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ShareApr. 19, 2010 — Individuals with the rare human genetic disease Fanconi anemia have an increased incidence of cancer. In many individuals, disease is caused by mutations in any one of 13 known genes (including FANCL) that generate proteins that function in one common signaling pathway that is known as the FA pathway. Whether this pathway has a role in human cancers in individuals who do not have Fanconi anemia has not been clearly determined.
But now, Peiwen Fei and colleagues, at the Mayo Clinic, Rochester, have identified a new form of the protein FANCL, which they named FAVL, that dysregulates the FA pathway in non-FA human tumor cells and acts as a tumor-promoting factor.
The authors therefore conclude that impairment of the FA pathway could contribute to the development of cancer in individuals who do not have Fanconia anemia.
The research appears in the Journal of Clinical Investigation.
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The above story is reprinted from materials provided by Journal of Clinical Investigation, via EurekAlert!, a service of AAAS.
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Journal Reference:
- Jun Zhang, Deping Zhao, Hwan Ki Park, Hong Wang, Roy B. Dyer, Wanguo Liu, George G. Klee, Mark A. Mcniven, Donald J. Tindall, Julian R. Molina and Peiwen Fei. FAVL elevation in human tumors disrupts Fanconi anemia pathway signaling and promotes genomic instability and tumor growth. Journal of Clinical Investigation, 2010; DOI: 10.1172/JCI40908
Note: If no author is given, the source is cited instead.
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