Summary To establish whether loss of heterozygosity (LOH) for chromosome 16q in Wilms' tumours confers an adverse prognosis, DNA from 40 Wilms' tumour/normal pairs were analysed using highly polymorphic microsatellite markers along the length of 1 6q. Fifteen per cent of tumours showed LOH for 16q. Although the common region of allele loss spanned the 16q24-qter region, a second distinct region of LOH was identified in 16q21. (Coppes et al. 1992: Maw et al. 1992: Grundy et al. 1994: Austruy et al. 1995: Redeker et al 1996. Using a panel of informative markers for the region 16ql2.2-qter. Maw et al (1992) were the first to demonstrate LOH for 16q in 9 (20%c) of 45 informatiVe patients by Southem blot analysis. A larger follow--on study. as part of NWTS4. involving 232 patients. found a similar frequency of LOH at 17%7. but used only polymorphic markers that mapped to the distal 16q22-qter region (Grundv et al. 1994). In the study by Coppes et al (1992). using only two polymorphic markers mapping to 16q22.2 and 16q24.3. LOH was identified in 20% of tumours. The most recent studv. albeit in a relatively small group of patients (Austruy et al. 1995). found the highest level of LOH (25%7c) using a large panel of restriction length polymorphisms and microsatellite probes. Furthermore. LOH for 16q has been associated with a worse outcome because these patients have a relapse rate 3.3 times higher than those with tumours retaining heterozygosity for 16q (Grundy et al 1994).Because cytogenetic and molecular studies of Wilms' tumours clearly suggest a role for grenes on 16q in the molecular pathology of this tumour. we have undertaken LOH analysis for 16q markers using a large. well-characterized series of sporadic Wilms' tumours. Our results clearly show that LOH is relatively frequent in Wilms' tumours. especially in patients with an adverse outcome.
MATERIALS AND METHODSDNA was prepared from tumour tissue and lymphocNies using standard phenol-chloroform extraction procedures described by Wadey et al (1990). The optimal polymerase chain reaction (PCR) conditions
The growth factor independent 1 (GFI1) gene encodes a zinc finger protein which acts as a transcriptional repressor and confers growth factor independence on tumor cells, as suggested by the study of its mouse ortholog, Gfi1. We previously isolated the human GFI1 gene but no information about the structure and location of the promotor of this gene has been reported. In this study we have cloned and characterized the human GFI1 promoter. The nucleotide sequence of the promoter region is GC‐rich and does not contain a typical TATA or CAAT box. Several Sp1 sites are present and computer predictions indicate that either of the two Sp1 sites might serve as the sites for transcription initiation. Analysis of various lengths of the promoter region using the luciferase reporter assay identifies a functional promoter that is active in NIH3T3 cells. The strongest activity lies within a region 312–602 basepairs upstream from the translation start site.
We have recently isolated a cloned cDNA coding for a cytochrome P-450 of human liver microsomal membranes, which corresponds to a major phenobarbital-inducible cytochrome P-450 of rat liver. This human cytochrome P-450 is encoded by a member of a multigene family. DNA extracted from a panel of 12 independent human-rodent somatic cell hybrids was analysed by Southern blot hybridization with the cloned cDNA. The results indicate that all components of this cytochrome P-450 gene family are located on chromosome 19. Evidence from hybrids derived from an individual carrying a balanced translocation suggests a regional localization of 19p13.2----qter. Analysis of human metaphase chromosomes by in situ hybridization localizes this cytochrome P-450 gene family further to the long arm of chromosome 19 in the region q13.1----qter. We propose the designation P450PB for this locus.
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