Q-omics provides the consensus-scored DEFB132 profile across patient tissues and cancer cell-line models. DEFB132 expression is associated with patient survival in 15 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, DEFB132 is differentially expressed in 8, with the highest sampling consensus in KIRC. Additionally, DEFB132 RNA expression shows 6,940 significant pathway-activity associations, with the highest sampling consensus in STAD. Together, these results highlight LUAD, KIRC, and STAD as cancer lineages where DEFB132 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 DEFB132 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DEFB132 survival associations across molecular data types. DEFB132 RNA expression shows survival associations in the most cancer types (15), followed by mutation status (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible DEFB132 RNA expression–survival associations across cancer types. High DEFB132 expression shows unfavorable associations in LUAD, UCS, SCLC and GBM, but favorable associations in BRCA and LIHC. The LUAD 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 LUAD as the clearest survival context for DEFB132 RNA expression.
This table summarizes DEFB132 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for DEFB132. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DEFB132 shows lower tumor expression in KIRC, KIRP, BRCA, KICH and PRAD and higher tumor expression in LIHC. The KIRC box plot shows higher DEFB132 RNA expression in normal versus tumor tissue (log2 FC = −0.521, t-test p < 0.001).
This table shows molecular features associated with DEFB132 in patient tissues and cancer cell lines. In patient samples, DEFB132 shows the broadest associations at the RNA and protein expression levels, with STAD recurring as the lineage with the largest associated feature set. In cancer cell lines, DEFB132 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and LARGE_INTESTINE.
