Q-omics provides the consensus-scored HTN1 profile across patient tissues and cancer cell-line models. HTN1 expression is associated with patient survival in 18 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, HTN1 is differentially expressed in 3, with the highest sampling consensus in HNSC. Additionally, HTN1 protein abundance shows 12,096 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight UVM, HNSC, and LUAD as cancer lineages where HTN1 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 HTN1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HTN1 survival associations across molecular data types. HTN1 RNA expression shows survival associations in the most cancer types (18), followed by mutation status (1) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible HTN1 RNA expression–survival associations across cancer types. High HTN1 expression shows unfavorable associations in UVM, CHOL, THYM, UCEC and KICH, but favorable associations in MESO. 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 HTN1 RNA expression.
This table summarizes HTN1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 3, while mass-spec protein shows differences in 5. The strongest signals are observed in HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for HTN1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HTN1 shows lower tumor expression in HNSC and KIRC and higher tumor expression in LUSC. The HNSC box plot shows higher HTN1 RNA expression in normal versus tumor tissue (log2 FC = −1.597, t-test p = .004).
This table shows molecular features associated with HTN1 in patient tissues and cancer cell lines. In patient samples, HTN1 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, HTN1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in SKIN and LUNG_SCLC.
