Q-omics provides the consensus-scored HORMAD2 profile across patient tissues and cancer cell-line models. HORMAD2 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, HORMAD2 is differentially expressed in 8, with the highest sampling consensus in LUAD. Additionally, HORMAD2 RNA expression shows 8,462 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight ACC, LUAD, and KIRP as cancer lineages where HORMAD2 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 HORMAD2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HORMAD2 survival associations across molecular data types. HORMAD2 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible HORMAD2 RNA expression–survival associations across cancer types. High HORMAD2 expression shows unfavorable associations in ACC, READ, UVM, LGG and CHOL, but favorable associations in KIRP. The ACC 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 ACC as the clearest survival context for HORMAD2 RNA expression.
This table summarizes HORMAD2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8. The strongest signals are observed in THCA for RNA.
This table ranks reproducible tumor–normal expression differences for HORMAD2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HORMAD2 shows lower tumor expression in BRCA, CHOL and KICH and higher tumor expression in LUAD, THCA and UCEC. The LUAD box plot shows higher HORMAD2 RNA expression in tumor versus normal tissue (log2 FC = +0.352, t-test p < 0.001).
This table shows molecular features associated with HORMAD2 in patient tissues and cancer cell lines. In patient samples, HORMAD2 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, HORMAD2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and SKIN.
