Q-omics provides the consensus-scored SALL3 profile across patient tissues and cancer cell-line models. SALL3 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, SALL3 is differentially expressed in 8, with the highest sampling consensus in KIRP. Additionally, SALL3 RNA expression shows 10,447 significant gene co-expression associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, KIRP, and GBM as cancer lineages where SALL3 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 SALL3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SALL3 survival associations across molecular data types. SALL3 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SALL3 RNA expression–survival associations across cancer types. High SALL3 expression shows unfavorable associations in KIRC, THCA, UVM, ACC and UCEC, but favorable associations in HNSC. The KIRC 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 KIRC as the clearest survival context for SALL3 RNA expression.
This table summarizes SALL3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8, while mass-spec protein shows differences in 1. The strongest signals are observed in KIRP for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for SALL3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SALL3 shows lower tumor expression in KIRP, KIRC and BLCA and higher tumor expression in BRCA, LUAD and LUSC. The KIRP box plot shows higher SALL3 RNA expression in normal versus tumor tissue (log2 FC = −1.357, t-test p < 0.001).
This table shows molecular features associated with SALL3 in patient tissues and cancer cell lines. In patient samples, SALL3 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, SALL3 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 UPPER_AERODIGESTIVE_TRACT and LARGE_INTESTINE.
