PRLTS gene alterations in human prostate cancer.
Journal: 1997/July - Japanese journal of cancer research : Gann
ISSN: 0910-5050
PUBMED: 9197531
Abstract:
Since loss of heterozygosity on 8p22-p21.3 has been found frequently in prostate cancer, the status of a candidate tumor suppressor gene named PRLTS gene, recently cloned from the same region in some human malignancies, was examined in the present study. DNAs were isolated from 69 Japanese prostate cancer patients (37 localized and 32 cancer-death cases). Loss of heterozygosity at this gene locus was observed in 15 of 36 (42%) localized prostate cancer patients and 22 of 32 (69%) cancer-death patients. One cancer-death patient had a missense mutation, ACG->>ATG (Thr->>Met) at codon 64 in metastatic tumor tissues of pelvic lymph node and liver, and these tissues showed loss of the homologous allele, indicating that "two-hit" mutation of the PRLTS gene had occurred in this case. The others did not show any mutation, regardless of the presence or absence of loss of heterozygosity. Although loss of heterozygosity at the PRLTS gene locus is a relatively common abnormality, mutation of this gene is rare in prostate cancer.
Relations:
Content
Citations
(6)
Diseases
(2)
Organisms
(1)
Processes
(5)
Anatomy
(1)
Affiliates
(1)
Similar articles
Articles by the same authors
Discussion board
Japanese Journal of Cancer Research : Gann. Mar/31/1997; 88(4): 389-393

PRLTS Gene Alterations in Human Prostate Cancer

+2 authors

Abstract

Since loss of heterozygosity on 8p22‐p21,3 has been found frequently in prostate cancer, the status of a candidate tumor suppressor gene named PRLTS gene, recently cloned from the same region in some human malignancies, was examined in the present study. DNAs were isolated from 69 Japanese prostate cancer patients (37 localized and 32 cancer‐death cases). Loss of heterozygosity at this gene locus was observed in 15 of 36 (42%) localized prostate cancer patients and 22 of 32 (69%) cancer‐death patients. One cancer‐death patient had a missense mutation, ACG→ATG (Thr→Met) at codon 64 in metastatic tumor tissues of pelvic lymph node and liver, and these tissues showed loss of the homologous allele, indicating that “two‐hit” mutation of the PRLTS gene had occurred in this case. The others did not show any mutation, regardless of the presence or absence of loss of heterozygosity. Although loss of heterozygosity at the PRLTS gene locus is a relatively common abnormality, mutation of this gene is rare in prostate cancer.

The abbreviations used are:

PRLTSplatelet‐derived growth factor receptor‐like tumor suppressorPCRpolymerase chain reactionSSCPsingle‐strand conformation polymorphismLOHloss of heterozygosityRFLPrestriction fragment length polymorphismPDGFRplatelet‐derived growth factor receptor

References

  • 1. )Emi,M.,Fujiwara,Y.,Nakajima,T.,Tsuchiya,E.,Tsuda,H.,Hirohashi,S.,Maeda,Y.,Tsuruta,K.,Miyaki,M.andNakamura,Y.Frequent loss of heterozygosity for loci on chromosome 8p in hepatocellular carcinoma, colorectal cancer, and lung cancer.Cancer Res.,52,53685372(1992).[PubMed][Google Scholar]
  • 2. )Knowles,M. A.,Shaw,M. E.andProctor,A. J.Deletion mapping of chromosome 8 in cancers of the urinary bladder using restriction fragment length polymorphisms and microsatellite polymorphisms.Oncogene,8,13571364(1993).[PubMed][Google Scholar]
  • 3. )Bergerheim,U. S. R.,Kunimi,K.,Collins,V. P.andEkman,P.Deletion mapping of chromosome 8, 10, and 16 in human prostatic carcinoma.Genes Chromosom. Cancer,3,215220(1991).[PubMed][Google Scholar]
  • 4. )Kunimi,K.,Bergerheim,U. S.R.,Larsson,I.‐L.,Ekman,P.andCollins,V. P.Allelotyping of human prostatic adenocarcinoma.Genomics,11,530536(1991).[PubMed][Google Scholar]
  • 5. )Suzuki,H.,Emi,M.,Komiya,A.,Fujiwara,Y.,Yatani,R.,Nakamura,Y.andShimazaki,J.Localization of a tumor suppressor gene associated with progression of human prostate cancer within a 1,2 Mb region of 8p22‐p21.3.Genes Chromosom. Cancer,13,168174(1995).[PubMed][Google Scholar]
  • 6. )Fujiwara,Y.,Ohata,H.,Kuroki,T.,Koyama,K.,Tsuchiya,E.,Monden,M.andNakamura,Y.Isolation of a candidate tumor suppressor gene on chromosome 8p2I.3‐p22 that is homologous to an extracellular domain of the PDGF receptor beta gene.Oncogene,10,891895(1995).[PubMed][Google Scholar]
  • 7. )Union Internationale Centre le Cancer.InTNM Atlas, Third Edition, 2nd Revision 1992,”ed.SptesslB.,BeahrsO. H.,HermanekP.,HutterR. V. P.,ScheibeO.,SobinL. H.andWagnerQ.,pp.241250(1992).Springer‐Verlag,Berlin, Heidelberg.
  • 8. )Emi,M.,Fujiwara,Y.andNakamura,Y.A primary genetic linkage map of 14 polymorphic loci for the short arm of human chromosome 8.Genomics,15,530534(1993).[PubMed][Google Scholar]
  • 9. )Fujiwara,Y.,Ohata,H.,Emi,M.,Okui,K.,Koyama,K.,Tsuchiya,E.,Nakajima,T.,Monden,M.,Mori,T.,Kurimasa,A.,Oshimura,M.andNakamura,Y.A 3‐Mb physical map of the chromosome region 8p21.3‐p22, including a 600‐kb region commonly deleted in human hepatocellular carcinoma, colorectal cancer, and non‐small cell lung cancer.Genes Chromosom. Cancer,10,714(1994).[PubMed][Google Scholar]
  • 10. )Suzuki,H.,Aida,S.,Akimoto,S.,Igarashi,T.,Yatani,R.andShimazaki,J.State of adenomatous polyposis coli gene and ras oncogenes in Japanese prostate cancer.Jpn. J. Cancer Res.,85,847857(1994).[PubMed][Google Scholar]
  • 11. )Komiya,A.,Suzuki,H.,Aida,S.,Yatani,R.andShimazaki,J.Mutational analysis of CDKN2(CDK4I/ MTS1) gene in tissues and cell lines of human prostate cancer.Jpn. J. Cancer Res.,86,622625(1995).[PubMed][Google Scholar]
  • 12. )Pentao,L.,Wise,C. A.,Chinault,A. C.,Patel,P. I.andLupski,J. R.Charcot‐Marie‐Tooth type 1A duplication appears to arise from recombination at repeat sequences flanking the 1.5 Mb monomer unit.Nat. Genet.,2,292300(1992).[PubMed][Google Scholar]
  • 13. )Raskind,W. H.,Williams,C. A.,Hudson,L. D.andBird,T. D.Complete deletion of the proteolipid protein gene (PLP) in a family with X‐linked Pelizaeus‐Merzbacher disease.Am. J. Hum. Genet.,49,13551360(1991).[PubMed][Google Scholar]
  • 14. )Chang,C.‐Y.,Riley,D. J.,Lee,E. Y.‐H. P.andLee,W.‐H.Quantitative effects of the retinoblastoma gene on mouse development and tissue‐specific tumorigenesis.Cell Growth Differ.,4,10571064(1993).[PubMed][Google Scholar]
  • 15. )Kemp,C. J.,Donehower,L. A.,Bradley,A.andBalmain,A.Reduction of p53 dosage does not increase initiation or promotion but enhances malignant progression of chemically induced skin tumors.Cell,74,813822(1993).[PubMed][Google Scholar]
Collaboration tool especially designed for Life Science professionals.Drag-and-drop any entity to your messages.