Q-omics provides the consensus-scored MTHFD2 profile across patient tissues and cancer cell-line models. MTHFD2 expression is associated with patient survival in 29 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, MTHFD2 is differentially expressed in 17, with the highest sampling consensus in HNSC. Additionally, MTHFD2 protein abundance shows 28,646 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRP, HNSC, and LUAD as cancer lineages where MTHFD2 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 MTHFD2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MTHFD2 survival associations across molecular data types. MTHFD2 RNA expression shows survival associations in the most cancer types (29), followed by mutation status (5) 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 MTHFD2 RNA expression–survival associations across cancer types. High MTHFD2 expression shows unfavorable associations in KIRP, KIRC, MESO, KICH, ACC and UCEC. The KIRP 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 KIRP as the clearest survival context for MTHFD2 RNA expression.
This table summarizes MTHFD2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 17, while mass-spec protein shows differences in 7. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for MTHFD2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MTHFD2 shows higher tumor expression in HNSC, LUAD, COAD, KIRC, STAD and BLCA. The HNSC box plot shows higher MTHFD2 RNA expression in tumor versus normal tissue (log2 FC = +1.839, t-test p < 0.001).
This table shows molecular features associated with MTHFD2 in patient tissues and cancer cell lines. In patient samples, MTHFD2 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, MTHFD2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BLOOD_Lymphoma.
