Q-omics provides the consensus-scored GTF2I profile across patient tissues and cancer cell-line models. GTF2I expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, GTF2I is differentially expressed in 12, with the highest sampling consensus in BLCA. Additionally, GTF2I protein abundance shows 25,518 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, BLCA, and GBM as cancer lineages where GTF2I 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 GTF2I — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GTF2I survival associations across molecular data types. GTF2I RNA expression shows survival associations in the most cancer types (26), followed by mutation status (3) 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 GTF2I RNA expression–survival associations across cancer types. High GTF2I expression shows unfavorable associations in CESC, PAAD and MESO, but favorable associations in KIRC, UCS and BRCA. 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 GTF2I RNA expression.
This table summarizes GTF2I 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 5. The strongest signals are observed in BLCA for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for GTF2I. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GTF2I shows lower tumor expression in THCA and higher tumor expression in BLCA, COAD, LIHC, LUAD and CHOL. The BLCA box plot shows higher GTF2I RNA expression in tumor versus normal tissue (log2 FC = +0.760, t-test p = .001).
This table shows molecular features associated with GTF2I in patient tissues and cancer cell lines. In patient samples, GTF2I shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, GTF2I RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in OVARY and BLOOD_Leukemia.
