Q-omics provides the consensus-scored LTBR profile across patient tissues and cancer cell-line models. LTBR expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, LTBR is differentially expressed in 15, with the highest sampling consensus in HNSC. Additionally, LTBR protein abundance shows 21,311 significant protein co-abundance associations, with the highest sampling consensus in CCRCC. Together, these results highlight UVM, HNSC, and CCRCC as cancer lineages where LTBR 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 LTBR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LTBR survival associations across molecular data types. LTBR RNA expression shows survival associations in the most cancer types (26), followed by mutation status (2) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LTBR RNA expression–survival associations across cancer types. High LTBR expression shows unfavorable associations in UVM, ACC, KIRC, LUAD, LGG and HNSC. The UVM 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 UVM as the clearest survival context for LTBR RNA expression.
This table summarizes LTBR 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 8. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for LTBR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LTBR shows higher tumor expression in HNSC, KIRC, KIRP, BLCA, LIHC and LUSC. The HNSC box plot shows higher LTBR RNA expression in tumor versus normal tissue (log2 FC = +1.060, t-test p < 0.001).
This table shows molecular features associated with LTBR in patient tissues and cancer cell lines. In patient samples, LTBR shows the broadest associations at the RNA and protein expression levels, with CCRCC recurring as the lineage with the largest associated feature set. In cancer cell lines, LTBR 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 BREAST and BLOOD_Leukemia.
