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Publication : Mouse proto-oncogene assignments (Abstracts of meeting presentations: Human gene mapping 7, Los Angeles Conference (1983) Seventh International Workshop on Human Gene Mapping)

First Author  Sakaguchi AY Year  1984
Journal  Cytogenet Cell Genet Volume  37 (1-4)
Pages  573-574 (Abstr.) (399-616) Mgi Jnum  J:4793
Mgi Id  MGI:53275 Citation  Sakaguchi AY, et al. (1984) Mouse proto-oncogene assignments (Abstracts of meeting presentations: Human gene mapping 7, Los Angeles Conference (1983) Seventh International Workshop on Human Gene Mapping). Cytogenet Cell Genet 37 (1-4):573-574 (Abstr.) (399-616)
abstractText  Abstracts of meeting pesentations. PAGE 573. Mouse proto-oncogene assignments. A.Y. Sakaguchi,1 P.A. Lalley,2 B.U. Zabel, l R. Ellis, 3 E. Scolnick, 3 and S.L. Naylor1. 1Roswell Park Memorial Institute, Buffalo, NY, 2 Oak Ridge National Laboratory, Oak Ridge, TN, and 3Merck, Sharp & Dohme Research Laboratories, West Point, PA. The mouse possesses normal cellular genes (proto-oncogenes) homologous with acutely transforming retrovirus oncogenes. This genetic kinship has fostered speculation of possible roles of proto-oncogenes in malignant transformation of cells, and prompted their chromosomal assignment. Mouse c-abl and c-mos have been assigned to chromosomes 2 and 4, respectively, by others. We have assigned six additional mouse proto-oncogenes using DNAs of 15 mouse-Chinese hamster somatic cell hybrids which were screened with 32p-labeled viral oncogenes probes (from J.M. Bishop) as described (Sakaguchi et al., Somat. Cell Genet. 9: 391, 1983; Sakaguchi et al., Human proto-oncogene assignments, this Workshop). We assigned a mouse c-src gene to chromosome 2, c-Ki-ras to 6, c-Ha-ras to 7, c-myb to 10, c-erb-a to 11, and c-myc to 15. Mouse c-src, c-Ki-ras, and c-Ha-ras appear to reside in conserved linkage groups in mouse and man; for example, c-src on human chromosome 20 (with ADA and ITP), c-Ki-ras2 on l2p (with TPI and GAPD), and c-Ha-ras on l l p (with INS, HBB, and LDHA). Hayata et al. (Cancer Res. 43: 367, 1983) have reported a deletion commonly encompassing bands C-D of chromosome 2 in 94% of myeloid leukemias. Whether these deletions affect the c-src gene is not presently known. Rearrangements of mouse c-myb and altered c-myb mRNA transcripts have been observed by others in mouse plasmacytoid lymphosarcomas (Mushinski et al., Science 220: 795, 1983). Whether the alterations in c-myb arise by intra- or inter-chromosomal events is not known. These assignments should be useful in assessing the significance of chromosome rearrangements in marine neoplasms.
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