Q-omics provides the consensus-scored MICAL2 profile across patient tissues and cancer cell-line models. MICAL2 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, MICAL2 is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, MICAL2 protein abundance shows 24,887 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight MESO, HNSC, and LSCC as cancer lineages where MICAL2 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 MICAL2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MICAL2 survival associations across molecular data types. MICAL2 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (6) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MICAL2 RNA expression–survival associations across cancer types. High MICAL2 expression shows unfavorable associations in MESO, LUSC, ACC, KIRP, CESC and UVM. The MESO 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 MESO as the clearest survival context for MICAL2 RNA expression.
This table summarizes MICAL2 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 9. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for MICAL2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MICAL2 shows lower tumor expression in COAD and LUSC and higher tumor expression in HNSC, KIRC, BRCA and LIHC. The HNSC box plot shows higher MICAL2 RNA expression in tumor versus normal tissue (log2 FC = +2.166, t-test p < 0.001).
This table shows molecular features associated with MICAL2 in patient tissues and cancer cell lines. In patient samples, MICAL2 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, MICAL2 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 URINARY_TRACT and BONE.
