Q-omics provides the consensus-scored HLA-A profile across patient tissues and cancer cell-line models. HLA-A expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, HLA-A is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, HLA-A RNA expression shows 14,974 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight UVM, and KIRC as cancer lineages where HLA-A 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 HLA-A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HLA-A survival associations across molecular data types. HLA-A RNA expression shows survival associations in the most cancer types (22), followed by mutation status (4) 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 HLA-A RNA expression–survival associations across cancer types. High HLA-A expression shows unfavorable associations in UVM, UCS, LGG and THYM, but favorable associations in SKCM and CESC. 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 HLA-A RNA expression.
This table summarizes HLA-A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 3. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for HLA-A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HLA-A shows higher tumor expression in KIRC, HNSC, LIHC, KIRP, STAD and THCA. The KIRC box plot shows higher HLA-A RNA expression in tumor versus normal tissue (log2 FC = +2.010, t-test p < 0.001).
This table shows molecular features associated with HLA-A in patient tissues and cancer cell lines. In patient samples, HLA-A 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, HLA-A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in SKIN and CNS.
