Q-omics provides the consensus-scored SMAP2 profile across patient tissues and cancer cell-line models. SMAP2 expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, SMAP2 is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, SMAP2 protein abundance shows 22,315 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight HNSC, KIRC, and LSCC as cancer lineages where SMAP2 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 SMAP2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SMAP2 survival associations across molecular data types. SMAP2 RNA expression shows survival associations in the most cancer types (20), followed by mutation status (3) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SMAP2 RNA expression–survival associations across cancer types. High SMAP2 expression shows unfavorable associations in KICH, ACC and LAML, but favorable associations in HNSC, SKCM and LUAD. 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 SMAP2 RNA expression.
This table summarizes SMAP2 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 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for SMAP2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SMAP2 shows lower tumor expression in BLCA, KICH and LUSC and higher tumor expression in KIRC, LIHC and HNSC. The KIRC box plot shows higher SMAP2 RNA expression in tumor versus normal tissue (log2 FC = +1.039, t-test p < 0.001).
This table shows molecular features associated with SMAP2 in patient tissues and cancer cell lines. In patient samples, SMAP2 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, SMAP2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in KIDNEY and UPPER_AERODIGESTIVE_TRACT.
