Q-omics provides the consensus-scored TMED2 profile across patient tissues and cancer cell-line models. TMED2 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, TMED2 is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, TMED2 protein abundance shows 26,011 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight HNSC, KIRC, and PDAC as cancer lineages where TMED2 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 TMED2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TMED2 survival associations across molecular data types. TMED2 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (4) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TMED2 RNA expression–survival associations across cancer types. High TMED2 expression shows unfavorable associations in HNSC, MESO, KIRP, UVM, CESC and LIHC. The HNSC 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 HNSC as the clearest survival context for TMED2 RNA expression.
This table summarizes TMED2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TMED2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TMED2 shows lower tumor expression in THCA and higher tumor expression in KIRC, BLCA, HNSC, KIRP and LUAD. The KIRC box plot shows higher TMED2 RNA expression in tumor versus normal tissue (log2 FC = +0.698, t-test p < 0.001).
This table shows molecular features associated with TMED2 in patient tissues and cancer cell lines. In patient samples, TMED2 shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, TMED2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and UPPER_AERODIGESTIVE_TRACT.
