Clinical Chemistry
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Clinical Chemistry 53: 796-798, 2007; 10.1373/clinchem.2006.084350
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(Clinical Chemistry. 2007;53:796-798.)
© 2007 American Association for Clinical Chemistry, Inc.


Letters to the Editor

Epigenetic Analysis of RASSF1A Gene in Cell-Free DNA in Amniotic Fluid

Fiona M.F. Lun1,2, Rossa W.K. Chiu1,2, Tak Y. Leung3, Tse N. Leung3, Tze K. Lau3 and Y.M. Dennis Lo1,2,a

Departments of1 Chemical Pathology, and3 Obstetrics and Gynaecology
2 Centre for Research into, Circulating Fetal Nucleic Acids, Li Ka Shing, Institute of Health Sciences, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong SAR

aAddress correspondence to this author at: Department of Chemical Pathology, Room 38023, 1/F, Clinical Sciences Building, Prince of Wales Hospital, 30–32 Ngan Shing Street, Shatin, Hong Kong SAR. Fax +852-2194 -6171; e-mail loym@cuhk.edu.hk.

The first 20% of the full text of this article appears below.


To the Editor:

Cell-free fetal nucleic acids exist not only in the maternal circulation (1) but also in amniotic fluid samples (2). Evidence suggests that DNA in maternal plasma that bears the fetal genotype is predominantly derived from the placenta (3). Although the cells in amniotic fluid are widely known to have originated from fetal urogenital, respiratory, and alimentary tracts, skin and amnion, the origin of cell-free fetal DNA in amniotic fluid remains unclear (2). It has been speculated that the latter might originate from the same sources as amniotic fluid cells or the placenta (2). Here, we applied the recent developments in epigenetics to this area of research (4)(5).

The promoter of RASSF1A has been shown to be hypermethylated in the placenta but essentially unmethylated in maternal blood cells and other fetal tissues (4). Chan et al. (5) adopted hypermethylated RASSF1A as a placental-specific epigenetic marker and developed an assay . . . [Full Text of this Article]







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Copyright © 2007 by the American Association for Clinical Chemistry.