Q-omics provides the consensus-scored FIBIN profile across patient tissues and cancer cell-line models. FIBIN expression is associated with patient survival in 19 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, FIBIN is differentially expressed in 8, with the highest sampling consensus in KICH. Additionally, FIBIN protein abundance shows 19,788 significant protein co-abundance associations, with the highest sampling consensus in BRCA. Together, these results highlight KIRC, KICH, and BRCA as cancer lineages where FIBIN 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 FIBIN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FIBIN survival associations across molecular data types. FIBIN RNA expression shows survival associations in the most cancer types (19), followed by mutation status (5) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible FIBIN RNA expression–survival associations across cancer types. High FIBIN expression shows unfavorable associations in KICH, ACC and STAD, but favorable associations in KIRC, DLBC and KIRP. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for FIBIN RNA expression.
This table summarizes FIBIN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8, while mass-spec protein shows differences in 4. The strongest signals are observed in THCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for FIBIN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FIBIN shows lower tumor expression in KICH, THCA, LUAD, LUSC, KIRC and UCEC. The KICH box plot shows higher FIBIN RNA expression in normal versus tumor tissue (log2 FC = −3.782, t-test p < 0.001).
This table shows molecular features associated with FIBIN in patient tissues and cancer cell lines. In patient samples, FIBIN shows the broadest associations at the RNA and protein expression levels, with BRCA recurring as the lineage with the largest associated feature set. In cancer cell lines, FIBIN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BONE.
