Q-omics provides the consensus-scored CHRAC1 profile across patient tissues and cancer cell-line models. CHRAC1 expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, CHRAC1 is differentially expressed in 13, with the highest sampling consensus in HNSC. Additionally, CHRAC1 protein abundance shows 25,147 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight UVM, HNSC, and LSCC as cancer lineages where CHRAC1 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 CHRAC1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CHRAC1 survival associations across molecular data types. CHRAC1 RNA expression shows survival associations in the most cancer types (20), followed by mutation status (2) 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 CHRAC1 RNA expression–survival associations across cancer types. High CHRAC1 expression shows unfavorable associations in UVM, KIRP, KICH, LIHC, LGG and LUAD. The UVM 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 UVM as the clearest survival context for CHRAC1 RNA expression.
This table summarizes CHRAC1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 7. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CHRAC1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CHRAC1 shows lower tumor expression in THCA and higher tumor expression in HNSC, KIRC, LIHC, LUSC and STAD. The HNSC box plot shows higher CHRAC1 RNA expression in tumor versus normal tissue (log2 FC = +1.306, t-test p < 0.001).
This table shows molecular features associated with CHRAC1 in patient tissues and cancer cell lines. In patient samples, CHRAC1 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, CHRAC1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and BLOOD_Lymphoma.
