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POLQ (DNA polymerase theta) is an enzyme. The public catalogues list it as an oncogene driver, a tumour suppressor and a DNA repair gene, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Lung cancer, Endometrial cancer, Breast cancer and 5 more.
Low-fidelity DNA polymerase with a putative helicase activity that promotes microhomology-mediated end-joining (MMEJ), an alternative non-homologous end-joining (NHEJ) machinery required to repair double-strand breaks in DNA during mitosis. MMEJ is an error-prone repair pathway that produces deletions of sequences from the strand being repaired and promotes genomic rearrangements, such as telomere fusions, some of them leading to cellular transformation. MMEJ is required during mitosis to repair persistent double-strand breaks that originate in S-phase.
Open Targets scores its association with cancer at 0.68 (direct and indirect evidence; datatypes literature 0.96, genetic association 0.18, somatic mutation 0.84, genetic literature 0.30). IntOGen calls it a driver in 4 cohorts (1 activating, 3 loss-of-function), covering Lung Squamous Cell Carcinoma, Melanoma, Endometrial Carcinoma.
In plain words · POLQ (DNA polymerase theta) is an enzyme. The public catalogues list it as an oncogene driver, a tumour suppressor and a DNA repair gene, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Lung cancer, Endometrial cancer, Breast cancer and 5 more.
POLQ (DNA polymerase theta) is an enzyme. The public catalogues list it as an oncogene driver, a tumour suppressor and a DNA repair gene, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Lung cancer, Endometrial cancer, Breast cancer and 5 more.
Low-fidelity DNA polymerase with a putative helicase activity that promotes microhomology-mediated end-joining (MMEJ), an alternative non-homologous end-joining (NHEJ) machinery required to repair double-strand breaks in DNA during mitosis.
No product in this corpus aims at POLQ yet. Inhibitors are shaped to fit the enzyme's active site so the reaction the cancer relies on stops.
First described 1998. Earliest sequence paper UniProt cites for the protein: Harris P.V. et al, 1998, "Catalytic activity of Pol eta, a new human DNA polymerase related to the bacterial DNA polymerase I family and Drosophila Mus308". Source.
Sources: HGNC HGNC:9186 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt O75417 (protein name, function text, keywords and locations (REST API)); Open Targets ENSG00000051341 (association with cancer (MONDO_0004992) 0.68; per-cancer scores at or above 0.5: non-small cell lung carcinoma 0.53, colorectal cancer 0.55, gastric cancer 0.52, ovarian cancer 0.50, melanoma 0.60, skin cancer 0.56 (GraphQL API, CC0)); IntOGen POLQ (driver in 4 cohorts (Act 1, LoF 3); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Low-fidelity DNA polymerase with a putative helicase activity that promotes microhomology-mediated end-joining (MMEJ), an alternative non-homologous end-joining (NHEJ) machinery required to repair double-strand breaks in DNA during mitosis. MMEJ is an error-prone repair pathway that produces deletions of sequences from the strand being repaired and promotes genomic rearrangements, such as telomere fusions, some of them leading to cellular transformation. MMEJ is required during mitosis to repair persistent double-strand breaks that originate in S-phase. Although error-prone, MMEJ protects against chromosomal instability and tumorigenesis. The polymerase acts by binding directly the 2 ends of resected double-strand breaks, allowing microhomologous sequences in the overhangs to form base pairs. It then extends each strand from the base-paired region using the opposing overhang as a template. Location: Nucleus; Chromosome (UniProt). Locus 3q13.33 (HGNC).
Query for this target: (TITLE:"POLQ" OR ABSTRACT:"POLQ" OR TITLE:"DNA polymerase theta" OR ABSTRACT:"DNA polymerase theta") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about POLQ, not a curated reading list.
Shares Synthetic lethality: paired dependencies, Endometrial cancer, Skin cancer (all types), Gastric & gastro-oesophageal junction cancer.
Shares Synthetic lethality: paired dependencies, DNA damage response & homologous recombination, Double-strand break repair: HR versus end joining, Open Targets Platform.
Shares Double-strand break repair: HR versus end joining, IntOGen, Gastric & gastro-oesophageal junction cancer, Ovarian cancer.
Shares Double-strand break repair: HR versus end joining, Breast cancer (all types), Open Targets Platform.
Shares DNA damage response & homologous recombination, Endometrial cancer, Ovarian cancer, Colorectal cancer.
Shares Synthetic lethality: paired dependencies, Double-strand break repair: HR versus end joining.
Shares Double-strand break repair: HR versus end joining, Open Targets Platform.
Shares Synthetic lethality: paired dependencies, DNA damage response & homologous recombination, Double-strand break repair: HR versus end joining, Endometrial cancer.