Q-omics provides the consensus-scored CLDN18 profile across patient tissues and cancer cell-line models. CLDN18 expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, CLDN18 is differentially expressed in 11, with the highest sampling consensus in LUAD. Additionally, CLDN18 RNA expression shows 18,173 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight UVM, and LUAD as cancer lineages where CLDN18 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 CLDN18 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CLDN18 survival associations across molecular data types. CLDN18 RNA expression shows survival associations in the most cancer types (28), followed by mutation status (7) 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 CLDN18 RNA expression–survival associations across cancer types. High CLDN18 expression shows unfavorable associations in UVM, LIHC, LUSC, LGG, MESO and KICH. 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 CLDN18 RNA expression.
This table summarizes CLDN18 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 3. The strongest signals are observed in LUAD for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for CLDN18. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CLDN18 shows lower tumor expression in LUAD, LUSC, KICH, BRCA and UCEC and higher tumor expression in HNSC. The LUAD box plot shows higher CLDN18 RNA expression in normal versus tumor tissue (log2 FC = −7.576, t-test p < 0.001).
This table shows molecular features associated with CLDN18 in patient tissues and cancer cell lines. In patient samples, CLDN18 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, CLDN18 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in STOMACH and SOFT_TISSUE.
