Q-omics provides the consensus-scored SLIT1 profile across patient tissues and cancer cell-line models. SLIT1 expression is associated with patient survival in 29 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, SLIT1 is differentially expressed in 11, with the highest sampling consensus in THCA. Additionally, SLIT1 RNA expression shows 17,262 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight HNSC, THCA, and UVM as cancer lineages where SLIT1 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 SLIT1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SLIT1 survival associations across molecular data types. SLIT1 RNA expression shows survival associations in the most cancer types (29), followed by mutation status (8) 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 SLIT1 RNA expression–survival associations across cancer types. High SLIT1 expression shows unfavorable associations in UVM, KIRC and UCEC, but favorable associations in HNSC, CESC 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 SLIT1 RNA expression.
This table summarizes SLIT1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 2. The strongest signals are observed in THCA for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for SLIT1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SLIT1 shows lower tumor expression in KICH and LUSC and higher tumor expression in THCA, KIRC, KIRP and HNSC. The THCA box plot shows higher SLIT1 RNA expression in tumor versus normal tissue (log2 FC = +4.448, t-test p < 0.001).
This table shows molecular features associated with SLIT1 in patient tissues and cancer cell lines. In patient samples, SLIT1 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, SLIT1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and BLOOD_Leukemia.
