Q-omics provides the consensus-scored TMPRSS5 profile across patient tissues and cancer cell-line models. TMPRSS5 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in THCA. Among the 18 cancer types available for tumor–normal comparison, TMPRSS5 is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, TMPRSS5 RNA expression shows 16,627 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight THCA, KIRC, and ACC as cancer lineages where TMPRSS5 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 TMPRSS5 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TMPRSS5 survival associations across molecular data types. TMPRSS5 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TMPRSS5 RNA expression–survival associations across cancer types. High TMPRSS5 expression shows unfavorable associations in THCA, KIRC, ACC and KIRP, but favorable associations in SCLC and BLCA. The THCA Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .002). Together, the overview and detailed table identify THCA as the clearest survival context for TMPRSS5 RNA expression.
This table summarizes TMPRSS5 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for TMPRSS5. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TMPRSS5 shows lower tumor expression in BRCA and higher tumor expression in KIRC, COAD, THCA, LIHC and STAD. The KIRC box plot shows higher TMPRSS5 RNA expression in tumor versus normal tissue (log2 FC = +0.167, t-test p < 0.001).
This table shows molecular features associated with TMPRSS5 in patient tissues and cancer cell lines. In patient samples, TMPRSS5 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, TMPRSS5 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and BLOOD_Leukemia.