A Quantitative Trait Locus in Major Histocompatibility Complex Determining Latent Period of Mouse Lymphomas

The effects of two host genes on retro virus‐induced murine lymphoma were evaluated by studying 114 F2 intercross mice between SL/Kh and AKR/Ms mice. Out of 47 T‐lymphoma‐bearing F2 mice, 45 had the AKR‐derived dominant allele at Tlsm‐1. The length of the lymphoma latent period was not related to type of tumor. Instead, it was significantly shortened by a recessive SL/Kh‐derived allele at a major histocompatibility complex (MHC)‐linked locus on Chr. 17. A quantitative trait analysis of the latent period yielded a maximal logarithm of likelihood ratio for linkage (LOD) score of 7.06 at a class II gene within MHC. The SL/Kh‐derived recessive gene was named lla (lymphoma latency acceleration).

[1]  A. Kawarai,et al.  T lymphomagenesis is determined by a dominant host gene thymic lymphoma susceptible mouse-1 (TLSM-1) in mouse models , 1994, The Journal of experimental medicine.

[2]  J. Crabbe,et al.  Genetic animal models of alcohol and drug abuse. , 1994, Science.

[3]  W. Vogel,et al.  Quantitative trait loci mapping of three loci controlling morphine preference using inbred mouse strains , 1994, Nature Genetics.

[4]  S. Toyokuni,et al.  Genetic predisposition to pre-B lymphomas in SL/Kh strain mice. , 1994, Cancer research.

[5]  T. Honjo,et al.  SL/KH strain of mice: a model of spontaneous pre-B-lymphomas. , 1993, Leukemia research.

[6]  B. Chesebro,et al.  Influence of MHC genes on spontaneous recovery from Friend retrovirus-induced leukemia. , 1992, Journal of immunology.

[7]  M. Melhem,et al.  Genetic control of susceptibility to diethylnitrosamine and dimethylbenzanthracene carcinogenesis in rats. , 1991, The American journal of pathology.

[8]  M. Zijlstra,et al.  Major histocompatibility complex class II-regulated immunity to murine leukemia virus protects against early T- but not late B-cell lymphomas , 1988, Journal of virology.

[9]  M. Daly,et al.  MAPMAKER: an interactive computer package for constructing primary genetic linkage maps of experimental and natural populations. , 1987, Genomics.

[10]  M. Zijlstra,et al.  THE H‐2 COMPLEX REGULATES BOTH THE SUSCEPTIBILITY TO MOUSE VIRAL LYMPHOMAGENESIS AND THE PHENOTYPE OF THE VIRUS‐INDUCED LYMPHOMAS , 1986, Journal of immunogenetics.

[11]  P. Debré,et al.  Genetic control of sensitivity to Moloney leukemia virus in mice. II. Mapping of three resistant genes within the H-2 complex. , 1979, Journal of immunology.

[12]  B. Chesebro,et al.  Rfv-1 and Rfv-2, two H-2-associated genes that influence recovery from Friend leukemia virus-induced splenomegaly. , 1978, Journal of immunology.

[13]  D. Meruelo,et al.  Genetic control of radiation leukemia virus-induced tumorigenesis. I. Role of the major murine histocompatibility complex, H-2 , 1977, The Journal of experimental medicine.

[14]  P. Lonai,et al.  Resistance genes to murine leukemia in the I immune response gene region of the H-2 complex , 1977, The Journal of experimental medicine.

[15]  F. Lilly,et al.  THE EFFECT OF HISTOCOMPATIBILITY-2 TYPE ON RESPONSE TO THE FRIEND LEUKEMIA VIRUS IN MICE , 1968, The Journal of experimental medicine.

[16]  N. Haran‐Ghera,et al.  Changes of H-2 antigen expression on thymocytes during leukemia development by radiation leukemia virus. , 1985, Leukemia research.

[17]  H. Hiai,et al.  Progression of mouse thymic leukemias in thymic microenvironments. , 1983, Princess Takamatsu symposia.