Q-omics provides the consensus-scored ANK2 profile across patient tissues and cancer cell-line models. ANK2 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, ANK2 is differentially expressed in 15, with the highest sampling consensus in COAD. Additionally, ANK2 protein abundance shows 36,247 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight UVM, COAD, and GBM as cancer lineages where ANK2 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 ANK2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ANK2 survival associations across molecular data types. ANK2 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (13) 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 ANK2 RNA expression–survival associations across cancer types. High ANK2 expression shows unfavorable associations in UVM, BLCA, LUSC and THCA, but favorable associations in LUAD and PAAD. The UVM Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .002). Together, the overview and detailed table identify UVM as the clearest survival context for ANK2 RNA expression.
This table summarizes ANK2 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 7. The strongest signals are observed in COAD for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for ANK2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ANK2 shows lower tumor expression in COAD, KICH, THCA, KIRC, BLCA and LUSC. The COAD box plot shows higher ANK2 RNA expression in normal versus tumor tissue (log2 FC = −1.786, t-test p < 0.001).
This table shows molecular features associated with ANK2 in patient tissues and cancer cell lines. In patient samples, ANK2 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, ANK2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and LARGE_INTESTINE.
