The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Cells Deficient in the FANC/BRCA Pathway Are Hypersensitive to Plasma Levels of Formaldehyde
Open accessAbstract
Formaldehyde is an aliphatic monoaldehyde and is a highly reactive environmental human carcinogen. Whereas humans are continuously exposed to exogenous formaldehyde, this reactive aldehyde is a naturally occurring biological compound that is present in human plasma at concentrations ranging from 13 to 97 μmol/L. It has been well documented that DNA-protein crosslinks (DPC) likely play an important role with regard to the genotoxicity and carcinogenicity of formaldehyde. However, little is known about which DNA damage response pathways are essential for cells to counteract formaldehyde. In the present study, we first assessed the DNA damage response to plasma levels of formaldehyde using chicken DT40 cells with targeted mutations in various DNA repair genes. Here, we show that the hypersensitivity to formaldehyde is detected in DT40 mutants deficient in the BRCA/FANC pathway, homologous recombination, or translesion DNA synthesis. In addition, FANCD2-deficient DT40 cells are hypersensitive to acetaldehyde, but not to acrolein, crotonaldehyde, glyoxal, and methylglyoxal. Human cells deficient in FANCC and FANCG are also hypersensitive to plasma levels of formaldehyde. These results indicate that the BRCA/FANC pathway is essential to counteract DPCs caused by aliphatic monoaldehydes. Based on the results obtained in the present study, we are currently proposing that endogenous formaldehyde might have an effect on highly proliferating cells, such as bone marrow cells, as well as an etiology of cancer in Fanconi anemia patients. [Cancer Res 2007;67(23):11117–22]
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Cogliano, V. J., Grosse, Y., Baan, R. A., Straif, K., Secretan, M. B., Ghissassi, F. E., & the Working Group for Volume 88 (2005) · Environmental Health Perspectives · doi:10.1289/ehp.7542 · Cited by 375
Cited by
Targeting Aldehyde Dehydrogenase 2: New Therapeutic Opportunities
Chen, C.-H., Ferreira, J. C. B., Gross, E. R., & Mochly-Rosen, D. (2014) · Physiological Reviews · doi:10.1152/physrev.00017.2013 · Cited by 614
Chen, C.-C., Feng, W., Lim, P. X., Kass, E. M., & Jasin, M. (2018) · Annual Review of Cancer Biology · doi:10.1146/annurev-cancerbio-030617-050502 · Cited by 317
Molecular pathogenesis and clinical management of Fanconi anemia
Kee, Y., & D’Andrea, A. D. (2012) · Journal of Clinical Investigation · doi:10.1172/jci58321 · Cited by 289
Hematopoietic stem cell defects in mice with deficiency of Fancd2 or Usp1
Parmar, K., Kim, J., Sykes, S. M., Shimamura, A., Stuckert, P., Zhu, K., Hamilton, A., Deloach, M. K., Kutok, J. L., Akashi, K., et al. (2010) · Stem Cells · doi:10.1002/stem.437 · Cited by 113
Gueranger, Q., Kia, A., Frith, D., & Karran, P. (2011) · Nucleic Acids Research · doi:10.1093/nar/gkr112 · Cited by 47
Metadata
- Authors
- Ridpath, J. R., Nakamura, A., Tano, K., Luke, A. M., Sonoda, E., Arakawa, H., Buerstedde, J.-M., Gillespie, D. A. F., Sale, J. E., Yamazoe, M., Bishop, D. K., Takata, M., Takeda, S., Watanabe, M., Swenberg, J. A., & Nakamura, J.
- Venue
- Cancer Research
- Published
- 2007-12-01
- Volume
- 67
- Issue
- 23
- Pages
- 11117-11122
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W2114624818
- Cited by
- 181
- References
- 1
- FWCI
- 3.59
- Type
- journal article
- Language
- en
- Open access
- bronze
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- The paper
- Ridpath, J. R., Nakamura, A., Tano, K., Luke, A. M., Sonoda, E., Arakawa, H., Buerstedde, J.-M., Gillespie, D. A. F., Sale, J. E., Yamazoe, M., Bishop, D. K., Takata, M., Takeda, S., Watanabe, M., Swenberg, J. A., & Nakamura, J. (2007). Cells Deficient in the FANC/BRCA Pathway Are Hypersensitive to Plasma Levels of Formaldehyde. Cancer Research. https://doi.org/10.1158/0008-5472.can-07-3028
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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