Q-omics provides the consensus-scored RSL24D1 profile across patient tissues and cancer cell-line models. RSL24D1 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, RSL24D1 is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, RSL24D1 protein abundance shows 27,298 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight HNSC, KIRC, and LSCC as cancer lineages where RSL24D1 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 RSL24D1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes RSL24D1 survival associations across molecular data types. RSL24D1 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (3) and mass-spec protein abundance (11). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible RSL24D1 RNA expression–survival associations across cancer types. High RSL24D1 expression shows unfavorable associations in HNSC, KIRP, ACC, LIHC and CESC, but favorable associations in KIRC. The HNSC 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 HNSC as the clearest survival context for RSL24D1 RNA expression.
This table summarizes RSL24D1 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 KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for RSL24D1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. RSL24D1 shows lower tumor expression in UCEC and higher tumor expression in KIRC, LIHC, HNSC, CHOL and COAD. The KIRC box plot shows higher RSL24D1 RNA expression in tumor versus normal tissue (log2 FC = +0.556, t-test p < 0.001).
This table shows molecular features associated with RSL24D1 in patient tissues and cancer cell lines. In patient samples, RSL24D1 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, RSL24D1 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 LUNG_SCLC and CNS.
