Q-omics provides the consensus-scored PLSCR4 profile across patient tissues and cancer cell-line models. PLSCR4 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PLSCR4 is differentially expressed in 12, with the highest sampling consensus in KICH. Additionally, PLSCR4 RNA expression shows 21,318 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRC, KICH, and LUAD as cancer lineages where PLSCR4 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 PLSCR4 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PLSCR4 survival associations across molecular data types. PLSCR4 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (5) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PLSCR4 RNA expression–survival associations across cancer types. High PLSCR4 expression shows favorable associations in KIRC, HNSC, UVM, MESO, UCS and SKCM. 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 PLSCR4 RNA expression.
This table summarizes PLSCR4 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 9. The strongest signals are observed in THCA for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for PLSCR4. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PLSCR4 shows lower tumor expression in KICH, THCA, COAD, LUAD, LIHC and KIRP. The KICH box plot shows higher PLSCR4 RNA expression in normal versus tumor tissue (log2 FC = −3.237, t-test p < 0.001).
This table shows molecular features associated with PLSCR4 in patient tissues and cancer cell lines. In patient samples, PLSCR4 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, PLSCR4 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in BREAST and LARGE_INTESTINE.
