Q-omics provides the consensus-scored TIMP3 profile across patient tissues and cancer cell-line models. TIMP3 expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, TIMP3 is differentially expressed in 13, with the highest sampling consensus in KIRP. Additionally, TIMP3 protein abundance shows 27,077 significant protein co-abundance associations, with the highest sampling consensus in UCEC. Together, these results highlight KIRC, KIRP, and UCEC as cancer lineages where TIMP3 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 TIMP3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TIMP3 survival associations across molecular data types. TIMP3 RNA expression shows survival associations in the most cancer types (28), followed by mutation status (6) and mass-spec protein abundance (12). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TIMP3 RNA expression–survival associations across cancer types. High TIMP3 expression shows unfavorable associations in LUSC, OV and MESO, but favorable associations in KIRC, UVM and UCS. The KIRC 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 KIRC as the clearest survival context for TIMP3 RNA expression.
This table summarizes TIMP3 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 9. The strongest signals are observed in KIRP for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for TIMP3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TIMP3 shows lower tumor expression in KIRP, KICH, THCA, LUAD and KIRC and higher tumor expression in HNSC. The KIRP box plot shows higher TIMP3 RNA expression in normal versus tumor tissue (log2 FC = −2.757, t-test p < 0.001).
This table shows molecular features associated with TIMP3 in patient tissues and cancer cell lines. In patient samples, TIMP3 shows the broadest associations at the RNA and protein expression levels, with UCEC recurring as the lineage with the largest associated feature set. In cancer cell lines, TIMP3 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 SKIN and BLOOD_Leukemia.
