Fanconi anemia gene mutations in young-onset pancreatic cancer.
Publication/Presentation Date
5-15-2003
Abstract
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.
Volume
63
Issue
10
First Page
2585
Last Page
2588
ISSN
0008-5472
Published In/Presented At
van der Heijden, M. S., Yeo, C. J., Hruban, R. H., & Kern, S. E. (2003). Fanconi anemia gene mutations in young-onset pancreatic cancer. Cancer research, 63(10), 2585–2588.
Disciplines
Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods
PubMedID
12750283
Department(s)
Administration and Leadership
Document Type
Article