Q-omics provides the consensus-scored NTPCR profile across patient tissues and cancer cell-line models. NTPCR expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, NTPCR is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, NTPCR RNA expression shows 19,226 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRP, KIRC, and LSCC as cancer lineages where NTPCR 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 NTPCR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NTPCR survival associations across molecular data types. NTPCR RNA expression shows survival associations in the most cancer types (24), followed by mutation status (2) 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 NTPCR RNA expression–survival associations across cancer types. High NTPCR expression shows unfavorable associations in KIRP, LUAD, ACC, LIHC and CESC, but favorable associations in COAD. 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 NTPCR RNA expression.
This table summarizes NTPCR 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 4. The strongest signals are observed in KIRC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for NTPCR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NTPCR shows lower tumor expression in KICH and higher tumor expression in KIRC, KIRP, HNSC, LIHC and CHOL. The KIRC box plot shows higher NTPCR RNA expression in tumor versus normal tissue (log2 FC = +0.505, t-test p < 0.001).
This table shows molecular features associated with NTPCR in patient tissues and cancer cell lines. In patient samples, NTPCR shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, NTPCR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Myeloma and UPPER_AERODIGESTIVE_TRACT.
