Q-omics provides the consensus-scored LTBP2 profile across patient tissues and cancer cell-line models. LTBP2 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, LTBP2 is differentially expressed in 11, with the highest sampling consensus in HNSC. Additionally, LTBP2 protein abundance shows 27,041 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRP, HNSC, and LUAD as cancer lineages where LTBP2 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 LTBP2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LTBP2 survival associations across molecular data types. LTBP2 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (7) 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 LTBP2 RNA expression–survival associations across cancer types. High LTBP2 expression shows unfavorable associations in KIRP, BLCA, ACC, MESO, LUSC and LGG. The KIRP Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify KIRP as the clearest survival context for LTBP2 RNA expression.
This table summarizes LTBP2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 6. The strongest signals are observed in HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for LTBP2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LTBP2 shows lower tumor expression in UCEC and LUSC and higher tumor expression in HNSC, COAD, LIHC and STAD. The HNSC box plot shows higher LTBP2 RNA expression in tumor versus normal tissue (log2 FC = +1.435, t-test p < 0.001).
This table shows molecular features associated with LTBP2 in patient tissues and cancer cell lines. In patient samples, LTBP2 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, LTBP2 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 OESOPHAGUS and LARGE_INTESTINE.
