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Suggestive evidence for a site specific prostate cancer gene on chromosome 1p36
  1. MICHAEL BADZIOCH*,218,
  2. ROS EELES,
  3. GILLES LEBLANC,
  4. WILLIAM D FOULKES§,
  5. GRAHAM GILES,
  6. STEVE EDWARDS,
  7. DAVID GOLDGAR*,
  8. JOHN L HOPPER**,
  9. D T BISHOP164,
  10. PAL MØLLER,
  11. KETIL HEIMDAL,
  12. DOUGLAS EASTON§§,
  13. THE CRC/BPG UK FAMILIAL PROSTATE CANCER STUDY COORDINATORS AND COLLABORATORS¶¶ ,
  14. THE EU BIOMED COLLABORATORS165,
  15. JACQUES SIMARD
  1. *Unit of Genetic Epidemiology, International Agency for Research on Cancer, Lyon, France
  2. †CRC Section of Cancer Genetics, Institute of Cancer Research and Royal Marsden NHS Trust, Sutton, Surrey, UK
  3. ‡Laboratory of Hereditary Cancers, MRC Group of Molecular Endocrinology, CHUL Research Centre, Quebec, Canada
  4. §Department of Medicine and Human Genetics, McGill University, Montreal General Hospital, Montreal, Quebec, Canada
  5. ¶Cancer Epidemiology Centre, Anti-Cancer Council of Victoria, Carlton, Australia
  6. **Centre for Genetic Epidemiology, The University of Melbourne, Carlton, Australia
  7. 164ICRF Genetic Epidemiology Laboratory, St James's Hospital, Leeds, UK
  8. ‡Unit of Medical Genetics, The Norwegian Radium Hospital, Oslo, Norway
  9. §§CRC Genetic Epidemiology Unit, Strangeways Research Laboratories, Cambridge, UK
  1. Dr Eeles, Section of Cancer Genetics, Institute of Cancer Research, Downs Road, Sutton, Surrey SM2 5PT, UK, ros{at}icr.ac.uk

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Editor—A report was recently published on the localisation of a chromosome segment at 1p36 which appeared to be linked (two point lod score=4.74) to a large number of families with multiple cases of early onset (mean age at diagnosis of <66 years) prostate cancer (PC) in which a brain tumour had been reported in a first or second degree relative of a PC case.1 This result is consistent with epidemiological evidence suggesting a familial relationship between brain cancer and PC as well as numerous studies of LOH at 1p36 in brain tumours.1 As part of the ACTANE (Anglo/Canadian/Texan/Australian/Norwegian/EU Biomed) familial PC Consortium, we have genotyped 207 multiple case PC families for five 1p36 tetranucleotide repeat polymorphisms, which were used by Gibbset al,1 and performed linkage analysis using GENEHUNTER2 with the following genetic map3: D1S1160 - 3.835 cM - D1S1597 - 4.339 cM - D1S407-2.611 cM - GATA29A05 (=D1S3669) - 6.520 cM - D1S552. In addition to our interest in assessing our families for evidence of linkage of prostate and primary brain cancer to this region, we also wanted to determine if any other cancer site(s) might be associated with a susceptibility locus in this region. To this end, the family histories of all cancers were abstracted from the databases of several Consortium members and included in the analysis.

Table 1 presents the characteristics of the families; details on how they were ascertained are included in the footnotes. The criteria used for the prostate cancer familial clusters in this study are more relaxed than those suggested by the Hopkins group (referred to as the “Hopkins criteria” in the field).4 The linkage analysis results of nine prostate-brain cancer families were partitioned according to mean age at diagnosis of PC in the …

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Footnotes

  • ¶¶ David Dearnaley, Robert Shearer, Audrey Ardern-Jones, Annette Murkin, Rachel Jackson, Dawn Teare, and the CRC/BPG collaborators (list available on request from Dr R Eeles)

  • 165 Names and addresses available on request from Professor D T Bishop

  • 218 Present address: Division of Medical Genetics, Box 357720, University of Washington Medical Center, Seattle, WA 98195, USA