC = +1.958, t-test p < 0.001).
This table shows molecular features associated with PIWIL1 in patient tissues and cancer cell lines. In patient samples, PIWIL1 shows the broadest associations at the RNA and protein expression levels, with BRCA recurring as the lineage with the largest associated feature set. In cancer cell lines, PIWIL1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and LARGE_INTESTINE.
