Q-omics provides the consensus-scored PLSCR2 profile across patient tissues and cancer cell-line models. PLSCR2 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in COAD. Among the 18 cancer types available for tumor–normal comparison, PLSCR2 is differentially expressed in 11, with the highest sampling consensus in THCA. Additionally, PLSCR2 RNA expression shows 14,425 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight COAD, THCA, and KIRP as cancer lineages where PLSCR2 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 PLSCR2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PLSCR2 survival associations across molecular data types. PLSCR2 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PLSCR2 RNA expression–survival associations across cancer types. High PLSCR2 expression shows unfavorable associations in COAD, UCEC, LGG, UVM and THYM, but favorable associations in MESO. The COAD 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 COAD as the clearest survival context for PLSCR2 RNA expression.
This table summarizes PLSCR2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11. The strongest signals are observed in THCA for RNA.
This table ranks reproducible tumor–normal expression differences for PLSCR2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PLSCR2 shows lower tumor expression in THCA, KICH and KIRC and higher tumor expression in LUAD, HNSC and STAD. The THCA box plot shows higher PLSCR2 RNA expression in normal versus tumor tissue (log2 FC = −0.450, t-test p < 0.001).
This table shows molecular features associated with PLSCR2 in patient tissues and cancer cell lines. In patient samples, PLSCR2 shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, PLSCR2 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 BREAST and OVARY.
