Q-omics provides the consensus-scored HDAC2 profile across patient tissues and cancer cell-line models. HDAC2 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in LIHC. Among the 18 cancer types available for tumor–normal comparison, HDAC2 is differentially expressed in 15, with the highest sampling consensus in COAD. Additionally, HDAC2 protein abundance shows 26,037 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight LIHC, COAD, and GBM as cancer lineages where HDAC2 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 HDAC2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HDAC2 survival associations across molecular data types. HDAC2 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (5) 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 HDAC2 RNA expression–survival associations across cancer types. High HDAC2 expression shows unfavorable associations in LIHC, ACC, KIRP, MESO, BRCA and SARC. The LIHC 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 LIHC as the clearest survival context for HDAC2 RNA expression.
This table summarizes HDAC2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 6. The strongest signals are observed in COAD for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for HDAC2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HDAC2 shows higher tumor expression in COAD, HNSC, BLCA, LUSC, STAD and LIHC. The COAD box plot shows higher HDAC2 RNA expression in tumor versus normal tissue (log2 FC = +0.916, t-test p < 0.001).
This table shows molecular features associated with HDAC2 in patient tissues and cancer cell lines. In patient samples, HDAC2 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, HDAC2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and LARGE_INTESTINE.
