Q-omics provides the consensus-scored MRPL23 profile across patient tissues and cancer cell-line models. MRPL23 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, MRPL23 is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, MRPL23 protein abundance shows 19,636 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight ACC, KIRC, and LSCC as cancer lineages where MRPL23 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 MRPL23 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MRPL23 survival associations across molecular data types. MRPL23 RNA expression shows survival associations in the most cancer types (23), followed by mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MRPL23 RNA expression–survival associations across cancer types. High MRPL23 expression shows unfavorable associations in ACC, KICH, LGG and KIRC, but favorable associations in UCEC and SCLC. 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 MRPL23 RNA expression.
This table summarizes MRPL23 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, 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 MRPL23. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MRPL23 shows higher tumor expression in KIRC, COAD, LIHC, KIRP, STAD and BRCA. The KIRC box plot shows higher MRPL23 RNA expression in tumor versus normal tissue (log2 FC = +0.881, t-test p < 0.001).
This table shows molecular features associated with MRPL23 in patient tissues and cancer cell lines. In patient samples, MRPL23 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, MRPL23 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 BONE and UPPER_AERODIGESTIVE_TRACT.
