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Origin of rare Ha-ras alleles: relationship of VTR length to a 5′ polymorphic Xho I site

Published online by Cambridge University Press:  14 April 2009

Glenn D. Baxter ,
Nicholas K. Hayward ,
Russell J. Collins  and
Martin F. Lavin
Glenn D. Baxter
Affiliation:
Queensland Institute of Medical Research, Herston, Brisbane 4006., Australia
Nicholas K. Hayward
Affiliation:
Queensland Institute of Medical Research, Herston, Brisbane 4006., Australia
Russell J. Collins
Affiliation:
Division of Immunology, Department of Pathology, Royal Brisbane Hospital, Brisbane, 4006
Martin F. Lavin*
Affiliation:
Queensland Institute of Medical Research, Herston, Brisbane 4006., Australia
*
*Corresponding author.
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Amongst the four common Ha-ras alleles in both controls and cancer patients, we detected the presence of a polymorphic Xho I site associated specifically with the 6·6 and 7·7 kb Bam HI fragments but absent from the 7·1 and 8·2 kb alleles, as recently reported by others. We have extended this study and report here, the consistent appearance of this Xho I site in unusual alleles close in size to the two common alleles of 6·6 and 7·7 kb, in control lymphoblastoid DNA samples in a variety of tumor DNAs. Unusual alleles grouped around the 7·1 and 8·2 kb common alleles on the other hand, did not possess the Xho I site. The consistent presence of the Xho I site polymorphism, in the unusual Ha-ras alleles surrounding the 6·6 and 7·7 kb common alleles and its absence in alleles around the 7·1 and 8·2 kb common alleles, suggests that the unusual ones are derived from the corresponding common alleles to which they are closest in size.

Type
Research Article
Information
Genetics Research , Volume 54 , Issue 2 , October 1989 , pp. 149 - 153
Copyright
Copyright © Cambridge University Press 1989

References

Capon, D. J., Chen, E. Y., Levinson, A. D., Seeburg, P. H. & Goeddel, D. V. (1983). Complete nucleotide sequences of the T24 human bladder carcinoma oncogene and its normal homologue. Nature 302, 33–37.Google Scholar
Carter, G., Worwood, M. & Jacobs, A. (1988). The Ha-ras polymorphism in sporadic and familial myelodysplasia. Blood 70, Suppl. 1, 276a.Google Scholar
Ceccherini-Nelli, L., De Re, V., Veil, A., Molaro, G., Zilli, L., Clemente, L. & Boiocchi, M. (1987). Ha-ras restriction fragment length polymorphism and susceptibility to colon adenocarcinoma. British Journal of Canter 56, 1–5.Google Scholar
Chandler, L. A., Ghazi, H., Jones, P. A., Boukamp, P. & Fusenig, N. E. (1987). Allele specific methylation of the human c-Ha-ras-1 gene. Cell 50, 711–717.Google Scholar
Chang, E. H., Furth, M., Scolnick, E. & Lowy, D. (1982). Tumorigenic transformaton of mammalian cells induced by a normal human gene homologous to the oncogene of Harvey murine sarcoma virus. Nature 297, 479–483.Google Scholar
Cohen, J. B., Walter, M. V. & Levinson, A. D. (1987). A repetitive sequence element 3′ of the human c-Ha-ras-1 gene has enhancer activity. Journal of Cellular Physiology, Suppl. 5, 75–81.Google Scholar
Damante, G., Filetti, S. & Rapoport, B. (1987). Nucleotide sequence and characterization of the 5′ flanking region of the rat Ha-ras proto-oncogene. Proceedings of the National Academy of Science, U.S.A. 84, 774–778.Google Scholar
Der, C. J., Krontiris, T. G. & Cooper, G. M. (1982). Transforming genes of human bladder and lung carcinoma cell lines are homologous to the ras genes of Harvey and Kirsten sarcoma viruses. Proceedings of the National Academy of Science, U.S.A. 79, 3637–3640.Google Scholar
Eva, A., Tronick, S. R., Gol, R. A., Pierce, J. H. & Aaronson, S. A. (1983). Transforming genes of human hemopoietic tumors: frequent detection of ras related oncogenes whose activation appears to be independent of tumor phenotype. Proceedings of the National Academy of Science, U.S.A. 80, 4926–4938.Google Scholar
Gerhard, D. S., Dracopoli, N. C., Bale, S. J., Houghton, A. N., Watkins, P., Payne, C. E., Green, M. H. & Housman, D. E. (1987). Evidence against Ha-ras-1 involvement in sporadic and familial melanoma. Nature 325, 73–75.Google Scholar
Hand, P. H., Vilasi, V., Thor, A., Ohuchi, N. & Schlom, J. (1987). Quantitation of Harvey ras p21 enhanced expression in human breast and colon carcinomas. Journal of the National Cancer Institute 79, 59–65.Google Scholar
Hayward, N. K., Keegan, R., Nancarrow, D. J., Little, M. H., Smith, P. J., Gardiner, R. A., Seymour, G. J., Kidson, C. & Lavin, M. F. (1988). c-Ha-ras-1 alleles in bladder cancer, Wilms’ tumour and malignant melanoma. Human Genetics 18, 115–120.Google Scholar
Heighway, J., Thatcher, N., Cerny, T. & Haselton, P. S. (1986). Genetic predisposition to human lung cancer. British Journal of Cancer 53. 453–457.Google Scholar
Ishii, S., Merlino, G. T. & Pastan, I. (1985). Promoter region of the human Harvey ras proto-oncogene: similarity to the EGF receptor promoter. Science 230, 1378–1382.Google Scholar
Ishii, S., Nagase, T. & Imamoto, F. (1986). Second Annual Meeting on Oncogenes, pp. III. Hood College. Frederic. Maryland.Google Scholar
Ishikawa, J., Maeda, S., Takahashi, R., Kamidono, S. & Sugiyama, T. (1987). Lack of correlation between Ha-ras alleles and urothelial cancer in Japan. International Journal of Cancer 40, 474–478.Google Scholar
Jeffreys, A. J., Royle, N. J.. Wilson, V. & Wong, Z. (1988). Spontaneous mutation rates to new length alleles al tandem repetitive hypervariable loci in human DNA. Nature 332, 278–281.Google Scholar
Krontiris, T. G. & Cooper, G. M. (1981). Transforming activity of human tumor DNAs. Proceedings of the National Academy of Science, U.S.A. 78, 1181–1184.Google Scholar
Krontiris, T. G., DiMartino, N. A., Colb, M. & Parkinson, D. R. (1985). Unique allelic restriction fragments of the human Ha-ras locus in leukocyte and tumor DNAs of cancer patients. Nature 313, 369–374.Google Scholar
Krontiris, T. G., DiMartino, N. A., Colb, M., Mitcheson, H. D. & Parkinson, D. R. (1986). Human restriction fragment length polymorphisms and cancer risk assessment. Journal of Cellular Biochemistry 30, 319–329.Google Scholar
Lidereau, R., Escot, C., Theillet, C., Champeme, M. H., Brunet, M., Gest, J. & Callahan, R. (1986). High frequency of rare alleles of the human c-Ha-ras-1 proto-oncogene in breast cancer patients. Journal of the National Cancer Institute 11, 697–701.Google Scholar
Perucho, M., Goldfarb, M., Shimizu, K., Lama, C., Fogh, J. & Wigler, M. (1981). Human tumor derived cell lines contain common and different transforming genes. Cell 27, 467–476.Google Scholar
Rabinowe, S. N. & Krontiris, T. G. (1987). Enhancement of human c-Ha-ras-1 transcription by the downstream variable tandem repeat (VTR). Blood 68, Suppl. 1, 262a.Google Scholar
Radice, P., Pierotti, M. A., Borrello, M. G., Illeni, M. T., Rovini, D. & Delia Porta, G. (1987). HRAS1 protooncogene polymorphisms in human malignant melanoma: Taq I defined alleles significantly associated with the disease. Oncogene 2, 91–95.Google Scholar
Reddy, E. P., Reynolds, R. K., Santos, E. & Barbacid, M. (1982). A point mutation is responsible for the acquisition of transforming properties by the T24 human bladder carcinoma oncogene. Nature 300, 149–152.Google Scholar
Shih, C., Padhy, L. C., Murray, M. & Weinberg, R. A. (1981). Transforming genes of carcinomas and neuro-blastomas introduced into mouse fibroblasts. Nature 290, 261–264.Google Scholar
Shih, C. & Weinberg, R. A. (1982). Isolation of a transforming sequence from a human bladder carcinoma cell line. Cell 29, 161–169.Google Scholar
Shimizu, K., Birnbaum, D., Ruley, M. A., Fasano, O., Suard, Y., Edlund, L., Taparowsky, E., Goldfarb, M. & Wigler, M. (1983). Structure of the Ki-ras gene of the human lung carcinoma cell line Calu-1. Nature 304, 497–500.Google Scholar
Southern, E. M. (1975). Detection of specific sequences among DNA fragments separated by gel electrophoresis. Journal of Molecular Biology 98, 503–517.Google Scholar
Spandidos, D. A. & Ker, I. B. (1984). Elevated expression of the human ras oncongene family in premalignant and malignant tumors of the colorectum. British Journal of Cancer 49, 681–688.Google Scholar
Stacey, D. W. & Kung, H. F. (1984). Transformation of NIH 3T3 cells by microinjection of Ha-ras p21 protein. Nature 310, 508–511.Google Scholar
Tabin, C. J., Bradley, S. M., Bargmann, C. I., Weinberg, R. A., Papageorge, A. G., Scolnick, E. M., Dhar, R., Lowy, D. R. & Chang, E. H. (1982). Mechanism of activation of a human oncogene. Nature 300, 143–149.Google Scholar
Tanaka, T., Slamon, D. J., Battifora, H. & Cline, M. J. (1986). Expression of p21 ras oncoproteins in human cancers. Cancer Research 46, 1465–1470.Google Scholar
Thein, S. L., Oscier, D. G., Flint, J. & Wainscoat, J. S. (1986). Ha-ras hypervariable alleles in myelodysplasia. Nature 321, 84–85.Google Scholar
Weeks, D. P., Beerman, N. & Griffith, O. M. (1986), A small scale, five hour procedure for isolating multiple samples of CsCl purified DNA: application to isolations from mammalian, insect, higher plant, algal, yeast, and bacterial sources. Analytical Biochemistry 152, 376–385.Google Scholar
Yokota, J., Tsunetsugu-Yokota, Y., Battifora, H., Le Fevre, C. & Cline, M. J. (1986). Alterations of myc, myb, and Ha-ras proto-oncogenes in cancers are frequent and show clinical correlation. Science 231, 261–265.Google Scholar