Q-omics provides the consensus-scored SFTA2 profile across patient tissues and cancer cell-line models. SFTA2 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in COAD. Among the 18 cancer types available for tumor–normal comparison, SFTA2 is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, SFTA2 RNA expression shows 15,055 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight COAD, KIRC, and LSCC as cancer lineages where SFTA2 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 SFTA2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SFTA2 survival associations across molecular data types. SFTA2 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (2) 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 SFTA2 RNA expression–survival associations across cancer types. High SFTA2 expression shows unfavorable associations in COAD, PAAD, LUSC and READ, but favorable associations in ACC and SARC. The COAD 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 COAD as the clearest survival context for SFTA2 RNA expression.
This table summarizes SFTA2 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 KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for SFTA2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SFTA2 shows lower tumor expression in KIRC, HNSC, KICH and LUSC and higher tumor expression in COAD and THCA. The KIRC box plot shows higher SFTA2 RNA expression in normal versus tumor tissue (log2 FC = −2.432, t-test p < 0.001).
This table shows molecular features associated with SFTA2 in patient tissues and cancer cell lines. In patient samples, SFTA2 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, SFTA2 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 LARGE_INTESTINE and BREAST.
