Q-omics provides the consensus-scored TMPRSS3 profile across patient tissues and cancer cell-line models. TMPRSS3 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, TMPRSS3 is differentially expressed in 14, with the highest sampling consensus in COAD. Additionally, TMPRSS3 RNA expression shows 15,110 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight SKCM, COAD, and KIRP as cancer lineages where TMPRSS3 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 TMPRSS3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TMPRSS3 survival associations across molecular data types. TMPRSS3 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TMPRSS3 RNA expression–survival associations across cancer types. High TMPRSS3 expression shows unfavorable associations in KIRP, LGG, LUAD and GBM, but favorable associations in SKCM and HNSC. 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 TMPRSS3 RNA expression.
This table summarizes TMPRSS3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14. The strongest signals are observed in COAD for RNA.
This table ranks reproducible tumor–normal expression differences for TMPRSS3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TMPRSS3 shows lower tumor expression in KIRC, THCA, KIRP, LUSC and KICH and higher tumor expression in COAD. The COAD box plot shows higher TMPRSS3 RNA expression in tumor versus normal tissue (log2 FC = +2.101, t-test p < 0.001).
This table shows molecular features associated with TMPRSS3 in patient tissues and cancer cell lines. In patient samples, TMPRSS3 shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, TMPRSS3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LUNG_NSCLC_LUAD.
