Q-omics provides the consensus-scored PTPRN2-AS1 profile across patient tissues and cancer cell-line models. PTPRN2-AS1 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, PTPRN2-AS1 is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, PTPRN2-AS1 RNA expression shows 15,509 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight HNSC, KIRC, and UVM as cancer lineages where PTPRN2-AS1 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 PTPRN2-AS1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PTPRN2-AS1 survival associations across molecular data types. PTPRN2-AS1 RNA expression shows survival associations in the most cancer types (21). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PTPRN2-AS1 RNA expression–survival associations across cancer types. High PTPRN2-AS1 expression shows unfavorable associations in LGG and UVM, but favorable associations in HNSC, SKCM, CESC and STAD. The HNSC 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 HNSC as the clearest survival context for PTPRN2-AS1 RNA expression.
This table summarizes PTPRN2-AS1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for PTPRN2-AS1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PTPRN2-AS1 shows lower tumor expression in LUAD and LUSC and higher tumor expression in KIRC, KIRP, THCA and STAD. The KIRC box plot shows higher PTPRN2-AS1 RNA expression in tumor versus normal tissue (log2 FC = +1.208, t-test p < 0.001).
This table shows molecular features associated with PTPRN2-AS1 in patient tissues and cancer cell lines. In patient samples, PTPRN2-AS1 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set.
