solute carrier family 38 member 5Genealiases: JM24 · SN2 · SNAT5 · pp7194
Q-omics provides the consensus-scored SLC38A5 profile across patient tissues and cancer cell-line models. SLC38A5 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, SLC38A5 is differentially expressed in 12, with the highest sampling consensus in COAD. Additionally, SLC38A5 RNA expression shows 16,133 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, COAD, and LSCC as cancer lineages where SLC38A5 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 SLC38A5 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SLC38A5 survival associations across molecular data types. SLC38A5 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (4) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SLC38A5 RNA expression–survival associations across cancer types. High SLC38A5 expression shows unfavorable associations in KIRC, STAD, KIRP, UVM and OV, but favorable associations in LUAD. The KIRC 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 KIRC as the clearest survival context for SLC38A5 RNA expression.
This table summarizes SLC38A5 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 8. The strongest signals are observed in COAD for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for SLC38A5. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SLC38A5 shows lower tumor expression in KICH and UCEC and higher tumor expression in COAD, STAD, BRCA and HNSC. The COAD box plot shows higher SLC38A5 RNA expression in tumor versus normal tissue (log2 FC = +2.480, t-test p < 0.001).
This table shows molecular features associated with SLC38A5 in patient tissues and cancer cell lines. In patient samples, SLC38A5 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, SLC38A5 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Myeloma, while CRISPR and shRNA rows add functional-dependency signals in CNS and BONE.
