Q-omics provides the consensus-scored CARS1 profile across patient tissues and cancer cell-line models. CARS1 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, CARS1 is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, CARS1 protein abundance shows 25,433 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight MESO, KIRC, and LUAD as cancer lineages where CARS1 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 CARS1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CARS1 survival associations across molecular data types. CARS1 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (8) and mass-spec protein abundance (13). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CARS1 RNA expression–survival associations across cancer types. High CARS1 expression shows unfavorable associations in MESO, KICH, KIRP, ACC, KIRC and LIHC. 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 CARS1 RNA expression.
This table summarizes CARS1 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 10. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CARS1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CARS1 shows higher tumor expression in KIRC, HNSC, COAD, LUAD, STAD and KIRP. The KIRC box plot shows higher CARS1 RNA expression in tumor versus normal tissue (log2 FC = +1.009, t-test p < 0.001).
This table shows molecular features associated with CARS1 in patient tissues and cancer cell lines. In patient samples, CARS1 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, CARS1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in CNS and BLOOD_Lymphoma.
