TIMP metallopeptidase inhibitor 2Genealiases: CSC-21K · DDC8
Q-omics provides the consensus-scored TIMP2 profile across patient tissues and cancer cell-line models. TIMP2 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, TIMP2 is differentially expressed in 13, with the highest sampling consensus in KICH. Additionally, TIMP2 protein abundance shows 22,781 significant protein co-abundance associations, with the highest sampling consensus in BRCA. Together, these results highlight ACC, KICH, and BRCA as cancer lineages where TIMP2 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 TIMP2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TIMP2 survival associations across molecular data types. TIMP2 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (3) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TIMP2 RNA expression–survival associations across cancer types. High TIMP2 expression shows unfavorable associations in ACC, BLCA, MESO, KIRP, STAD and LUSC. The ACC 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 ACC as the clearest survival context for TIMP2 RNA expression.
This table summarizes TIMP2 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 5. The strongest signals are observed in KICH for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TIMP2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TIMP2 shows lower tumor expression in KICH, BLCA, UCEC and LUSC and higher tumor expression in HNSC and KIRP. The KICH box plot shows higher TIMP2 RNA expression in normal versus tumor tissue (log2 FC = −1.646, t-test p < 0.001).
This table shows molecular features associated with TIMP2 in patient tissues and cancer cell lines. In patient samples, TIMP2 shows the broadest associations at the RNA and protein expression levels, with BRCA recurring as the lineage with the largest associated feature set. In cancer cell lines, TIMP2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BLOOD_Leukemia.
