Hypermethylation of RASSF1A in Human and Rhesus Placentas

Chiu, Rossa W.̉K.; Chim, Stephen S.C.; Wong, Ivy; Wong, Ching On; Lee, Wing Shan; To, Ka Fai; Tong, Joanna H.M.; Yuen, Ryan K.C.; Shum, Alisa S.W.; Chan, John; Chan, Lisa; Yuen, Jessie W.F.; Yu, Tong; Weier, Jingly F.; Ferlatte, Christy; Leung, Tse Ngong; Lau, Tze Kin; Lo, Kwok Wai; Lo, Y.M. Dennis

doi:10.2353/ajpath.2007.060641

Cited by 130 publications

(105 citation statements)

References 42 publications

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“…Conversely, RASSF1 methylation is not maintained in CVC. Chiu et al 20 analyzed the RASSF1 methylation profile in CVF by a semi-quantitative approach and found it to be hypermethylated compared to fetal tissues. Here, we confirmed this observation in CVF.…”

Section: Discussionmentioning

confidence: 99%

Beckwith–Wiedemann syndrome prenatal diagnosis by methylation analysis in chorionic villi

et al. 2015

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Beckwith-Wiedemann syndrome (BWS) is an imprinting disorder that can be prenatally suspected or diagnosed based on established clinical guidelines. Molecular confirmation is commonly performed on amniocytes. The possibility to use fresh (CVF) and cultured (CVC) chorionic villi has never been investigated. To verify whether CVF and CVC are reliable sources of DNA to study fetal methylation, we used pyrosequencing to test the methylation level of a number of differentially methylated regions (DMRs) at several imprinted loci (ICR1, ICR2, H19, PWS/AS-ICR, GNASXL, GNAS1A, ZAC/PLAGL1, and MEST) and at non-imprinted MGMT and RASSF1A promoters. We analyzed these regions in 19 healthy pregnancies and highlighted stable methylation levels between CVF and CVC at ICR1, ICR2, GNASXL, PWS/AS-ICR, and MEST. Conversely, the methylation levels at H19 promoter, GNAS1A and ZAC/PLAGL1 were different in CVC compared to fresh CV. We also investigated ICR1 and ICR2 methylation level of CVF/CVC of 2 BWS-suspected fetuses (P1 and P2). P1 showed ICR2 hypomethylation, P2 showed normal methylation at both ICR1 and ICR2. Our findings, although limited to one case of BWS fetus with an imprinting defect, can suggest that ICR1 and ICR2, but not H19, could be reliable targets for prenatal BWS diagnosis by methylation test in CVF and CVC. In addition, PWS/AS-ICR, GNASXL, and MEST, but not GNAS1A and ZAC/PLAGL1, are steadily hemimethylated in CV from healthy pregnancies, independently from culture. Thus, prenatal investigation of genomic imprinting in CV needs to be validated in a locus-specific manner.

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Section: Discussionmentioning

confidence: 99%

Beckwith–Wiedemann syndrome prenatal diagnosis by methylation analysis in chorionic villi

et al. 2015

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“…26,27 Some of these same promoter regions have also been reported to be methylated in placenta. [19][20][21]28 On the other hand, most normal tissues exhibit low methylation in these genomic regions, suggesting some molecular methylation signatures of tumor suppressor genes are shared by tumors and placenta. If this epigenetic signature is driven by the placental cell type with invasive behavior, it would be expected that methylation of tumor suppressor genes in cytotrophoblasts should be higher than in fibroblasts.…”

Section: ©2 0 1 1 L a N D E S B I O S C I E N C E D O N O T D I S Tmentioning

confidence: 99%

“…Table 1 presents an annotated list of the probes and Figure 5 shows their methylation levels in cytotrophoblasts and fibroblasts for the genes represented by multiple probes. Two genes, APC 19,20 and RASSF1, 21 have been previously reported to exhibit unique methylation patterns in placentas and in cancer. Others not previously reported (TP73, RASSF5, DAB2IP, PRKCDBP, MORF4L1) are also shown by our data to have probes in the promoter region that are more methylated in (Fig.…”

Section: O N O T D I S T R I B U T Ementioning

confidence: 99%

Cell specific patterns of methylation in the human placenta

Grigoriu¹,

Ferreira²,

Choufani³

et al. 2011

Epigenetics

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“…The location of SERPINB5 on chromosome 18 has also provided a valuable opportunity to test the application of this epigenetic approach for the prenatal detection of fetal chromosomal aneuploidy, using trisomy 18 as a model system (see later sections) (20 ). Since the development of the SERPINB5 marker, many other fetal epigenetic markers suitable for detection in maternal plasma have been described, including the RASSF1A gene on chromosome 3 (21,22 ) and numerous markers on chromosome 21 (23,24 ). Through the targeting of such fetus-specific DNA methylation markers in maternal plasma, the detected signal is virtually completely fetal in origin.…”

Section: Molecular Enrichment Strategies: Fetal Epigenetic Markers Anmentioning

confidence: 99%

Noninvasive Prenatal Diagnosis of Fetal Chromosomal Aneuploidies by Maternal Plasma Nucleic Acid Analysis

Lo¹,

Chiu

2008

Clinical Chemistry

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BACKGROUND:The discovery of circulating cell-free fetal nucleic acids in maternal plasma has opened up new possibilities for noninvasive prenatal diagnosis. The potential application of this technology for the noninvasive prenatal detection of fetal chromosomal aneuploidies is an aspect of this field that is being actively investigated. The main challenge of work in this area is the fact that cell-free fetal nucleic acids represent only a minor fraction of the total nucleic acids in maternal plasma.

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Hypermethylation of RASSF1A in Human and Rhesus Placentas

Cited by 130 publications

References 42 publications

Beckwith–Wiedemann syndrome prenatal diagnosis by methylation analysis in chorionic villi

Beckwith–Wiedemann syndrome prenatal diagnosis by methylation analysis in chorionic villi

Cell specific patterns of methylation in the human placenta

Noninvasive Prenatal Diagnosis of Fetal Chromosomal Aneuploidies by Maternal Plasma Nucleic Acid Analysis

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