Q-omics provides the consensus-scored ANAPC7 profile across patient tissues and cancer cell-line models. ANAPC7 expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, ANAPC7 is differentially expressed in 15, with the highest sampling consensus in COAD. Additionally, ANAPC7 protein abundance shows 23,289 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, COAD, and LSCC as cancer lineages where ANAPC7 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 ANAPC7 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ANAPC7 survival associations across molecular data types. ANAPC7 RNA expression shows survival associations in the most cancer types (28), followed by mutation status (9) 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 ANAPC7 RNA expression–survival associations across cancer types. High ANAPC7 expression shows unfavorable associations in KIRC, ACC, MESO, KICH, LIHC and UVM. The KIRC 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 KIRC as the clearest survival context for ANAPC7 RNA expression.
This table summarizes ANAPC7 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 ANAPC7. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ANAPC7 shows higher tumor expression in COAD, LIHC, KIRP, LUSC, LUAD and STAD. The COAD box plot shows higher ANAPC7 RNA expression in tumor versus normal tissue (log2 FC = +1.334, t-test p < 0.001).
This table shows molecular features associated with ANAPC7 in patient tissues and cancer cell lines. In patient samples, ANAPC7 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, ANAPC7 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUSC, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and BLOOD_Lymphoma.
