Q-omics provides the consensus-scored MCM3 profile across patient tissues and cancer cell-line models. MCM3 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, MCM3 is differentially expressed in 15, with the highest sampling consensus in COAD. Additionally, MCM3 protein abundance shows 32,007 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight MESO, COAD, and LSCC as cancer lineages where MCM3 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 MCM3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MCM3 survival associations across molecular data types. MCM3 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (8) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MCM3 RNA expression–survival associations across cancer types. High MCM3 expression shows unfavorable associations in MESO, ACC, LIHC, KICH and LGG, but favorable associations in OV. The MESO Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify MESO as the clearest survival context for MCM3 RNA expression.
This table summarizes MCM3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, 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 MCM3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MCM3 shows higher tumor expression in COAD, HNSC, BLCA, KIRP, LIHC and STAD. The COAD box plot shows higher MCM3 RNA expression in tumor versus normal tissue (log2 FC = +1.612, t-test p < 0.001).
This table shows molecular features associated with MCM3 in patient tissues and cancer cell lines. In patient samples, MCM3 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, MCM3 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 LIVER and BLOOD_Leukemia.
