Skip to main content
Log in

The QM gene is X-linked and therefore not involved in suppression of tumorigenesis in Wilms' tumor

  • Short Communications
  • Published:
Human Genetics Aims and scope Submit manuscript

Summary

Inactivation of one or more tumor-suppressor genes on the short arm of chromosome 11 is thought to play a role in the etiology of Wilms' tumor. A candidate gene, QM, was recently isolated by subtractive hybridization between a tumorigenic cell line (deleted for part of 11p) and a non-tumorigenic cell line (the tumorigenic cell line carrying an extra t(X;11)copy). We show here with an exon-specific polymerase chain reaction that the genomic homolog of the QM cDNA is located in the G6PD-color vision genes region in Xq28. No homologous sequences could be detected on 11p. Our experiments indicate that the QM gene is not involved in the suppression of Wilms' tumor.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

References

  • Beckwith JB (1983) Wilms' tumor and other renal tumors of childhood: a selective review from the National Wilms' tumor study pathology center. Hum Pathol 14:481–492

    Google Scholar 

  • Dao DD, Schroeder WT, Chao L-Y, Kikuchi H, Strong LC, Riccardi VM, Pathak S, Nichols WW, Lewis WH, Saunders GF (1987) Genetic mechanisms of tumor-specific loss of 11p DNA sequences in Wilms' tumor. Am J Hum Genet 41:202–217

    Google Scholar 

  • Dowdy SF, Fasching CL, Araujo D, Lai K-M, Livanos E, Weissman BE, Stanbridge EJ (1991a) Suppression of tumorigenicity in Wilms' tumor by the p15.5-p14 region of chromosome 11. Science 254:293–295

    Google Scholar 

  • Dowdy SF, Lai K-M, Weissman BE, Matsui Y, Hogan BLM, Stanbridge EJ (1991b) The isolation and characterization of a novel cDNA demonstrating an altered mRNA level in non-tumorigenic Wilms' microcell hybrid cells. Nucleic Acids Res 19:5763–5769

    Google Scholar 

  • Glaser T, Housman D, Lewis WH, Gerhard D, Jones C (1989) A fine-structure deletion map of human chromsome 11p: analysis of J1 series hybrids. Somat Cell Mol Genet 15:477–501

    Google Scholar 

  • Hoovers JMN, Mannens M, John R, Bliek J, Heyningen V van, Porteous DJ, Leschot NJ, Westerveld A, Little PFR (1992) High-resolution localization of 69 potential human zinc finger protein genes: a number are clustered. Genomics 12:254–263

    Google Scholar 

  • Knudson AG, Strong LC (1972) Mutation and cancer: a model for Wilms' tumor of the kidney. J Natl Cancer Inst 48:313–324

    Google Scholar 

  • Maestrini E, Rivella S, Tribioli C, Rocchi M, Camerino G, Santachiara-Benerecetti S, Parolini O, Notarangelo LD, Toniolo D (1992) Identification of novel RFLPs in the vicintity of CpG islands in Xq28: application to the analysis of the pattern of X chromosome inactivation. Am J Hum Genet 50:156–163

    Google Scholar 

  • Mannens M, Slater RM, Heyting C, Bliek J, Kraker J de, Coad N, Pagter-Holthuizen P de, Pearson PL (1988) Molecular nature of genetic changes resulting in loss of heterozygosity of chromosome 11 in Wilms' tumours. Hum Genet 81:41–48

    Google Scholar 

  • Mannens M, Hoovers JMN, Bleeker-Wagemakers EM, Redeker E, Bliek J, Overbeeke-Melkert M, Saunders G, Williams B, Van Heyningen V, Junien C, Haber D, Speleman F, Heyting C, Slater RM, Leschot NJ, Westerveld A (1991) The distal region of 11p13 and associated genetic diseases. Genomics 11:284–293

    Google Scholar 

  • Moore JW, Hyman S, Antonarakis SE, Mules EH, Thomas GH (1986) Familial isolated aniridia associated with a translocation involving chromosomes 11 and 22 [t(11;22)(p13;q12.2)]. Hum Genet 72:297–302

    Google Scholar 

  • Porteous D, Wilkinson MM, Fletcher JM, Heyningen V van (1989) Human-mouse hybrids carrying fragments of single human chromosomes selected by tumor growth. Genomics 5:680–684

    Google Scholar 

  • Suthers GK, Hyland VJ, Callen DF, Oberle I, Rocchi M, Thomas NS, Morris' CP, Schwartz CE, Schmidt M, Ropers HH, Baker E, Oostra BA, Dahl N, Wilson PJ, Hopwood JJ, Sutherland GR (1990) Physical mapping of new DNA probes near the fragile X mutation (FRAXA) by using a panel of cell lines. Am J Hum Genet 47:187–195

    Google Scholar 

  • Traupe H, Ouweland AMW van den, Oost BA van, Vogel W. Vetter U, Warren ST, Rocchi M, Darlison MG, Ropers H-H (1992) Fine mapping of the human biglycan gene (proteoglycan 1) within the Xq28 region employing a hybrid cell panel. Genomics 13:481–483

    Google Scholar 

  • Van Heyningen V, Hastie ND (1992) Wilms' tumour: reconciling genetics and biology. Trends Genet 8:16–21

    Google Scholar 

  • Verkerk AJMH, Pieretti M, Sutcliffe JS, Fu Y-H, Kuhl DPA, Pizzuti A, Reiner O, Richards S, Victoria MF, Zhang F, Eussen BE, Ommen G-JB van, Blonden LAJ, Riggens GJ, Chastain JL, Kunst CB, Galjaard H, Caskey CT, Nelson DL, Oostra BA, Warren ST (1991) Identification of a gene (FMR-1) containing a CGG repeat coincident with a breakpoint cluster region exhibiting lenght variation in fragile X syndrome. Cell 65:905–914

    Google Scholar 

  • Warren ST, Knight SJL, Peters JF, Stayton CL, Consalez GG, Zhang F (1990) Isolation of the human chromosomal band Xq28 within somatic cell hybrids by fragile X site breakage. Proc Natl Acad Sci USA 871:3856–3860

    Google Scholar 

  • Wiedemann HR (1983) Tumours and hemihypertrophy associated with Wiedemann-Beckwith syndrome. Eur J Pediatr 141:129

    Google Scholar 

  • Weissman BE, Saxon PJ, Pasquale SR, Jones GR, Geiser AG, Stanbridge EJ (1987) Introduction of a normal human chromosome 11 into a Wilms' tumor cell line controls its tumorigenic expression. Science 236:175–180

    Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

van den Ouweland, A.M.W., Verdijk, M., Mannens, M.M.A.M. et al. The QM gene is X-linked and therefore not involved in suppression of tumorigenesis in Wilms' tumor. Hum Genet 90, 144–146 (1992). https://doi.org/10.1007/BF00210759

Download citation

  • Received:

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF00210759

Keywords

Navigation