Q-omics provides the consensus-scored MPPED2 profile across patient tissues and cancer cell-line models. MPPED2 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, MPPED2 is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, MPPED2 RNA expression shows 19,797 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, and GBM as cancer lineages where MPPED2 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 MPPED2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MPPED2 survival associations across molecular data types. MPPED2 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (6) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MPPED2 RNA expression–survival associations across cancer types. High MPPED2 expression shows favorable associations in KIRC, PAAD, HNSC, UVM, LUAD and ACC. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for MPPED2 RNA expression.
This table summarizes MPPED2 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 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for MPPED2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MPPED2 shows lower tumor expression in KIRC, THCA, KIRP, COAD and BRCA and higher tumor expression in LIHC. The KIRC box plot shows higher MPPED2 RNA expression in normal versus tumor tissue (log2 FC = −2.439, t-test p < 0.001).
This table shows molecular features associated with MPPED2 in patient tissues and cancer cell lines. In patient samples, MPPED2 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, MPPED2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in KIDNEY and BREAST.
