Q-omics provides the consensus-scored SALL1 profile across patient tissues and cancer cell-line models. SALL1 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, SALL1 is differentially expressed in 13, with the highest sampling consensus in HNSC. Additionally, SALL1 RNA expression shows 17,053 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, HNSC, and UVM as cancer lineages where SALL1 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 SALL1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SALL1 survival associations across molecular data types. SALL1 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (12) 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 SALL1 RNA expression–survival associations across cancer types. High SALL1 expression shows unfavorable associations in LGG and LUAD, but favorable associations in KIRC, COAD, UCEC and READ. 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 SALL1 RNA expression.
This table summarizes SALL1 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 7. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for SALL1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SALL1 shows lower tumor expression in KICH, COAD, KIRC and KIRP and higher tumor expression in HNSC and LUSC. The HNSC box plot shows higher SALL1 RNA expression in tumor versus normal tissue (log2 FC = +0.611, t-test p < 0.001).
This table shows molecular features associated with SALL1 in patient tissues and cancer cell lines. In patient samples, SALL1 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, SALL1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and CNS.
