solute carrier family 7 member 6Genealiases: LAT-2 · LAT3 · y+LAT-2
Q-omics provides the consensus-scored SLC7A6 profile across patient tissues and cancer cell-line models. SLC7A6 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, SLC7A6 is differentially expressed in 11, with the highest sampling consensus in COAD. Additionally, SLC7A6 protein abundance shows 29,497 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRP, COAD, and LUAD as cancer lineages where SLC7A6 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 SLC7A6 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SLC7A6 survival associations across molecular data types. SLC7A6 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (4) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SLC7A6 RNA expression–survival associations across cancer types. High SLC7A6 expression shows unfavorable associations in KIRP, BLCA, UVM, MESO, ACC and LGG. 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 SLC7A6 RNA expression.
This table summarizes SLC7A6 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 9. The strongest signals are observed in HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for SLC7A6. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SLC7A6 shows lower tumor expression in THCA and higher tumor expression in COAD, HNSC, LIHC, STAD and BLCA. The COAD box plot shows higher SLC7A6 RNA expression in tumor versus normal tissue (log2 FC = +1.605, t-test p < 0.001).
This table shows molecular features associated with SLC7A6 in patient tissues and cancer cell lines. In patient samples, SLC7A6 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, SLC7A6 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and BLOOD_Leukemia.
