Q-omics provides the consensus-scored RSPH1 profile across patient tissues and cancer cell-line models. RSPH1 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in BRCA. Among the 18 cancer types available for tumor–normal comparison, RSPH1 is differentially expressed in 13, with the highest sampling consensus in KICH. Additionally, RSPH1 RNA expression shows 18,182 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight BRCA, KICH, and KIRP as cancer lineages where RSPH1 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 RSPH1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes RSPH1 survival associations across molecular data types. RSPH1 RNA expression shows survival associations in the most cancer types (22), 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 RSPH1 RNA expression–survival associations across cancer types. High RSPH1 expression shows unfavorable associations in LIHC, STAD, LGG, COAD and ESCA, but favorable associations in BRCA. The BRCA Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .002). Together, the overview and detailed table identify BRCA as the clearest survival context for RSPH1 RNA expression.
This table summarizes RSPH1 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 LUAD for protein.
This table ranks reproducible tumor–normal expression differences for RSPH1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. RSPH1 shows lower tumor expression in KICH, KIRC, THCA, LUSC and LUAD and higher tumor expression in STAD. The KICH box plot shows higher RSPH1 RNA expression in normal versus tumor tissue (log2 FC = −3.113, t-test p < 0.001).
This table shows molecular features associated with RSPH1 in patient tissues and cancer cell lines. In patient samples, RSPH1 shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, RSPH1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in CNS and BREAST.
