Association of human papillomavirus with Fanconi anemia promotes carcinogenesis in Fanconi anemia patients |
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| Authors: | Guang Bin Liu Jiezhong Chen Zhan He Wu Kong‐Nan Zhao |
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| Affiliation: | 1. School of Health and Wellbeing, Faculty of Health, Engineering and Sciences, The University of Southern Queensland, Toowoomba, Australia;2. School of Biomedical Sciences, The University of Queensland, Brisbane, Australia;3. Faculty of Science, Medicine and Health, University of Wollongong, Wollongong, Australia;4. Western Sydney Genomic Diagnosis, The Children's Hospital at Westmead, Sydney, Australia;5. Institute of Molecular Virology and Immunology, Department of Medical Microbiology and Immunology, Wenzhou Medical University, Wenzhou, China;6. Centre for Kidney Disease Research—Venomics Research, The University of Queensland School of Medicine, Translational Research Institute, Brisbane, Australia |
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| Abstract: | ![]()
Fanconi anemia (FA) is a rare recessive disorder associated with chromosomal fragility. FA patients are at very high risk of cancers, especially head and neck squamous cell carcinomas and squamous cell carcinomas caused by infection of human papillomaviruses (HPVs). By integrating into the host genome, HPV oncogenes E6 and E7 drive the genomic instability to promote DNA damage and gene mutations necessary for carcinogenesis in FA patients. Furthermore, E6 and E7 oncoproteins not only inhibit p53 and retinoblastoma but also impair the FANC/BRCA signaling pathway to prevent DNA damage repair and alter multiple signals including cell‐cycle checkpoints, telomere function, cell proliferation, and interference of the host immune system leading to cancer development in FA patients. In this review, we summarize recent advances in unraveling the molecular mechanisms of FA susceptibility to HPV‐induced cancers, which facilitate rational preventive and therapeutic strategies. Copyright © 2015 John Wiley & Sons, Ltd. |
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