Congenic rats with higher arylamine N-acetyltransferase 2 activity exhibit greater carcinogen-induced mammary tumor susceptibility independent of carcinogen metabolism

Author:

Stepp Marcus W.,Doll Mark A.,Samuelson David J.,Sanders Mary Ann G.,States J. Christopher,Hein David W.

Funder

National Cancer Institute

National Institute of Environmental Health Sciences

Publisher

Springer Science and Business Media LLC

Subject

Cancer Research,Genetics,Oncology

Reference58 articles.

1. Hein DW, Doll MA, Fretland AJ, Leff MA, Webb SJ, Xiao GH, Devanoboyina US, Nangju NA, Feng Y. Molecular genetics and epidemiology of the NAT1 and NAT2 acetylation polymorphisms. Cancer Epidemiol Biomark Prev. 2000;9(1):29–42.

2. Boukouvala S, Sim E. Structural analysis of the genes for human arylamine N-acetyltransferases and characterisation of alternative transcripts. Basic Clin Pharmacol Toxicol. 2005;96(5):343–51.

3. Pacifici GM, Bencini C, Rane A. Acetyltransferase in humans - development and tissue distribution. Pharmacology. 1986;32(5):283–91.

4. Millner LM, Doll MA, Cai J, States JC, Hein DW. Phenotype of the most common “slow acetylator” arylamine N-acetyltransferase 1 genetic variant (NAT1*14B) is substrate-dependent. Drug Metab Dispos. 2011;40(1):198–204.

5. Adam PJ, Berry J, Loader JA, Tyson KL, Craggs G, Smith P, De Belin J, Steers G, Pezzella F, Sachsenmeir KF, et al. Arylamine N-Acetyltransferase-1 is highly expressed in breast cancers and conveys enhanced growth and resistance to etoposide in vitro. Mol Cancer Res. 2003;1(11):826–35.

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