Q-omics provides the consensus-scored HDAC3 profile across patient tissues and cancer cell-line models. HDAC3 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KICH. Among the 18 cancer types available for tumor–normal comparison, HDAC3 is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, HDAC3 protein abundance shows 19,100 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KICH, KIRC, and GBM as cancer lineages where HDAC3 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 HDAC3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HDAC3 survival associations across molecular data types. HDAC3 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (5) 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 HDAC3 RNA expression–survival associations across cancer types. High HDAC3 expression shows unfavorable associations in KICH, LGG, MESO, KIRP and LUSC, but favorable associations in READ. The KICH 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 KICH as the clearest survival context for HDAC3 RNA expression.
This table summarizes HDAC3 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 5. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for HDAC3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HDAC3 shows lower tumor expression in THCA and higher tumor expression in KIRC, COAD, HNSC, LIHC and LUAD. The KIRC box plot shows higher HDAC3 RNA expression in tumor versus normal tissue (log2 FC = +0.742, t-test p < 0.001).
This table shows molecular features associated with HDAC3 in patient tissues and cancer cell lines. In patient samples, HDAC3 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, HDAC3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in OVARY and LARGE_INTESTINE.
