Research Papers:

Mutated Fanconi anemia pathway in non-Fanconi anemia cancers

Yihang Shen, Yuan-Hao Lee, Jayabal Panneerselvam, Jun Zhang, Lenora W. M. Loo and Peiwen Fei _

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Oncotarget. 2015; 6:20396-20403. https://doi.org/10.18632/oncotarget.4056

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Yihang Shen1, Yuan-Hao Lee1, Jayabal Panneerselvam1, Jun Zhang2, Lenora W. M. Loo3 and Peiwen Fei1

1 Program of Cancer Biology, University of Hawaii Cancer Center, University of Hawaii, Honolulu, HI, USA

2 Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA

3 Program of Epidemiology, University of Hawaii Cancer Center, University of Hawaii, Honolulu, HI, USA

Correspondence to:

Peiwen Fei, email:

Keywords: Fanconi anemia genes, TCGA, the mutated FA pathway, tumorigenesis, cancer treatment

Received: March 10, 2015 Accepted: April 22, 2015 Published: May 09, 2015


An extremely high cancer incidence and the hypersensitivity to DNA crosslinking agents associated with Fanconi Anemia (FA) have marked it to be a unique genetic model system to study human cancer etiology and treatment, which has emerged an intense area of investigation in cancer research. However, there is limited information about the relationship between the mutated FA pathway and the cancer development or/and treatment in patients without FA. Here we analyzed the mutation rates of the seventeen FA genes in 68 DNA sequence datasets. We found that the FA pathway is frequently mutated across a variety of human cancers, with a rate mostly in the range of 15 to 35 % in human lung, brain, bladder, ovarian, breast cancers, or others. Furthermore, we found a statistically significant correlation (p < 0.05) between the mutated FA pathway and the development of human bladder cancer that we only further analyzed. Together, our study demonstrates a previously unknown fact that the mutated FA pathway frequently occurs during the development of non-FA human cancers, holding profound implications directly in advancing our understanding of human tumorigenesis as well as tumor sensitivity/resistance to crosslinking drug-relevant chemotherapy.

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