Q-omics provides the consensus-scored RSAD2 profile across patient tissues and cancer cell-line models. RSAD2 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, RSAD2 is differentially expressed in 13, with the highest sampling consensus in HNSC. Additionally, RSAD2 RNA expression shows 16,355 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight SKCM, HNSC, and UVM as cancer lineages where RSAD2 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 RSAD2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes RSAD2 survival associations across molecular data types. RSAD2 RNA expression shows survival associations in the most cancer types (25), 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 RSAD2 RNA expression–survival associations across cancer types. High RSAD2 expression shows unfavorable associations in UVM, UCEC and LGG, but favorable associations in SKCM, KIRC and CHOL. The SKCM 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 SKCM as the clearest survival context for RSAD2 RNA expression.
This table summarizes RSAD2 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 4. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for RSAD2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. RSAD2 shows lower tumor expression in KICH, LUSC and UCEC and higher tumor expression in HNSC, BLCA and BRCA. The HNSC box plot shows higher RSAD2 RNA expression in tumor versus normal tissue (log2 FC = +4.000, t-test p < 0.001).
This table shows molecular features associated with RSAD2 in patient tissues and cancer cell lines. In patient samples, RSAD2 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, RSAD2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in CNS and BONE.
