Q-omics provides the consensus-scored TGM3 profile across patient tissues and cancer cell-line models. TGM3 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, TGM3 is differentially expressed in 13, with the highest sampling consensus in HNSC. Additionally, TGM3 RNA expression shows 10,421 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight KIRC, HNSC, and KIRP as cancer lineages where TGM3 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 TGM3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TGM3 survival associations across molecular data types. TGM3 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (8) 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 TGM3 RNA expression–survival associations across cancer types. High TGM3 expression shows unfavorable associations in KIRC, KICH, ACC and SKCM, but favorable associations in UVM and LUSC. The KIRC 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 KIRC as the clearest survival context for TGM3 RNA expression.
This table summarizes TGM3 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 1. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for TGM3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TGM3 shows lower tumor expression in HNSC and KICH and higher tumor expression in LIHC, KIRC, THCA and BRCA. The HNSC box plot shows higher TGM3 RNA expression in normal versus tumor tissue (log2 FC = −4.918, t-test p < 0.001).
This table shows molecular features associated with TGM3 in patient tissues and cancer cell lines. In patient samples, TGM3 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, TGM3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in BREAST and LARGE_INTESTINE.
