ReviewCancer science2008
Clinical relevance of the homologous recombination machinery in cancer therapy.
Review in Cancer science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 57 citations in OpenAlex.
- Impact of double-strand breaks induced by uv radiation on neuroinflammation and neurodegenerative disorders.Molecular biology reports · 2024Review
- Fanconi anemia associated protein 20 (FAAP20) plays an essential role in homology-directed repair of DNA double-strand breaks.Communications biology · 2023Article
- Article
- Utility of ctDNA in predicting response to neoadjuvant chemoradiotherapy and prognosis assessment in locally advanced rectal cancer: A prospective cohort study.PLoS medicine · 2021Article
- Overexpression of Progerin Results in Impaired Proliferation and Invasion of Non-Small Cell Lung Cancer Cells.OncoTargets and therapy · 2020Article
- Asparagine Synthetase and Filamin A Have Different Roles in Ovarian Cancer.Frontiers in oncology · 2019Article
- Article
- Article
- Rad51 expression is a useful predictive factor for the efficacy of neoadjuvant chemoradiotherapy in squamous cell carcinoma of the esophagus.Annals of surgical oncology · 2014Article
- Epistatic role of base excision repair and mismatch repair pathways in mediating cisplatin cytotoxicity.Nucleic acids research · 2013Article
- Imatinib radiosensitizes bladder cancer by targeting homologous recombination.Cancer research · 2013Article
- Article
- The role and clinical significance of DNA damage response and repair pathways in primary brain tumors.Cell & bioscience · 2013Article
- DNA double-strand break repair as determinant of cellular radiosensitivity to killing and target in radiation therapy.Frontiers in oncology · 2013Article
- Rad51 promoter-targeted gene therapy is effective for in vivo visualization and treatment of cancer.Molecular therapy : the journal of the American Society of Gene Therapy · 2012Article
- Novel role of base excision repair in mediating cisplatin cytotoxicity.The Journal of biological chemistry · 2011Article
- Enhancing radiotherapy through a greater understanding of homologous recombination.Seminars in radiation oncology · 2010Review
- Combination of bifunctional alkylating agent and arsenic trioxide synergistically suppresses the growth of drug-resistant tumor cells.Neoplasia (New York, N.Y.) · 2010Article
- Enhancing survival of mouse oocytes following chemotherapy or aging by targeting Bax and Rad51.PloS one · 2010Article
- Drug resistance in lung cancer.Lung Cancer (Auckland, N.Z.) · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer chemotherapy and radiotherapy kill cancer cells by inducing DNA damage, unless the lesions are repaired by intrinsic repair pathways. DNA double-strand breaks (DSB) are the most deleterious type of damage caused by cancer therapy. Homologous recombination (HR) is one of the major repair pathways for DSB and is thus a potential target of cancer therapy. Cells with a defect in HR have been shown to be sensitive to a variety of DNA-damaging agents, particularly interstrand crosslink (ICL)-inducing agents such as mitomycin C and cisplatin. These findings have recently been applied to clinical studies of cancer therapy. ERCC1, a structure-specific endonuclease involved in nucleotide excision repair (NER) and HR, confers resistance to cisplatin. Patients with ERCC1-negative non-small-cell lung cancer were shown to benefit from adjuvant cisplatin-based chemotherapy. Imatinib, an inhibitor of the c-Abl kinase, has been investigated as a sensitizer in DNA-damaging therapy, because c-Abl activates Rad51, which plays a key role in HR. Furthermore, proteins involved in HR have been shown to repair DNA damage induced by a variety of other chemotherapeutic agents, including camptothecin and gemcitabine. These findings highlight the importance of HR machinery in cancer therapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.