Q-omics provides the consensus-scored CSF3R profile across patient tissues and cancer cell-line models. CSF3R expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, CSF3R is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, CSF3R RNA expression shows 24,362 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight HNSC, KIRC, and LSCC as cancer lineages where CSF3R 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 CSF3R — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CSF3R survival associations across molecular data types. CSF3R RNA expression shows survival associations in the most cancer types (24), followed by mutation status (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CSF3R RNA expression–survival associations across cancer types. High CSF3R expression shows unfavorable associations in LGG, LUSC, KIRC and STAD, but favorable associations in HNSC and SKCM. The HNSC 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 HNSC as the clearest survival context for CSF3R RNA expression.
This table summarizes CSF3R tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 1. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for CSF3R. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CSF3R shows lower tumor expression in LUAD and LIHC and higher tumor expression in KIRC, KIRP, HNSC and THCA. The KIRC box plot shows higher CSF3R RNA expression in tumor versus normal tissue (log2 FC = +1.974, t-test p < 0.001).
This table shows molecular features associated with CSF3R in patient tissues and cancer cell lines. In patient samples, CSF3R 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, CSF3R RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in LIVER and BLOOD_Leukemia.
