Q-omics provides the consensus-scored NECTIN3 profile across patient tissues and cancer cell-line models. NECTIN3 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, NECTIN3 is differentially expressed in 11, with the highest sampling consensus in COAD. Additionally, NECTIN3 RNA expression shows 20,093 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, COAD, and UVM as cancer lineages where NECTIN3 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 NECTIN3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NECTIN3 survival associations across molecular data types. NECTIN3 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (5) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible NECTIN3 RNA expression–survival associations across cancer types. High NECTIN3 expression shows unfavorable associations in ACC, UVM, MESO and CESC, but favorable associations in KIRC and UCS. The KIRC 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 KIRC as the clearest survival context for NECTIN3 RNA expression.
This table summarizes NECTIN3 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 5. The strongest signals are observed in COAD for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for NECTIN3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NECTIN3 shows lower tumor expression in COAD, THCA, LUAD, BRCA, READ and LUSC. The COAD box plot shows higher NECTIN3 RNA expression in normal versus tumor tissue (log2 FC = −1.488, t-test p < 0.001).
This table shows molecular features associated with NECTIN3 in patient tissues and cancer cell lines. In patient samples, NECTIN3 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, NECTIN3 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 SOFT_TISSUE and BLOOD_Leukemia.
