Q-omics provides the consensus-scored PRMT7 profile across patient tissues and cancer cell-line models. PRMT7 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, PRMT7 is differentially expressed in 16, with the highest sampling consensus in KIRC. Additionally, PRMT7 protein abundance shows 20,032 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight MESO, KIRC, and LSCC as cancer lineages where PRMT7 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 PRMT7 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRMT7 survival associations across molecular data types. PRMT7 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4) 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 PRMT7 RNA expression–survival associations across cancer types. High PRMT7 expression shows unfavorable associations in LUSC, ACC, SKCM and HNSC, but favorable associations in MESO and UCEC. The MESO Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .007). Together, the overview and detailed table identify MESO as the clearest survival context for PRMT7 RNA expression.
This table summarizes PRMT7 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 CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PRMT7. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRMT7 shows lower tumor expression in KICH and THCA and higher tumor expression in KIRC, COAD, LIHC and HNSC. The KIRC box plot shows higher PRMT7 RNA expression in tumor versus normal tissue (log2 FC = +0.475, t-test p < 0.001).
This table shows molecular features associated with PRMT7 in patient tissues and cancer cell lines. In patient samples, PRMT7 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, PRMT7 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 LIVER and UPPER_AERODIGESTIVE_TRACT.
