Q-omics provides the consensus-scored FHAD1 profile across patient tissues and cancer cell-line models. FHAD1 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, FHAD1 is differentially expressed in 12, with the highest sampling consensus in KICH. Additionally, FHAD1 RNA expression shows 17,742 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, KICH, and UVM as cancer lineages where FHAD1 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 FHAD1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FHAD1 survival associations across molecular data types. FHAD1 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible FHAD1 RNA expression–survival associations across cancer types. High FHAD1 expression shows unfavorable associations in KIRC, LGG, COAD and MESO, but favorable associations in SKCM and CESC. The KIRC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .004). Together, the overview and detailed table identify KIRC as the clearest survival context for FHAD1 RNA expression.
This table summarizes FHAD1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 2. The strongest signals are observed in KICH for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for FHAD1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FHAD1 shows lower tumor expression in KICH and LUSC and higher tumor expression in HNSC, COAD, LIHC and BRCA. The KICH box plot shows higher FHAD1 RNA expression in normal versus tumor tissue (log2 FC = −0.432, t-test p < 0.001).
This table shows molecular features associated with FHAD1 in patient tissues and cancer cell lines. In patient samples, FHAD1 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, FHAD1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and LUNG_NSCLC_LUAD.
