Q-omics provides the consensus-scored ANKRD60 profile across patient tissues and cancer cell-line models. ANKRD60 expression is associated with patient survival in 13 of 34 cancer types, with the highest sampling consensus in KICH. Among the 18 cancer types available for tumor–normal comparison, ANKRD60 is differentially expressed in 2, with the highest sampling consensus in ESCA. Additionally, ANKRD60 protein abundance shows 7,830 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KICH, ESCA, and GBM as cancer lineages where ANKRD60 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 ANKRD60 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ANKRD60 survival associations across molecular data types. ANKRD60 RNA expression shows survival associations in the most cancer types (13), followed by mutation status (1) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ANKRD60 RNA expression–survival associations across cancer types. High ANKRD60 expression shows unfavorable associations in KICH, KIRC, LUSC, STAD, LIHC and MESO. 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 ANKRD60 RNA expression.
This table summarizes ANKRD60 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 2, while mass-spec protein shows differences in 2. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for ANKRD60. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ANKRD60 shows higher tumor expression in ESCA and KIRC. The ESCA box plot shows higher ANKRD60 RNA expression in tumor versus normal tissue (log2 FC = +0.055, t-test p = .008).
This table shows molecular features associated with ANKRD60 in patient tissues and cancer cell lines. In patient samples, ANKRD60 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, ANKRD60 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and LARGE_INTESTINE.
