Q-omics provides the consensus-scored PLS1 profile across patient tissues and cancer cell-line models. PLS1 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PLS1 is differentially expressed in 16, with the highest sampling consensus in KICH. Additionally, PLS1 RNA expression shows 19,969 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, KICH, and ACC as cancer lineages where PLS1 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 PLS1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PLS1 survival associations across molecular data types. PLS1 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (5) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PLS1 RNA expression–survival associations across cancer types. High PLS1 expression shows unfavorable associations in ACC, PAAD, MESO and LUAD, but favorable associations in KIRC and KIRP. 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 PLS1 RNA expression.
This table summarizes PLS1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 6. The strongest signals are observed in KICH for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PLS1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PLS1 shows lower tumor expression in KICH, COAD, READ and KIRC and higher tumor expression in LUAD and BRCA. The KICH box plot shows higher PLS1 RNA expression in normal versus tumor tissue (log2 FC = −3.042, t-test p < 0.001).
This table shows molecular features associated with PLS1 in patient tissues and cancer cell lines. In patient samples, PLS1 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, PLS1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in BREAST and UPPER_AERODIGESTIVE_TRACT.
