Q-omics provides the consensus-scored SPEM2 profile across patient tissues and cancer cell-line models. SPEM2 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, SPEM2 is differentially expressed in 6, with the highest sampling consensus in KIRC. Additionally, SPEM2 RNA expression shows 8,007 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight MESO, KIRC, and TGCT as cancer lineages where SPEM2 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 SPEM2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SPEM2 survival associations across molecular data types. SPEM2 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SPEM2 RNA expression–survival associations across cancer types. High SPEM2 expression shows unfavorable associations in MESO, THCA, UVM and PRAD, but favorable associations in PAAD and UCS. 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 SPEM2 RNA expression.
This table summarizes SPEM2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 6. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for SPEM2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SPEM2 shows lower tumor expression in THCA and higher tumor expression in KIRC, KIRP, BRCA, LUSC and LIHC. The KIRC box plot shows higher SPEM2 RNA expression in tumor versus normal tissue (log2 FC = +0.102, t-test p < 0.001).
This table shows molecular features associated with SPEM2 in patient tissues and cancer cell lines. In patient samples, SPEM2 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, SPEM2 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 KIDNEY and LARGE_INTESTINE.
