Q-omics provides the consensus-scored HSD17B1 profile across patient tissues and cancer cell-line models. HSD17B1 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in BLCA. Among the 18 cancer types available for tumor–normal comparison, HSD17B1 is differentially expressed in 10, with the highest sampling consensus in HNSC. Additionally, HSD17B1 RNA expression shows 19,851 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight BLCA, HNSC, and KIRP as cancer lineages where HSD17B1 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 HSD17B1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HSD17B1 survival associations across molecular data types. HSD17B1 RNA expression shows survival associations in the most cancer types (22), 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 HSD17B1 RNA expression–survival associations across cancer types. High HSD17B1 expression shows unfavorable associations in BLCA, ACC, KICH and KIRP, but favorable associations in UVM and PAAD. The BLCA 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 BLCA as the clearest survival context for HSD17B1 RNA expression.
This table summarizes HSD17B1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for HSD17B1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HSD17B1 shows lower tumor expression in KIRC and KICH and higher tumor expression in HNSC, BLCA, LIHC and LUSC. The HNSC box plot shows higher HSD17B1 RNA expression in tumor versus normal tissue (log2 FC = +1.006, t-test p < 0.001).
This table shows molecular features associated with HSD17B1 in patient tissues and cancer cell lines. In patient samples, HSD17B1 shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, HSD17B1 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 LUNG_SCLC and BLOOD_Leukemia.
