Localization of the human HF.10 finger gene on a chromosome region (3p21–22) frequently deleted in human cancers
✍ Scribed by Emilio Donti; Luisa Lanfrancone; Kay Huebner; Anna Pascucci; Giovanna Venti; Gina Pengue; Fausto Grignani; Carlo M. Croce; Luigi Lania; Pier Giuseppe Pelicci
- Publisher
- Springer
- Year
- 1990
- Tongue
- English
- Weight
- 642 KB
- Volume
- 84
- Category
- Article
- ISSN
- 0340-6717
No coin nor oath required. For personal study only.
✦ Synopsis
The finger motif is a tandemly repeated DNA-binding domain recently identified in the primary structure of several eukaryotic transcriptional regulatory proteins. It has been proposed that some members of the finger-gene family are implicated in both normal cell proliferation and differentiation. We isolated several human finger genes by means of hybridization with a finger motif-containing DNA probe. One of these finger genes, HF.10, is expressed at low levels in a variety of human tissues and is down-regulated during the in vitro terminal differentiation of human leukemic myeloid cell lines. By in situ hybridization experiments and analysis of interspecific somatic cell hybrids we mapped the HF. 10 gene to 3p21-22, a chromosome region frequently involved in karyotypic rearrangements associated with lung and renal cancer.
📜 SIMILAR VOLUMES
To isolate a putative tumor suppressor gene(+ we have constructed a physical map and a detailed deletion map of chromosome region 8p2 I .3-p22, where loss of heterozygosity (LOH) has been frequently seen in human hepatocellular carcinomas (HCC), colorectal cancers (CRC), and non-small cell lung canc
Human prostate cancers frequently show loss of heterozygosity at loci on the short arm of chromosome 8. In order t o take a step toward isolation of the putative tumor suppressor gene(s) on 8p via positional cloning, we performed high-resolution deletion mapping in 46 prostate cancers (stage B, 20 c
Genetic studies of chromosome arm 9p have indicated the presence of one or more tumor suppressor genes involved in genetic susceptibility to various types of human cancers. To define the extent of the specific deletion of 9p2 1-22 in human breast cancer, we have analyzed loss of heterozygosity and h