Bardenheuer W, Szymanski S, Lux A, Lüdecke H J, Horsthemke B, Claussen U, Senger G, Smith D I, Wang N D, LePaslier D
Department of Medical Oncology (Cancer Research), University of Essen Medical School, Federal Republic of Germany.
Genomics. 1994 Jan 15;19(2):291-7. doi: 10.1006/geno.1994.1060.
Structural alterations in human chromosome region 3p14-p23 resulting in the inactivation of one or more tumor suppressor genes are thought to play a pathogenic role in small cell lung cancer, renal cell carcinoma, and other human neoplasms. To identify putative tumor suppressor genes, 428 recombinant clones from a microdissection library specific for human chromosome region 3p14 were isolated and characterized. Ninety-six of these (22.5%) were human single-copy DNA sequences, 57 of which were unique sequence clones. Forty-four of these were mapped to the microdissected region using a cell hybrid mapping panel. Within this mapping panel, four probes detected two new chromosome breakpoints that were previously indistinguishable from the translocation breakpoint t(3;8) in 3p14.2 in hereditary renal cell carcinoma. One probe maps to the homozygously deleted region of the small cell lung cancer cell line U2020. In addition, microdissection clones have been shown to be suitable for isolation of yeast artificial chromosomes.
