Gene imprinting in developmental toxicology: a possible interface between physiology and pathology

被引：51

作者：

McLachlan, JA

Burow, M

Chiang, TC

Li, SF

机构：

[1] Tulane Univ, Ctr Bioenvironm Res, Environm Endocrinol Lab, New Orleans, LA 70112 USA

[2] Xavier Univ, New Orleans, LA 70112 USA

[3] Tulane Univ, Hlth Sci Ctr, Dept Pharmacol, New Orleans, LA 70112 USA

来源：

TOXICOLOGY LETTERS | 2001年 / 120卷 / 1-3期

关键词：

developmental toxicology; gene imprinting; endocrine disruption; estrogen; methylation;

D O I：

10.1016/S0378-4274(01)00295-8

中图分类号：

R99 [毒物学（毒理学）];

学科分类号：

100405 ;

摘要：

Gene imprinting is an epigenetic mechanism for accomplishing persistent change in gene expression. In this brief paper, we explore the mechanisms for imprinting genes and present data showing that the synthetic estrogen, diethylstilbestrol (DES) can developmentally imprint genes by changing the pattern of DNA methylation. We further discuss the implications of this and other findings for non-mutagenic aspects of developmental toxicology, and suggest ways to use this concept in modifying in vitro screening for developmental toxicants. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.

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收藏

页码：161 / 164

页数：4

相关论文

共 20 条

[1] DIETHYLSTILBESTROL INDUCES NEOPLASTIC TRANSFORMATION WITHOUT MEASURABLE GENE MUTATION AT 2 LOCI [J].

BARRETT, JC ;

WONG, A ;

MCLACHLAN, JA .

SCIENCE, 1981, 212 (4501) :1402-1404

[2]

BUROW ME, 2000, UNPUB ESTROGEN RECEP

[3] Physicological coupling of growth factor and steroid receptor signaling pathways: Estrogen receptor knockout mice lack estrogen-like response to epidermal growth factor [J].

Curtis, SW ;

Washburn, T ;

Sewall, C ;

DiAugustine, R ;

Lindzey, J ;

Couse, JF ;

Korach, KS .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (22) :12626-12630

[4]

DEGEN GH, 1987, ARCH TOXICOL, P264

[5] High frequency of hypermethylation at the 14-3-3 σ locus leads to gene silencing in breast cancer [J].

Ferguson, AT ;

Evron, E ;

Umbricht, CB ;

Pandita, TK ;

Chan, TA ;

Hermeking, H ;

Marks, JR ;

Lambers, AR ;

Futreal, PA ;

Stampfer, MR ;

Sukumar, S .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (11) :6049-6054

[6]

HERTZ R, 1976, CANCER-AM CANCER SOC, V38, P534, DOI 10.1002/1097-0142(197607)38:1<534::AID-CNCR2820380177>3.0.CO

[7]

2-G

[8] COUPLING OF DUAL SIGNALING PATHWAYS - EPIDERMAL GROWTH-FACTOR ACTION INVOLVES THE ESTROGEN-RECEPTOR [J].

IGNARTROWBRIDGE, DM ;

NELSON, KG ;

BIDWELL, MC ;

CURTIS, SW ;

WASHBURN, TF ;

MCLACHLAN, JA ;

KORACH, KS .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (10) :4658-4662

[9] Genomic imprinting and cancer [J].

Jirtle, RL .

EXPERIMENTAL CELL RESEARCH, 1999, 248 (01) :18-24

[10] Expression of estrogen receptor and proto-oncogene messenger ribonucleic acids in reproductive tracts of neonatally diethylstilbestrol-exposed female mice with or without postpuberal estrogen administration [J].

Kamiya, K ;

Sato, T ;

Nishimura, N ;

Goto, Y ;

Kano, K ;

Iguchi, T .

EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES, 1996, 104 (02) :111-122