Q-omics provides the consensus-scored STIM1 profile across patient tissues and cancer cell-line models. STIM1 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in ESCA. Among the 18 cancer types available for tumor–normal comparison, STIM1 is differentially expressed in 10, with the highest sampling consensus in KIRP. Additionally, STIM1 protein abundance shows 21,806 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight ESCA, KIRP, and PDAC as cancer lineages where STIM1 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 STIM1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes STIM1 survival associations across molecular data types. STIM1 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (3) 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 STIM1 RNA expression–survival associations across cancer types. High STIM1 expression shows unfavorable associations in BLCA, LUAD, UVM and HNSC, but favorable associations in ESCA and KIRC. The ESCA Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .002). Together, the overview and detailed table identify ESCA as the clearest survival context for STIM1 RNA expression.
This table summarizes STIM1 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 7. The strongest signals are observed in KIRP for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for STIM1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. STIM1 shows lower tumor expression in COAD and BRCA and higher tumor expression in KIRP, KICH, LIHC and KIRC. The KIRP box plot shows higher STIM1 RNA expression in tumor versus normal tissue (log2 FC = +1.000, t-test p < 0.001).
This table shows molecular features associated with STIM1 in patient tissues and cancer cell lines. In patient samples, STIM1 shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, STIM1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Myeloma, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BLOOD_Leukemia.
