Q-omics provides the consensus-scored HSPB11 profile across patient tissues and cancer cell-line models. HSPB11 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, HSPB11 is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, HSPB11 protein abundance shows 31,176 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight ACC, KIRC, and PDAC as cancer lineages where HSPB11 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 HSPB11 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HSPB11 survival associations across molecular data types. HSPB11 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (2) and mass-spec protein abundance (10). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible HSPB11 RNA expression–survival associations across cancer types. High HSPB11 expression shows unfavorable associations in ACC, KICH, LIHC, KIRC, LGG and 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 HSPB11 RNA expression.
This table summarizes HSPB11 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 11. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for HSPB11. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HSPB11 shows lower tumor expression in THCA and KICH and higher tumor expression in KIRC, HNSC, LIHC and BLCA. The KIRC box plot shows higher HSPB11 RNA expression in tumor versus normal tissue (log2 FC = +0.707, t-test p < 0.001).
This table shows molecular features associated with HSPB11 in patient tissues and cancer cell lines. In patient samples, HSPB11 shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, HSPB11 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BLOOD_Leukemia.
