SERTA domain containing 1Genealiases: SEI1 · TRIP-Br1 · TRIPBR1
Q-omics provides the consensus-scored SERTAD1 profile across patient tissues and cancer cell-line models. SERTAD1 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, SERTAD1 is differentially expressed in 11, with the highest sampling consensus in KICH. Additionally, SERTAD1 RNA expression shows 17,850 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight ACC, and KICH as cancer lineages where SERTAD1 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 SERTAD1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SERTAD1 survival associations across molecular data types. SERTAD1 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SERTAD1 RNA expression–survival associations across cancer types. High SERTAD1 expression shows unfavorable associations in ACC, LUSC, LGG, KIRP, READ and LAML. The ACC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify ACC as the clearest survival context for SERTAD1 RNA expression.
This table summarizes SERTAD1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11. The strongest signals are observed in KICH for RNA.
This table ranks reproducible tumor–normal expression differences for SERTAD1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SERTAD1 shows lower tumor expression in KICH, LUSC, LUAD, BLCA, KIRP and UCEC. The KICH box plot shows higher SERTAD1 RNA expression in normal versus tumor tissue (log2 FC = −2.858, t-test p < 0.001).
This table shows molecular features associated with SERTAD1 in patient tissues and cancer cell lines. In patient samples, SERTAD1 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, SERTAD1 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 LARGE_INTESTINE and SOFT_TISSUE.
