Q-omics provides the consensus-scored GREM1 profile across patient tissues and cancer cell-line models. GREM1 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, GREM1 is differentially expressed in 10, with the highest sampling consensus in BLCA. Additionally, GREM1 RNA expression shows 21,560 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRP, BLCA, and LSCC as cancer lineages where GREM1 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 GREM1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GREM1 survival associations across molecular data types. GREM1 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (5) 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 GREM1 RNA expression–survival associations across cancer types. High GREM1 expression shows unfavorable associations in KIRP, UVM, KIRC, ACC, LGG and THYM. The KIRP 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 KIRP as the clearest survival context for GREM1 RNA expression.
This table summarizes GREM1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 5. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for GREM1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GREM1 shows lower tumor expression in KIRC and KICH and higher tumor expression in BLCA, HNSC, LUAD and LUSC. The BLCA box plot shows higher GREM1 RNA expression in tumor versus normal tissue (log2 FC = +2.910, t-test p < 0.001).
This table shows molecular features associated with GREM1 in patient tissues and cancer cell lines. In patient samples, GREM1 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, GREM1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in SKIN and SOFT_TISSUE.
