FRA7G is an aphidicolin-inducible common fragile site at human chromosomal band 7q31.2. This region is frequently altered in a number of dierent tumor types including prostate, breast, and ovarian cancer. It has also been hypothesized that this region contains an important tumor suppressor gene which is mutated during the development of these cancers or an oncogene which is ampli®ed. We previously used a FISH-based approach to isolate YAC clones which spanned FRA7G. In this report, we describe the isolation and restriction endonuclease mapping of three overlapping P1 clones which cover FRA7G and the region frequently altered in the dierent cancers. FISH-based analysis of these clones reveals that aphidicolin-induced breakage in the FRA7G region occurs over a region of at least 300 Kb in length. We have also localized a previously sequenced BAC clone to this region. The sequence obtained from this clone reveals the presence of an endogenous retroviral sequence (HERV-H) in the midst of the FRA7G region as well as sequences with homology to small polydispersed circular DNAs (spcDNAs). Thus for the ®rst two cloned common fragile sites, FRA7G and FRA3B, there is an association with both spcDNAs and hot-spots for viral integration.

Plasma levels of Aspartate aminotransferase (AST), a liver enzyme, are elevated in patients with visceral obesity. The purpose of this study was to examine if adipocyte volume is under the influence of genetic factors and to evaluate its genetic correlations with AST. Fasting plasma of 374 pedigreed baboons from the Southwest National Primate Research Center at the Southwest Foundation for Biomedical Research, San Antonio, TX were assayed for AST. Adipocyte volume was measured using biopsies of omental adipose tissue. Adipocyte volume, body weight and plasma AST were heritable. Genetic correlations between the measured adiposity -related phenotypes and AST were significant. A QTL (LOD score of 3.2) for adipocyte volume was identified on the baboon homologue of human chromosome 6 near marker D6S1028. These results suggest that omental adipocyte volume is under genetic regulation and that shared genetic factors influence adiposity associated traits and AST.

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