Q-omics provides the consensus-scored LSM11 profile across patient tissues and cancer cell-line models. LSM11 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, LSM11 is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, LSM11 RNA expression shows 20,653 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight KIRC, HNSC, and KIRP as cancer lineages where LSM11 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 LSM11 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LSM11 survival associations across molecular data types. LSM11 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (4) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LSM11 RNA expression–survival associations across cancer types. High LSM11 expression shows unfavorable associations in LIHC, BLCA, MESO, CESC and LUAD, but favorable associations in KIRC. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for LSM11 RNA expression.
This table summarizes LSM11 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 2. The strongest signals are observed in HNSC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for LSM11. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LSM11 shows lower tumor expression in THCA and higher tumor expression in HNSC, LIHC, KIRP, KIRC and LUAD. The HNSC box plot shows higher LSM11 RNA expression in tumor versus normal tissue (log2 FC = +0.637, t-test p < 0.001).
This table shows molecular features associated with LSM11 in patient tissues and cancer cell lines. In patient samples, LSM11 shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, LSM11 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and SOFT_TISSUE.
