Q-omics provides the consensus-scored SLFN5 profile across patient tissues and cancer cell-line models. SLFN5 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, SLFN5 is differentially expressed in 13, with the highest sampling consensus in KIRP. Additionally, SLFN5 RNA expression shows 18,916 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight HNSC, KIRP, and UVM as cancer lineages where SLFN5 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 SLFN5 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SLFN5 survival associations across molecular data types. SLFN5 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (5) 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 SLFN5 RNA expression–survival associations across cancer types. High SLFN5 expression shows unfavorable associations in LGG, PAAD and KIRP, but favorable associations in HNSC, KIRC and ACC. The HNSC 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 HNSC as the clearest survival context for SLFN5 RNA expression.
This table summarizes SLFN5 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 5. The strongest signals are observed in KIRP for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for SLFN5. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SLFN5 shows lower tumor expression in KICH and BRCA and higher tumor expression in KIRP, HNSC, KIRC and THCA. The KIRP box plot shows higher SLFN5 RNA expression in tumor versus normal tissue (log2 FC = +1.446, t-test p < 0.001).
This table shows molecular features associated with SLFN5 in patient tissues and cancer cell lines. In patient samples, SLFN5 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, SLFN5 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in OESOPHAGUS and SOFT_TISSUE.
