Q-omics provides the consensus-scored LST1 profile across patient tissues and cancer cell-line models. LST1 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, LST1 is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, LST1 RNA expression shows 23,253 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight SKCM, KIRC, and LSCC as cancer lineages where LST1 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 LST1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LST1 survival associations across molecular data types. LST1 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (3) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LST1 RNA expression–survival associations across cancer types. High LST1 expression shows unfavorable associations in UVM and LAML, but favorable associations in SKCM, HNSC, CESC and UCEC. The SKCM 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 SKCM as the clearest survival context for LST1 RNA expression.
This table summarizes LST1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 2. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for LST1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LST1 shows lower tumor expression in LUAD and LUSC and higher tumor expression in KIRC, THCA, KIRP and STAD. The KIRC box plot shows higher LST1 RNA expression in tumor versus normal tissue (log2 FC = +2.336, t-test p < 0.001).
This table shows molecular features associated with LST1 in patient tissues and cancer cell lines. In patient samples, LST1 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, LST1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and BLOOD_Leukemia.
