Q-omics provides the consensus-scored HSBP1 profile across patient tissues and cancer cell-line models. HSBP1 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in STAD. Among the 18 cancer types available for tumor–normal comparison, HSBP1 is differentially expressed in 12, with the highest sampling consensus in THCA. Additionally, HSBP1 RNA expression shows 19,606 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight STAD, THCA, and UVM as cancer lineages where HSBP1 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 HSBP1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HSBP1 survival associations across molecular data types. HSBP1 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (1) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible HSBP1 RNA expression–survival associations across cancer types. High HSBP1 expression shows unfavorable associations in STAD, ACC and LIHC, but favorable associations in KIRP, UCEC and OV. The STAD Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .004). Together, the overview and detailed table identify STAD as the clearest survival context for HSBP1 RNA expression.
This table summarizes HSBP1 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 5. The strongest signals are observed in THCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for HSBP1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HSBP1 shows lower tumor expression in THCA and KICH and higher tumor expression in BLCA, KIRP, COAD and LIHC. The THCA box plot shows higher HSBP1 RNA expression in normal versus tumor tissue (log2 FC = −1.197, t-test p < 0.001).
This table shows molecular features associated with HSBP1 in patient tissues and cancer cell lines. In patient samples, HSBP1 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, HSBP1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in BONE and UPPER_AERODIGESTIVE_TRACT.
