Q-omics provides the consensus-scored NSG2 profile across patient tissues and cancer cell-line models. NSG2 expression is associated with patient survival in 19 of 34 cancer types, with the highest sampling consensus in THCA. Among the 18 cancer types available for tumor–normal comparison, NSG2 is differentially expressed in 11, with the highest sampling consensus in COAD. Additionally, NSG2 RNA expression shows 13,713 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight THCA, COAD, and GBM as cancer lineages where NSG2 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 NSG2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NSG2 survival associations across molecular data types. NSG2 RNA expression shows survival associations in the most cancer types (19), followed by mutation status (1) 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 NSG2 RNA expression–survival associations across cancer types. High NSG2 expression shows unfavorable associations in THCA, UCEC, MESO, LIHC and UVM, but favorable associations in LGG. The THCA 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 THCA as the clearest survival context for NSG2 RNA expression.
This table summarizes NSG2 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 COAD for RNA.
This table ranks reproducible tumor–normal expression differences for NSG2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NSG2 shows lower tumor expression in COAD, KIRP, STAD, KIRC and READ and higher tumor expression in BRCA. The COAD box plot shows higher NSG2 RNA expression in normal versus tumor tissue (log2 FC = −1.900, t-test p < 0.001).
This table shows molecular features associated with NSG2 in patient tissues and cancer cell lines. In patient samples, NSG2 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, NSG2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LUNG_SCLC.
