Q-omics provides the consensus-scored CPT1B profile across patient tissues and cancer cell-line models. CPT1B expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in BLCA. Among the 18 cancer types available for tumor–normal comparison, CPT1B is differentially expressed in 14, with the highest sampling consensus in BLCA. Additionally, CPT1B RNA expression shows 16,146 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight BLCA, and UVM as cancer lineages where CPT1B 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 CPT1B — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CPT1B survival associations across molecular data types. CPT1B RNA expression shows survival associations in the most cancer types (27), followed by mutation status (3) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CPT1B RNA expression–survival associations across cancer types. High CPT1B expression shows unfavorable associations in KIRC, COAD, ACC and MESO, but favorable associations in BLCA and HNSC. The BLCA 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 BLCA as the clearest survival context for CPT1B RNA expression.
This table summarizes CPT1B 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 BLCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CPT1B. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CPT1B shows higher tumor expression in BLCA, LIHC, LUSC, STAD, THCA and UCEC. The BLCA box plot shows higher CPT1B RNA expression in tumor versus normal tissue (log2 FC = +1.201, t-test p < 0.001).
This table shows molecular features associated with CPT1B in patient tissues and cancer cell lines. In patient samples, CPT1B shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, CPT1B RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in LIVER and BLOOD_Leukemia.
