Aryl hydrocarbon hydroxylase induction levels in patients with malignant tumors associated with smoking

1984 ◽  
Vol 108 (3) ◽  
pp. 286-289 ◽  
Author(s):  
Rolf Korsgaard ◽  
Erik Trell ◽  
Bo G. Simonsson ◽  
G�ran Stiksa ◽  
Lars Janzon ◽  
...  
Keyword(s):  
Malignant Tumors ◽  
Aryl Hydrocarbon Hydroxylase ◽  
Aryl Hydrocarbon

scholarly journals The genetic basis of susceptibility to leukemia induction in mice by 3-methylcholanthrene applied percutaneously.

1978 ◽  
Vol 147 (2) ◽  
pp. 459-469 ◽  
Author(s):  
M L Duran-Reynals ◽  
F Lilly ◽  
A Bosch ◽  
K J Blank
Keyword(s):  
Genetic Basis ◽  
Tumor Response ◽  
Malignant Tumors ◽  
Skin Tumors ◽  
Skin Tumor ◽  
Aryl Hydrocarbon Hydroxylase ◽  
Aryl Hydrocarbon ◽  
High Incidence ◽  
High Level ◽  
Skin Painting

Susceptibility to leukemia induction in mice by skin painting with 3-methylcholanthrene (MCA) is strain-specific, occurring only in strains relatively resistant to MCA-induced skin tumors. The Ah locus, which has a dominant allele (Ahb) for inducibility of the aryl hydrocarbon hydroxylase (AHH) enzyme system and a recessive allele (Ahd) for noninducibility, appears to be the major determinant of this trait. MCA-painted mice of strains and crosses carrying the Ahb allele usually show a high incidence of skin tumors (papillomas which may evolve into malignant tumors) and little or no leukemia, whereas in mice homozygous for the Ahd allele the treatment usually induces a high incidence of leukemia and few or no skin tumors. Among mice of a segregating backcross generation including both Ahb/Ahd heterozygotes and Ahd homozygotes, the occurrence of skin tumors was correlated directly with AHH inducibility and inversely with the leukemic response. Mice of Ahb strains with a high level of endogenous murine leukemia (MuLV) expression (C58, PL) show a much weaker skin tumor response than expected but no increase in leukemia incidence, and this observation tends to confirm the previous finding that MuLV infection of mice of low-MuLV strains results in reduced susceptibility to MCA tumorigenesis.

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