Q-omics provides the consensus-scored LSS profile across patient tissues and cancer cell-line models. LSS expression is associated with patient survival in 30 of 34 cancer types, with the highest sampling consensus in CESC. Among the 18 cancer types available for tumor–normal comparison, LSS is differentially expressed in 8, with the highest sampling consensus in THCA. Additionally, LSS RNA expression shows 18,288 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight CESC, THCA, and ACC as cancer lineages where LSS 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 LSS — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LSS survival associations across molecular data types. LSS RNA expression shows survival associations in the most cancer types (30), followed by mutation status (6) 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 LSS RNA expression–survival associations across cancer types. High LSS expression shows unfavorable associations in CESC, BLCA, BRCA, KICH, ACC and OV. The CESC 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 CESC as the clearest survival context for LSS RNA expression.
This table summarizes LSS tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8, while mass-spec protein shows differences in 6. The strongest signals are observed in THCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for LSS. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LSS shows lower tumor expression in THCA, LUAD and KIRC and higher tumor expression in COAD, LIHC and HNSC. The THCA box plot shows higher LSS RNA expression in normal versus tumor tissue (log2 FC = −0.734, t-test p < 0.001).
This table shows molecular features associated with LSS in patient tissues and cancer cell lines. In patient samples, LSS shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, LSS RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and BLOOD_Lymphoma.
