Q-omics provides the consensus-scored SPRTN profile across patient tissues and cancer cell-line models. SPRTN expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, SPRTN is differentially expressed in 13, with the highest sampling consensus in BLCA. Additionally, SPRTN RNA expression shows 21,087 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight ACC, and BLCA as cancer lineages where SPRTN 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 SPRTN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SPRTN survival associations across molecular data types. SPRTN RNA expression shows survival associations in the most cancer types (22), followed by mutation status (4) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SPRTN RNA expression–survival associations across cancer types. High SPRTN expression shows unfavorable associations in ACC, UVM, KICH and READ, but favorable associations in KIRC and LUSC. The ACC 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 ACC as the clearest survival context for SPRTN RNA expression.
This table summarizes SPRTN 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 2. The strongest signals are observed in BLCA for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for SPRTN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SPRTN shows lower tumor expression in THCA and KICH and higher tumor expression in BLCA, HNSC, LIHC and STAD. The BLCA box plot shows higher SPRTN RNA expression in tumor versus normal tissue (log2 FC = +0.524, t-test p < 0.001).
This table shows molecular features associated with SPRTN in patient tissues and cancer cell lines. In patient samples, SPRTN 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, SPRTN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in BONE and BLOOD_Leukemia.
