Q-omics provides the consensus-scored SHMT2 profile across patient tissues and cancer cell-line models. SHMT2 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, SHMT2 is differentially expressed in 16, with the highest sampling consensus in KIRC. Additionally, SHMT2 protein abundance shows 24,485 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight ACC, KIRC, and LUAD as cancer lineages where SHMT2 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 SHMT2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SHMT2 survival associations across molecular data types. SHMT2 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (3) 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 SHMT2 RNA expression–survival associations across cancer types. High SHMT2 expression shows unfavorable associations in ACC, KICH, MESO, LUAD, UVM and BRCA. The ACC 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 ACC as the clearest survival context for SHMT2 RNA expression.
This table summarizes SHMT2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for SHMT2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SHMT2 shows higher tumor expression in KIRC, COAD, BLCA, KIRP, HNSC and THCA. The KIRC box plot shows higher SHMT2 RNA expression in tumor versus normal tissue (log2 FC = +2.357, t-test p < 0.001).
This table shows molecular features associated with SHMT2 in patient tissues and cancer cell lines. In patient samples, SHMT2 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, SHMT2 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 BREAST and UPPER_AERODIGESTIVE_TRACT.
