International Mammalian Genome Society

The 15th International Mouse Genome Conference (2001)


POSTER 36 - TESTICULAR GERM CELL TUMOR (TGCT) SUSCEPTIBILITY LOCI ON MOUSE CHR 19 CONTRIBUTE ADDITIVELY TOWARDS TUMOR DEVELOPMENT

Dr Angabin Matin
Case Western Reserve University
Dept. of Genetics, BRB 609b
School of Medicine
Cleveland OH 44106-4955
USA

Co-Authors: Youngren, Y, Nadeau, J.
Institutions: Case Western Reserve University

Males of the 129/Sv strain are predisposed towards developing TGCTs at a low frequency (~10%).  Genetic analysis indicates that TGCT predisposition is a complex polygenic trait.  The Ter mutation increases TGCT frequency to 17% in heterozygote (129/Sv-Ter/+) males.  To identify other TGCT predisposing loci we analysed progeny from a sensitized backcross with the 129/Sv-Ter/+ and MOLF/Ei strains.  A genome-wide scan of tumor-bearing males indicated that multiple loci on MOLF-derived Chr 19 increased TGCT incidence.  To verify this, a 129.MOLF-Chr 19 consomic strain (or Chromosome Substitution Strain) was made in which Chr 19 of the MOLF substituted for that of the 129 strain.  The Ter mutation was not included.  Eighty percent of the consomic males develop TGCT indicating that loci on MOLF Chr 19, in the context of the 129 background and even in the absence of Ter, strongly predispose to tumorigenesis.  To determine the number of MOLF-derived loci which contribute to tumorigenesis, we have derived a series of congenic strains from the consomic.   The tumor frequency of the males of the congenic lines indicate at least 3 regions on Chr 19 independently cause tumor development.  Moreover, congenics which carry multiple loci show additive effects with regard to tumor frequencies.  Thus, the use of sensitized crosses, consomic and congenic strains have been fruitful for identifying TGCT susceptibility loci.


Abstracts * Officers * Bylaws * Application Form * Meeting Calendar * Contact Information * Home * Resources * News and Views * Membership

Base url http://imgs.org
Last modified: Saturday, November 3, 2012