Q-omics provides the consensus-scored TGM2 profile across patient tissues and cancer cell-line models. TGM2 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in LUSC. Among the 18 cancer types available for tumor–normal comparison, TGM2 is differentially expressed in 14, with the highest sampling consensus in COAD. Additionally, TGM2 protein abundance shows 28,346 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight LUSC, COAD, and LSCC as cancer lineages where TGM2 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 TGM2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TGM2 survival associations across molecular data types. TGM2 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (6) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TGM2 RNA expression–survival associations across cancer types. High TGM2 expression shows unfavorable associations in LUSC, PAAD and KIRC, but favorable associations in UCS, SKCM and THYM. The LUSC 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 LUSC as the clearest survival context for TGM2 RNA expression.
This table summarizes TGM2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 7. The strongest signals are observed in COAD for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TGM2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TGM2 shows lower tumor expression in LUAD and LUSC and higher tumor expression in COAD, KIRC, HNSC and THCA. The COAD box plot shows higher TGM2 RNA expression in tumor versus normal tissue (log2 FC = +0.940, t-test p < 0.001).
This table shows molecular features associated with TGM2 in patient tissues and cancer cell lines. In patient samples, TGM2 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, TGM2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in KIDNEY and BLOOD_Leukemia.
