Q-omics provides the consensus-scored DDR2 profile across patient tissues and cancer cell-line models. DDR2 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, DDR2 is differentially expressed in 15, with the highest sampling consensus in THCA. Additionally, DDR2 RNA expression shows 23,107 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRP, THCA, and LSCC as cancer lineages where DDR2 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 DDR2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DDR2 survival associations across molecular data types. DDR2 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (5) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible DDR2 RNA expression–survival associations across cancer types. High DDR2 expression shows unfavorable associations in KIRP, LGG, UVM and BLCA, but favorable associations in ACC and UCS. The KIRP Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRP as the clearest survival context for DDR2 RNA expression.
This table summarizes DDR2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 4. The strongest signals are observed in THCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for DDR2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DDR2 shows lower tumor expression in THCA, COAD, BLCA, LUSC, KICH and KIRP. The THCA box plot shows higher DDR2 RNA expression in normal versus tumor tissue (log2 FC = −1.667, t-test p < 0.001).
This table shows molecular features associated with DDR2 in patient tissues and cancer cell lines. In patient samples, DDR2 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, DDR2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BLOOD_Lymphoma.
