Q-omics provides the consensus-scored SPRR1A profile across patient tissues and cancer cell-line models. SPRR1A expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KICH. Among the 18 cancer types available for tumor–normal comparison, SPRR1A is differentially expressed in 12, with the highest sampling consensus in COAD. Additionally, SPRR1A RNA expression shows 11,016 significant gene co-expression associations, with the highest sampling consensus in ESCA. Together, these results highlight KICH, COAD, and ESCA as cancer lineages where SPRR1A 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 SPRR1A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SPRR1A survival associations across molecular data types. SPRR1A RNA expression shows survival associations in the most cancer types (24), followed by 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 SPRR1A RNA expression–survival associations across cancer types. High SPRR1A expression shows unfavorable associations in KICH, SKCM, BRCA, MESO and COAD, but favorable associations in LUSC. The KICH 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 KICH as the clearest survival context for SPRR1A RNA expression.
This table summarizes SPRR1A 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 4. The strongest signals are observed in COAD for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for SPRR1A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SPRR1A shows lower tumor expression in KICH, KIRC and KIRP and higher tumor expression in COAD, LUSC and LUAD. The COAD box plot shows higher SPRR1A RNA expression in tumor versus normal tissue (log2 FC = +1.262, t-test p < 0.001).
This table shows molecular features associated with SPRR1A in patient tissues and cancer cell lines. In patient samples, SPRR1A shows the broadest associations at the RNA and protein expression levels, with ESCA recurring as the lineage with the largest associated feature set. In cancer cell lines, SPRR1A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in BONE and URINARY_TRACT.
