Q-omics provides the consensus-scored CFTR profile across patient tissues and cancer cell-line models. CFTR expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, CFTR is differentially expressed in 12, with the highest sampling consensus in HNSC. Additionally, CFTR protein abundance shows 20,691 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight LUAD, HNSC, and LSCC as cancer lineages where CFTR 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 CFTR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CFTR survival associations across molecular data types. CFTR RNA expression shows survival associations in the most cancer types (23), followed by mutation status (8) 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 CFTR RNA expression–survival associations across cancer types. High CFTR expression shows favorable associations in LUAD, READ, LGG, LAML, UCS and BRCA. The LUAD 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 LUAD as the clearest survival context for CFTR RNA expression.
This table summarizes CFTR tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 5. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for CFTR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CFTR shows lower tumor expression in HNSC, LUAD, KIRC, LUSC and BRCA and higher tumor expression in KICH. The HNSC box plot shows higher CFTR RNA expression in normal versus tumor tissue (log2 FC = −1.563, t-test p < 0.001).
This table shows molecular features associated with CFTR in patient tissues and cancer cell lines. In patient samples, CFTR 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, CFTR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and LARGE_INTESTINE.
