Q-omics provides the consensus-scored SSTR3 profile across patient tissues and cancer cell-line models. SSTR3 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, SSTR3 is differentially expressed in 11, with the highest sampling consensus in COAD. Additionally, SSTR3 RNA expression shows 19,384 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight HNSC, COAD, and GBM as cancer lineages where SSTR3 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 SSTR3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SSTR3 survival associations across molecular data types. SSTR3 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (11). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SSTR3 RNA expression–survival associations across cancer types. High SSTR3 expression shows unfavorable associations in UVM and KIRC, but favorable associations in HNSC, SKCM, BLCA and ESCA. 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 SSTR3 RNA expression.
This table summarizes SSTR3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11. The strongest signals are observed in COAD for RNA.
This table ranks reproducible tumor–normal expression differences for SSTR3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SSTR3 shows lower tumor expression in COAD, KIRP, UCEC and KICH and higher tumor expression in THCA and HNSC. The COAD box plot shows higher SSTR3 RNA expression in normal versus tumor tissue (log2 FC = −0.365, t-test p < 0.001).
This table shows molecular features associated with SSTR3 in patient tissues and cancer cell lines. In patient samples, SSTR3 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, SSTR3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BLOOD_Leukemia.
