Q-omics provides the consensus-scored TMIGD2 profile across patient tissues and cancer cell-line models. TMIGD2 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in BLCA. Among the 18 cancer types available for tumor–normal comparison, TMIGD2 is differentially expressed in 8, with the highest sampling consensus in COAD. Additionally, TMIGD2 RNA expression shows 17,915 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight BLCA, COAD, and GBM as cancer lineages where TMIGD2 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 TMIGD2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TMIGD2 survival associations across molecular data types. TMIGD2 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (6) 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 TMIGD2 RNA expression–survival associations across cancer types. High TMIGD2 expression shows unfavorable associations in KIRP, but favorable associations in BLCA, UCEC, HNSC, MESO and THCA. The BLCA 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 BLCA as the clearest survival context for TMIGD2 RNA expression.
This table summarizes TMIGD2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8. The strongest signals are observed in COAD for RNA.
This table ranks reproducible tumor–normal expression differences for TMIGD2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TMIGD2 shows lower tumor expression in COAD, LUSC and LUAD and higher tumor expression in KIRC, KIRP and KICH. The COAD box plot shows higher TMIGD2 RNA expression in normal versus tumor tissue (log2 FC = −1.101, t-test p < 0.001).
This table shows molecular features associated with TMIGD2 in patient tissues and cancer cell lines. In patient samples, TMIGD2 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, TMIGD2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in KIDNEY and BLOOD_Leukemia.
