Q-omics provides the consensus-scored HS3ST3A1 profile across patient tissues and cancer cell-line models. HS3ST3A1 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, HS3ST3A1 is differentially expressed in 11, with the highest sampling consensus in LUAD. Additionally, HS3ST3A1 RNA expression shows 15,231 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight UVM, and LUAD as cancer lineages where HS3ST3A1 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 HS3ST3A1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HS3ST3A1 survival associations across molecular data types. HS3ST3A1 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible HS3ST3A1 RNA expression–survival associations across cancer types. High HS3ST3A1 expression shows unfavorable associations in UVM, KIRC, OV and BLCA, but favorable associations in LAML and UCEC. The UVM 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 UVM as the clearest survival context for HS3ST3A1 RNA expression.
This table summarizes HS3ST3A1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11. The strongest signals are observed in LUAD for RNA.
This table ranks reproducible tumor–normal expression differences for HS3ST3A1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HS3ST3A1 shows lower tumor expression in LIHC and KIRP and higher tumor expression in LUAD, COAD, BLCA and LUSC. The LUAD box plot shows higher HS3ST3A1 RNA expression in tumor versus normal tissue (log2 FC = +0.873, t-test p < 0.001).
This table shows molecular features associated with HS3ST3A1 in patient tissues and cancer cell lines. In patient samples, HS3ST3A1 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, HS3ST3A1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Myeloma and BONE.