By Jeffery C. Hall
Advances in Genetics raises its specialize in smooth human genetics and its relation to medication with the merger of this long-standing serial with Molecular Genetic medication . This merger affirms theAcademic Press dedication to submit very important stories of the broadest curiosity to geneticists and their colleagues in affiliated disciplines.
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Tumor Suppressor Genes Implicated in Sporadic Cancers 94 C. Mechanisms of Disrupting Tumor Suppressor Function in Human Cancers Advances in Genetics, Val. OO 94 45 46 Melissa A. Brown IV. Conclusions References 105 107 Ideas contributing to our understanding of tumorigenic mechanisms date from the 1700s, when early records of cancer families suggested that cancer was a genetic disease. Most of our present knowledge, however, is built on the contributions of researchers in this century (reviewed in Witkowski, 1990).
Mice deficient in the gene for connexin32 show pathological changes in peripheral nerves. 5th Annu. Eur. , London, 1996. , Lensch, M. , Hanemann, C. , Muller, H. , Bird, T. , and Chance, P. F. (1992). 2associated with Charcot-Marie-Tooth 1A. Nat. Genet. 1:176-179. McAlpine, P. , Hahn. A. , Kaita, H.. , Cox, D. , and Yee, W. C. (1990). Localisation of a locus for Charcot-Marie-Tooth neuropathy type la (CMTlA) to chromosome 17. Genomics 7:408-415. Milks, L. , Kumar, N. , and Gilula, N. B. (1988).
And Werner, R. (1988). Structure of a gap junction gene: Rat connexin32. Biosci. Rep. 8:455-464. Mostacciuolo, M. , Micaglio, G . , and Danieli, G. A. (1991). X-linked Charcot-Marie-Toothdisease. A linkage study in a large family by using 12 probes of the pericentromeric region. Hum. Genet. 87:23-27. ,and van Broeckhoven, C . (1994a). Linkage and mutation analysis in an extended family with Charcot-Marie-Tooth neuropathy type 1B. J. Med. Genet. 3:811-815. , and van Broeckhoven, C. Identification of a 5’ splice site mutation in the PMP-22 gene in autosoinal dominant Charcot-Marie-Tooth disease type 1.