Q-omics provides the consensus-scored EFCAB11 profile across patient tissues and cancer cell-line models. EFCAB11 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, EFCAB11 is differentially expressed in 15, with the highest sampling consensus in THCA. Additionally, EFCAB11 RNA expression shows 20,241 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, THCA, and ACC as cancer lineages where EFCAB11 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 EFCAB11 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes EFCAB11 survival associations across molecular data types. EFCAB11 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible EFCAB11 RNA expression–survival associations across cancer types. High EFCAB11 expression shows unfavorable associations in HNSC and ACC, but favorable associations in KIRC, BRCA, READ and UCEC. 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 EFCAB11 RNA expression.
This table summarizes EFCAB11 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 1. The strongest signals are observed in THCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for EFCAB11. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. EFCAB11 shows lower tumor expression in THCA, KICH and KIRC and higher tumor expression in BLCA, COAD and LIHC. The THCA box plot shows higher EFCAB11 RNA expression in normal versus tumor tissue (log2 FC = −0.695, t-test p < 0.001).
This table shows molecular features associated with EFCAB11 in patient tissues and cancer cell lines. In patient samples, EFCAB11 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, EFCAB11 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and STOMACH.
