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[Cancer Research 63, 2585-2588, May 15, 2003]
© 2003 American Association for Cancer Research

Molecular Biology and Genetics

Fanconi Anemia Gene Mutations in Young-onset Pancreatic Cancer1

Michiel S. van der Heijden, Charles J. Yeo, Ralph H. Hruban and Scott E. Kern2

Departments of Oncology [M. S. v. d. H., S. E. K., R. H. H.], Pathology [R. H. H., S. E. K.], and Surgery [C. J. Y.], The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland 21231

Genes of the Fanconi complementation groups [Fanconi anemia (FA) genes] are suggested to be involved in homologous DNA recombination and produce FA when two allelic mutations are inherited. BRCA2 is an FA gene and additionally conveys an inherited risk for breast, ovarian, and pancreatic cancer for individuals carrying a single mutated allele [N. G. Howlett et al., Science (Wash. DC), 297: 606–609, 2002]. Here we report inherited and somatic mutations of FANCC and FANCG present in young-onset pancreatic cancer. This may imply a general involvement of Fanconi genes with an inherited risk of cancer. The known hypersensitivity of Fanconi cells to mitomycin and other therapeutic agents [M. S. Sasaki, Nature (Lond.), 257: 501–503, 1975] suggests a therapeutic utility for a more complete characterization of the DNA repair defects and their causative genetic mutations in pancreatic cancer.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
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Copyright © 2003 by the American Association for Cancer Research.