Localization of the human aryl hydrocarbon hydroxylase gene to the 2q31→2pter region of chromosome 2

Ocraft, Kevin; Muskett, J. M.; Brown, S.

doi:10.1111/j.1469-1809.1985.tb01697.x

Cited by 11 publications

(4 citation statements)

References 6 publications

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“…It is possible that the locus on 2 is a receptor or a regulatory locus but in view of the lack of evidence the designation AHH has been left unchanged. Recent work has supported the original assignment and localized AHH to 2pter-2q31 (Ocraft et al 1985).…”

Section: Confirmations and Regional Localizationmentioning

confidence: 89%

“…The gene symbols are given at the top of the figure; the references are given by the numbers at the bottom. Davis et al (1983); (16) Rabin et al (1984); (17) Popescu et al (1985); (18) Francke et al (1983); (19) Cook and Hamerton (HGM6); (20) Cousineau et al (1984); (21) Kao et al (1984); (22) Bock et al (1985); (23 Lackner et al (1984); (27) Knott et al (1984); (28) (1) Kanda et al (1983); (2) Kohl et al (1983); (3) Schwab et al (1984) ; (4) (23) Sukhatme et al (1985); (24) Ocraft et al (1985). …”

Section: Note For All Chromosome Diagramsmentioning

confidence: 99%

See 1 more Smart Citation

Report of the committee on the genetic constitution of chromosomes 1 and 2

Povey¹,

Morton²,

Sherman³

1985

Cytogenet Genome Res

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Section: Confirmations and Regional Localizationmentioning

confidence: 89%

Section: Note For All Chromosome Diagramsmentioning

confidence: 99%

Report of the committee on the genetic constitution of chromosomes 1 and 2

Povey¹,

Morton²,

Sherman³

1985

Cytogenet Genome Res

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“…Human studies Cell culture experiments in humans have identified the regulatory Ah locus and assigned it to chromosome 2 (Wiebel et al, 1981;Ocraft et al, 1985). Amsbaugh et al (1986) have isolated the human PI-450 structural locus.…”

Section: Phase II Conjugationmentioning

confidence: 99%

Genetic predisposition to lung cancer

1990

Br J Cancer

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In Britain, the life-time risk of lung cancer in men who smoke 20 or more cigarettes per day is about 15%. That most smokers never develop lung cancer has promoted interest in the role of host factors. While chance, other environmental factors and the competing effect of other diseases, some of which are also smoking related, are all likely to affect individual lung cancer risk, genetic factors may also be important. This review examines the evidence for genetic predisposition to smoking related lung cancer.The review concentrates on the numerous metabolic studies that have sought differences between individuals in the genetic control of biochemical pathways that could be involved in the metabolism of carcinogens in tobacco smoke. Insights gained are likely to have wider implications for other environmental carcinogens. Other studies that have sought simple evidence, such as familial clustering or associations of lung cancer with blood group, HLA and other naturally occurring antigens, are also examined. The field of chromosomal abnormalities in lung cancer and the difficulties in interpreting them is reviewed only briefly, since this area may not directly relate to tobacco smoking and has been reviewed elsewhere (Birrer & Minna, 1988). Various sources of bias important in the interpretation of the metabolic studies in particular are outlined. Future research is likely to be dominated by the recent advances in molecular genetics that offer the possibility of circumventing bias by the direct identification of genes, but at present this is possible only to a limited extent. Familial clustering of lung cancer casesFamilial clustering of a cancer (or indeed of any disease) is an insensitive indicator of genetic predisposition. Peto (1980) and Bodmer (1986) have pointed out that a cancer can have a major genetic component yet show no detectable familial clustering. The ratio of the incidence of the cancer in relatives of known cases to that in age-matched controls is the only measure of familial clustering (in the absence of a marker). This ratio will be much smaller than the ratio of the incidence in genetically susceptible to non-susceptible individuals, which is the direct measure of the magnitude of the genetic effect. It is a question of dilution -not all patients with cancer will be genetically susceptible individuals, fewer of their relatives will be, and tne general population contains susceptibles as well as non-susceptibles. (1980) showed that even with a very large cancer risk in susceptibles, the incidence of cancer in relatives will generally be increased by no more than 1.5-3-fold. It is difficult in a family study to show that such a modest increase could not be due to chance, shared exposure or other bias.Five studies have examined lung cancer incidence in relatives of cases, but three (Tokuhata & Lilienfeld, 1963b;

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“…Previously described somatic cell fusion studies indicated that the presence of human chromosome 2pter->q22 was required for the AHH inducibility in Balb/cd mouse RAG cells (Brown et al, 1976;Ocraft et al, 1985;Wiebel et al, 1981). Since these initial reports, a number of genes known to play a role in the regulation of AHH activity have been localized, but none of them map to human chromosome 2.…”

Section: Discussionmentioning

confidence: 99%

Chromosomal localization of the human AHR locus encoding the structural gene for the Ah receptor to 7p21→p15

Beau

Carver

Espinosa

et al. 1994

Cytogenet Genome Res

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The AHR locus encodes the structural gene for the Ah receptor, a ligand activated transcription factor that regulates the expression of a number of enzymes involved in the metabolism of chemical carcinogens and that appears to mediate the tumor promoting properties of compounds such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Using polymerase chain reaction (PCR), we amplified exon-10 and intron-D of the AHR gene from human genomic DNA. By using PCR analysis of somatic cell hybrids and fluorescence in situ hybridization of metaphase cells, we localized AHR to human chromosome 7, bands p21→pl5. This mapping data should prove useful in determining the role that the AHR locus plays in human cancer incidence and in the identification of human populations with altered susceptibilities to the toxic/carcinogenic effects of planar aromatic hydrocarbons.

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Localization of the human aryl hydrocarbon hydroxylase gene to the 2q31→2pter region of chromosome 2

Cited by 11 publications

References 6 publications

Report of the committee on the genetic constitution of chromosomes 1 and 2

Report of the committee on the genetic constitution of chromosomes 1 and 2

Genetic predisposition to lung cancer

Chromosomal localization of the human AHR locus encoding the structural gene for the Ah receptor to 7p21→p15

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