Q-omics provides the consensus-scored ANKRD1 profile across patient tissues and cancer cell-line models. ANKRD1 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, ANKRD1 is differentially expressed in 10, with the highest sampling consensus in LUSC. Additionally, ANKRD1 RNA expression shows 17,664 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight HNSC, LUSC, and LSCC as cancer lineages where ANKRD1 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 ANKRD1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ANKRD1 survival associations across molecular data types. ANKRD1 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (7) 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 ANKRD1 RNA expression–survival associations across cancer types. High ANKRD1 expression shows unfavorable associations in HNSC, LUSC, KIRC, KIRP, BLCA and CESC. The HNSC 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 HNSC as the clearest survival context for ANKRD1 RNA expression.
This table summarizes ANKRD1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 1. The strongest signals are observed in LUSC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for ANKRD1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ANKRD1 shows lower tumor expression in LUSC, LUAD and KICH and higher tumor expression in STAD, UCEC and COAD. The LUSC box plot shows higher ANKRD1 RNA expression in normal versus tumor tissue (log2 FC = −6.402, t-test p < 0.001).
This table shows molecular features associated with ANKRD1 in patient tissues and cancer cell lines. In patient samples, ANKRD1 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, ANKRD1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in LIVER and BONE.
