Q-omics provides the consensus-scored FSBP profile across patient tissues and cancer cell-line models. FSBP expression is associated with patient survival in 16 of 34 cancer types, with the highest sampling consensus in READ. Among the 18 cancer types available for tumor–normal comparison, FSBP is differentially expressed in 6, with the highest sampling consensus in KIRC. Additionally, FSBP RNA expression shows 17,033 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight READ, KIRC, and LSCC as cancer lineages where FSBP 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 FSBP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FSBP survival associations across molecular data types. FSBP RNA expression shows survival associations in the most cancer types (16), followed by mutation status (1) 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 FSBP RNA expression–survival associations across cancer types. High FSBP expression shows unfavorable associations in READ, LGG, UCEC, KIRP and PAAD, but favorable associations in CHOL. The READ 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 READ as the clearest survival context for FSBP RNA expression.
This table summarizes FSBP tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 6, while mass-spec protein shows differences in 1. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for FSBP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FSBP shows lower tumor expression in PRAD and KICH and higher tumor expression in KIRC, PAAD, STAD and LUAD. The KIRC box plot shows higher FSBP RNA expression in tumor versus normal tissue (log2 FC = +0.020, t-test p < 0.001).
This table shows molecular features associated with FSBP in patient tissues and cancer cell lines. In patient samples, FSBP 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, FSBP 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 LIVER and BONE.
