Placental P-glycoprotein and breast cancer resistance protein: Influence of polymorphisms on fetal drug exposure and physiology

Hutson, J.R.; Koren, G.; Matthews, S.G.

doi:10.1016/j.placenta.2010.02.010

Cited by 45Drug Transport and Resistance MechanismsPharmacogenetics and Drug MetabolismPregnancy and Medication Impact

Placental P-glycoprotein and breast cancer resistance protein: Influence of polymorphisms on fetal drug exposure and physiology

Hutson, J.R., Koren, G., Matthews, S.G.·2010·Placenta

DOI 10.1016/j.placenta.2010.02.010

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Abstract

Recent studies have illustrated the importance of placental drug transport proteins, such as P-glycoprotein (Pgp) and breast cancer resistance protein (BCRP) in limiting fetal exposure to drugs and toxins. Moreover, increasing evidence supports a role for Pgp and BCRP in the normal development and physiological function of the placenta. Several single nucleotide polymorphisms (SNPs) in the genes encoding Pgp and BCRP have been described and are associated with altered protein expression, transporter activity, and clinical outcome in studies focusing on tissues other than the placenta. This review aims to summarize current research regarding the association between these polymorphisms and expression and function in the placenta. The influence of these genotypes on fetal drug exposure and altered placental physiology or development is also presented. To date, evidence suggests that SNPs in both ABCB1 and ABCG1 can alter expression of their respective protein; however, the functional significance of these polymorphisms is less clear. An understanding of this genotype-phenotype relationship will allow for prediction of susceptible or favorable genotypes in order to personalize medication choices to minimize fetal exposure to teratogens, or to maximize pharmacological therapy to the fetus.

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Perturbations of placental barrier function due to mechanical damage, polymorphisms, or environmental factors may lead to increased fetal exposure.
“Nonetheless, perturbations of this function due to mechanical damage, polymorphisms (267), or environmental factors (287), may lead to increased fetal exposure.”
From Placental Origins of Chronic Disease (2016) · cites this paper as [267]

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Pharmacogenetics of Drug-Induced Birth Defects: The Role of Polymorphisms of Placental Transporter Proteins
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Authors: Hutson, J. R., Koren, G., & Matthews, S. G.
Affiliations: University of Toronto (CA)
Corresponding author: Matthews, S.G.
ORCID: Hutson, J.R.
Koren, G.
Matthews, S.G.
Venue: Placenta
Publisher: Elsevier BV
Published: 2010-05
Volume: 31
Issue: 5
Pages: 351-357
ISSN: 0143-4004 (ISSN-L)
DOI: 10.1016/j.placenta.2010.02.010
OpenAlex: W2020220205
Cited by: 45
References: 85
Citations by year: 2026: 1 · 2025: 1 · 2024: 1 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2019: 5 · 2018: 2 · 2017: 1 · 2016: 6 · 2015: 2 · 2014: 6 · 2013: 6 · 2012: 5
FWCI: 2.50
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Placenta (publishedVersion)
PubMed (publishedVersion)
Funders: Canadian Institutes of Health Research
Topics: Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Pharmacogenetics and Drug Metabolism
Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Pregnancy and Medication Impact
Keywords: ABCG2, P-glycoprotein, ABCG1, single nucleotide polymorphisms, prenatal drug exposure, placental physiology, placental development, genotype-phenotype correlation, teratogens
MeSH terms: ATP Binding Cassette Transporter, Subfamily G, Member 2, Adult, Biological Transport, Female, Fetus, Genotype, Humans, Maternal-Fetal Exchange, Neoplasm Proteins, Placenta, Pregnancy, Xenobiotics, Drug Resistance, Multiple, ATP-Binding Cassette Transporters, ATP Binding Cassette Transporter, Subfamily B, Member 1, Polymorphism, Single Nucleotide

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Placental P-glycoprotein and breast cancer resistance protein: Influence of polymorphisms on fetal drug exposure and physiology

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