Q-omics provides the consensus-scored SULT6B1 profile across patient tissues and cancer cell-line models. SULT6B1 expression is associated with patient survival in 18 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, SULT6B1 is differentially expressed in 4, with the highest sampling consensus in KICH. Additionally, SULT6B1 RNA expression shows 6,751 significant pathway-activity associations, with the highest sampling consensus in STAD. Together, these results highlight HNSC, KICH, and STAD as cancer lineages where SULT6B1 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 SULT6B1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SULT6B1 survival associations across molecular data types. SULT6B1 RNA expression shows survival associations in the most cancer types (18), followed by mutation status (4) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SULT6B1 RNA expression–survival associations across cancer types. High SULT6B1 expression shows unfavorable associations in KICH, KIRC, BRCA and KIRP, but favorable associations in HNSC and BLCA. The HNSC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .006). Together, the overview and detailed table identify HNSC as the clearest survival context for SULT6B1 RNA expression.
This table summarizes SULT6B1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 4, while mass-spec protein shows differences in 2. The strongest signals are observed in KICH for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for SULT6B1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SULT6B1 shows lower tumor expression in KICH and THCA and higher tumor expression in HNSC and STAD. The KICH box plot shows higher SULT6B1 RNA expression in normal versus tumor tissue (log2 FC = −0.053, t-test p < 0.001).
This table shows molecular features associated with SULT6B1 in patient tissues and cancer cell lines. In patient samples, SULT6B1 shows the broadest associations at the RNA and protein expression levels, with STAD recurring as the lineage with the largest associated feature set. In cancer cell lines, SULT6B1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and BLOOD_Leukemia.
