Q-omics provides the consensus-scored MID2 profile across patient tissues and cancer cell-line models. MID2 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in COAD. Among the 18 cancer types available for tumor–normal comparison, MID2 is differentially expressed in 11, with the highest sampling consensus in KICH. Additionally, MID2 RNA expression shows 19,163 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight COAD, KICH, and THYM as cancer lineages where MID2 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 MID2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MID2 survival associations across molecular data types. MID2 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (4) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MID2 RNA expression–survival associations across cancer types. High MID2 expression shows unfavorable associations in COAD, STAD and MESO, but favorable associations in KIRC, ACC and LUAD. The COAD 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 COAD as the clearest survival context for MID2 RNA expression.
This table summarizes MID2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 4. The strongest signals are observed in KICH for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for MID2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MID2 shows lower tumor expression in KICH, THCA, UCEC, BLCA and STAD and higher tumor expression in LIHC. The KICH box plot shows higher MID2 RNA expression in normal versus tumor tissue (log2 FC = −0.871, t-test p < 0.001).
This table shows molecular features associated with MID2 in patient tissues and cancer cell lines. In patient samples, MID2 shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, MID2 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 LUNG_SCLC and UPPER_AERODIGESTIVE_TRACT.
