Q-omics provides the consensus-scored ASB2 profile across patient tissues and cancer cell-line models. ASB2 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, ASB2 is differentially expressed in 14, with the highest sampling consensus in BLCA. Additionally, ASB2 RNA expression shows 15,731 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight LUAD, BLCA, and LSCC as cancer lineages where ASB2 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 ASB2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ASB2 survival associations across molecular data types. ASB2 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 ASB2 RNA expression–survival associations across cancer types. High ASB2 expression shows unfavorable associations in LAML, LGG and READ, but favorable associations in LUAD, UCEC and OV. The LUAD 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 LUAD as the clearest survival context for ASB2 RNA expression.
This table summarizes ASB2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 2. The strongest signals are observed in BLCA for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for ASB2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ASB2 shows lower tumor expression in BLCA, COAD, UCEC, BRCA and STAD and higher tumor expression in KIRC. The BLCA box plot shows higher ASB2 RNA expression in normal versus tumor tissue (log2 FC = −4.745, t-test p < 0.001).
This table shows molecular features associated with ASB2 in patient tissues and cancer cell lines. In patient samples, ASB2 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, ASB2 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 UPPER_AERODIGESTIVE_TRACT and SKIN.
