Q-omics provides the consensus-scored HSPBAP1 profile across patient tissues and cancer cell-line models. HSPBAP1 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, HSPBAP1 is differentially expressed in 13, with the highest sampling consensus in HNSC. Additionally, HSPBAP1 RNA expression shows 20,323 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, HNSC, and UVM as cancer lineages where HSPBAP1 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 HSPBAP1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HSPBAP1 survival associations across molecular data types. HSPBAP1 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (3) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible HSPBAP1 RNA expression–survival associations across cancer types. High HSPBAP1 expression shows unfavorable associations in KIRC, OV, LGG, ACC, LIHC and UCEC. The KIRC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .005). Together, the overview and detailed table identify KIRC as the clearest survival context for HSPBAP1 RNA expression.
This table summarizes HSPBAP1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 2. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for HSPBAP1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HSPBAP1 shows lower tumor expression in THCA and higher tumor expression in HNSC, COAD, LIHC, STAD and BLCA. The HNSC box plot shows higher HSPBAP1 RNA expression in tumor versus normal tissue (log2 FC = +1.151, t-test p < 0.001).
This table shows molecular features associated with HSPBAP1 in patient tissues and cancer cell lines. In patient samples, HSPBAP1 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, HSPBAP1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in OVARY and BREAST.
