Q-omics provides the consensus-scored LSM12 profile across patient tissues and cancer cell-line models. LSM12 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, LSM12 is differentially expressed in 14, with the highest sampling consensus in LUAD. Additionally, LSM12 protein abundance shows 22,809 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRP, LUAD, and LSCC as cancer lineages where LSM12 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 LSM12 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LSM12 survival associations across molecular data types. LSM12 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (1) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LSM12 RNA expression–survival associations across cancer types. High LSM12 expression shows unfavorable associations in KIRP, HNSC, UVM, KICH and LIHC, but favorable associations in BRCA. The KIRP 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 KIRP as the clearest survival context for LSM12 RNA expression.
This table summarizes LSM12 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 7. The strongest signals are observed in LUAD for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for LSM12. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LSM12 shows higher tumor expression in LUAD, HNSC, BLCA, LUSC, LIHC and STAD. The LUAD box plot shows higher LSM12 RNA expression in tumor versus normal tissue (log2 FC = +1.048, t-test p < 0.001).
This table shows molecular features associated with LSM12 in patient tissues and cancer cell lines. In patient samples, LSM12 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, LSM12 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 BREAST and UPPER_AERODIGESTIVE_TRACT.
