Q-omics provides the consensus-scored TXLNGY profile across patient tissues and cancer cell-line models. TXLNGY expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, TXLNGY is differentially expressed in 9, with the highest sampling consensus in KIRP. Additionally, TXLNGY RNA expression shows 7,681 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight HNSC, KIRP, and TGCT as cancer lineages where TXLNGY 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 TXLNGY — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TXLNGY survival associations across molecular data types. TXLNGY RNA expression shows survival associations in the most cancer types (23), followed by 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 TXLNGY RNA expression–survival associations across cancer types. High TXLNGY expression shows unfavorable associations in THCA, OV, DLBC and LGG, but favorable associations in HNSC and MESO. 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 TXLNGY RNA expression.
This table summarizes TXLNGY tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9. The strongest signals are observed in KIRP for RNA.
This table ranks reproducible tumor–normal expression differences for TXLNGY. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TXLNGY shows lower tumor expression in KIRP, KICH, LUSC and HNSC and higher tumor expression in CHOL and PRAD. The KIRP box plot shows higher TXLNGY RNA expression in normal versus tumor tissue (log2 FC = −1.192, t-test p < 0.001).
This table shows molecular features associated with TXLNGY in patient tissues and cancer cell lines. In patient samples, TXLNGY shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, TXLNGY RNA and mutation anchors are most strongly linked to RNA-expression features, especially in STOMACH, while CRISPR and shRNA rows add functional-dependency signals in BREAST.
