Q-omics provides the consensus-scored FAM83D profile across patient tissues and cancer cell-line models. FAM83D expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, FAM83D is differentially expressed in 13, with the highest sampling consensus in LUAD. Additionally, FAM83D RNA expression shows 25,615 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRP, LUAD, and LSCC as cancer lineages where FAM83D 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 FAM83D — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FAM83D survival associations across molecular data types. FAM83D RNA expression shows survival associations in the most cancer types (28), followed by mutation status (5) 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 FAM83D RNA expression–survival associations across cancer types. High FAM83D expression shows unfavorable associations in KIRP, ACC, MESO, UVM, KICH and LIHC. The KIRP 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 KIRP as the clearest survival context for FAM83D RNA expression.
This table summarizes FAM83D 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 3. The strongest signals are observed in LUAD for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for FAM83D. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FAM83D shows higher tumor expression in LUAD, LIHC, COAD, LUSC, KIRC and UCEC. The LUAD box plot shows higher FAM83D RNA expression in tumor versus normal tissue (log2 FC = +3.251, t-test p < 0.001).
This table shows molecular features associated with FAM83D in patient tissues and cancer cell lines. In patient samples, FAM83D 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, FAM83D RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in CNS and BLOOD_Lymphoma.
