Q-omics provides the consensus-scored MFAP3L profile across patient tissues and cancer cell-line models. MFAP3L expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, MFAP3L is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, MFAP3L RNA expression shows 18,610 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, and UVM as cancer lineages where MFAP3L 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 MFAP3L — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MFAP3L survival associations across molecular data types. MFAP3L RNA expression shows survival associations in the most cancer types (26), followed by mutation status (5) 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 MFAP3L RNA expression–survival associations across cancer types. High MFAP3L expression shows unfavorable associations in THCA, STAD, LUAD and UCS, but favorable associations in KIRC and BLCA. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for MFAP3L RNA expression.
This table summarizes MFAP3L tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, 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 MFAP3L. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MFAP3L shows lower tumor expression in KIRC, THCA, KICH, LUAD, LIHC and KIRP. The KIRC box plot shows higher MFAP3L RNA expression in normal versus tumor tissue (log2 FC = −1.675, t-test p < 0.001).
This table shows molecular features associated with MFAP3L in patient tissues and cancer cell lines. In patient samples, MFAP3L 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, MFAP3L RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in CNS and LARGE_INTESTINE.
