Genetic breakdown in Fanconi anemia may have link to HPV-associa... (ell growth and skin thickness. In a reve...)

Genetic breakdown in Fanconi anemia may have link to HPV-associated cancer

Date:12/3/2008

ell growth and skin thickness. In a reverse experiment, the researchers took FA-normal cells, where the FA gene pathway is not broken. The FA-normal cells also carried the HPV cancer genes E6/E7. The investigators then switched off two Fanconi anemia genes in the cells (FANCA and FANCD2). This disabled the FA pathway and resulted in irregular cell growth and thickening of epithelial/skin tissue.

The HPV E6/E7 genes are known to inhibit natural tumor suppression and promote chromosomal instability in the cell replication cycle. Dr. Wells and her colleagues believe FA deficiency may accelerate tumor development by promoting genomic instability, which then cooperates with HPV's inactivation of the body's natural tumor suppressors. Restoring the FA gene pathway, they suggest, can block cell cycle abnormalities stimulated by high-risk HPV E6/E7.

The researchers also experimented with standard cell cultures that aren't as close to mimicking living skin. In those experiments, cellular abnormalities did not occur until the researchers introduced DNA damaging agents, such as the chemotherapy agent mitomycin C. After exposure the cells experienced programmed death. This may explain why skin lesions develop in some Fanconi anemia patients who have residual DNA damage following certain treatments. Dr. Wells said it's also possible residual DNA damage mutates surviving cells, which can cause cancer. The results show how sensitive FANCA-deficient skin cells are to DNA damage from external sources, highlighting in part the vulnerability Fanconi anemia patients can have to certain forms of cancer treatment.

The study's results also have potential implications for cancers not linked to Fanconi anemia. Previous research has shown inactivation of the FA pathway has been detected in some cancers affecting people without the blood disorder. The skin cell model researchers developed for the current study could be used to advance research of FA-deficient squamo
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Contact: Nick Miller
nicholas.miller@cchmc.org
513-803-6035
Cincinnati Children's Hospital Medical Center
Source:Eurekalert

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