Q-omics provides the consensus-scored NLGN3 profile across patient tissues and cancer cell-line models. NLGN3 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, NLGN3 is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, NLGN3 RNA expression shows 20,591 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRP, KIRC, and PDAC as cancer lineages where NLGN3 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 NLGN3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NLGN3 survival associations across molecular data types. NLGN3 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (3) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible NLGN3 RNA expression–survival associations across cancer types. High NLGN3 expression shows unfavorable associations in KIRP, UVM, THCA, KIRC, COAD and SCLC. The KIRP 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 KIRP as the clearest survival context for NLGN3 RNA expression.
This table summarizes NLGN3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for NLGN3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NLGN3 shows lower tumor expression in KIRC, KICH, THCA, COAD, UCEC and BRCA. The KIRC box plot shows higher NLGN3 RNA expression in normal versus tumor tissue (log2 FC = −0.845, t-test p < 0.001).
This table shows molecular features associated with NLGN3 in patient tissues and cancer cell lines. In patient samples, NLGN3 shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, NLGN3 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 UPPER_AERODIGESTIVE_TRACT and BLOOD_Leukemia.
