NDLI: Loss of the transmembrane but not the soluble Kit ligand isoform increases testicular germ cell tumor susceptibility in mice

Content Provider	PubMed Central
Author	Heaney, Jason D. Lam, Man-yee J. Michelson, Megan V. Nadeau, Joseph H.
Abstract	Several genetic variants act as modifiers of testicular germ cell tumor (TGCT) susceptibility in the 129/Sv mouse model of human pediatric TGCTs. One such modifier, the Steel locus, encodes the transmembrane-bound and soluble ligand of the kit receptor. Some (Sl and SlJ) but not all (Sld) mutations of the Steel locus increase TGCT incidence in heterozygous mutant mice. Because Sl and SlJ are large deletions that affect multiple transcripts and Sld is an intragenic deletion of the kit ligand (Kitl) from which only the soluble protein is produced, it was uncertain whether Kitl or a neighboring gene is a modifier of TGCT susceptibility. We tested the effect of the small Steel grizzle-belly (Slgb) deletion on TGCT susceptibility to determine whether Kitl is a TGCT modifier gene. An increase in TGCT incidence was observed in Slgb/+ heterozygotes and fine-mapping of the deletion breakpoints revealed that Kitl is the only conventional gene deleted by the mutation, suggesting that Kitl is the TGCT modifier gene at the Steel locus. Additionally, we propose that soluble KITL in Sld/+ heterozygous mutant mice complements a dosage effect of transmembrane-associated KITL on TGCT susceptibility and that the kit receptor (Kit) is haplosufficient for primordial germ cell (PGC) development.
Related Links	http://dx.doi.org/10.1158/0008-5472.can-08-0779
Ending Page	5197
Page Count	5
Starting Page	5193
File Format	PDF
ISSN	00085472
e-ISSN	15387445
Journal	Cancer research
Issue Number	13
Volume Number	68
Language	English
Publisher Date	2008-07-01
Access Restriction	Open
Subject Keyword	Cancer Research Oncology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cancer Research Oncology

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