Q-omics provides the consensus-scored NTRK2 profile across patient tissues and cancer cell-line models. NTRK2 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in BLCA. Among the 18 cancer types available for tumor–normal comparison, NTRK2 is differentially expressed in 13, with the highest sampling consensus in KICH. Additionally, NTRK2 RNA expression shows 21,627 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight BLCA, KICH, and LSCC as cancer lineages where NTRK2 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 NTRK2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NTRK2 survival associations across molecular data types. NTRK2 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (9) 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 NTRK2 RNA expression–survival associations across cancer types. High NTRK2 expression shows unfavorable associations in BLCA, but favorable associations in KIRC, HNSC, LUSC, BRCA and LIHC. The BLCA 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 BLCA as the clearest survival context for NTRK2 RNA expression.
This table summarizes NTRK2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 3. The strongest signals are observed in KIRC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for NTRK2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NTRK2 shows lower tumor expression in KICH, KIRC, LUAD, THCA, COAD and KIRP. The KICH box plot shows higher NTRK2 RNA expression in normal versus tumor tissue (log2 FC = −4.530, t-test p < 0.001).
This table shows molecular features associated with NTRK2 in patient tissues and cancer cell lines. In patient samples, NTRK2 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, NTRK2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in KIDNEY and BLOOD_Leukemia.
