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Analysis of human prostate century by fluorescent differential display

Research Project

Project/Area Number 12670171
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Human pathology
Research InstitutionSecond Department of Pathology, Nara Medical University

Principal Investigator

KONISHI Noboru  Second Department of Pathology, Nara Medical University, Professor, 医学部, 教授 (20145832)

Project Period (FY) 2000 – 2002
Project Status Completed (Fiscal Year 2002)
Budget Amount *help
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2002: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2001: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2000: ¥1,300,000 (Direct Cost: ¥1,300,000)
Keywordsprostate cancer / gene / differential / PIN / PCA-1 / antibody / Differential display
Research Abstract

A number of genetic changes have been shown to occur in prostate tumorigenesis, yet it is difficult to translate this molecular knowledge into diagnostic and prognostic criteriae widely applicable for the management and treatment of the disease. Recent molecular studies have demonstrated several candidate genes important in hereditary prostate cancer; however, no specific molecular marker for this tumor has as yet been found. In searching for potential gene markers for prostate carcinoma, we explored the molecular profile relating to the gene expression patterns in tumors using fluorescent differential display (FDD) analysis. We have identified a novel gene, designated prostate cancer antigen-1 (PCA-1), which shows increased expression in prostate carcinoma. The full-length transcript corresponding to the PCR product was cloned by rapid amplification of CDNA ends. Analysis of the deduced amino acid sequence demonstrated that this gene encodes a novel 50-Kda putative protein immunohistochemically expressed in a high number of prostate carcinomas (63/70; 90%) as well as in the atypical cells in high-grade prostatic intraepithelial neoplasias. Western blot analysis indicates that PCA-1 is also up-regulated in prostate cancer cell lines PC-3 and DU 145, but not in LNCaP Other human cancers, such as thyroid, gastric colorectal, lung, breast, and renal cell cancers, proved negative for PCA-1 , indicating specificity for prostatic lesions. Although there appears to be no significant correlation between immunoreactivity and histological tumor grade or pathological stage, the gene may be relevant to the early stages of the tumor development, thus making it useful as a diagnostic and therapeutic tool for dealing with prostate cancer.

Report

(4 results)
  • 2002 Annual Research Report   Final Research Report Summary
  • 2001 Annual Research Report
  • 2000 Annual Research Report
  • Research Products

    (27 results)

All Other

All Publications (27 results)

  • [Publications] Matsumoto K., et al.: "ELISA for a complexed antigen with a monoclonal antibody blocking reactior with the free antigen-assay-specific for complexed prostate-specific antigen"J.Immunol.Methods. 234. 99-106 (2000)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Konishi, N., et al.: "Heterogenous methylation and deletion patterns of the INK4a/ARF locus within prostate carcinomas"Am.J.Pathol.. 160. 1207-1214 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Konishi, N., et al.: "DNA hypermethylation status of multip1e genes in prostate adenocarcinomas"Jpn.J.Cancer Res.. 93. 767-773 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Shimada, K., et al.: "Contributions of mitogenactivated protein kinase and nuclear factor kappa B to N-(4-hydroxyphenyl)retinamide-induced apoptosis in prostate cancer cells"Mol.Carcinog.. 35. 127-137 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Shimada, K., et al.: "Phosphorylation of Fas-associated death domain contributes to enhancement of etoposide-induced apoptosiss in prostate cancer cells"Jpn.J.Cancer Res.. 93. 1164-1174 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Shimada, K., et al.: "c-Jun NH2-terminal kinase-dependent Fas activation contributes to etoposide-induced apoptosis in p53-mutated prostate cancer cells"The Prostate. (In press).

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Matsumoto K., Konishi, N., Samori, T., Kimura, E., Doi, M., Kato, S., Yuki Y.: "ELISA for a complexed antigen with a monoclonal antibody blocking reaction with the free antigen-assay-specific for complexed prostate-specific antigen"J. Immunol. Methods. 234. 99-106 (2000)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Konishi, N., Nakamura, M., Kishi, M., Nishimine, M., Ishida, E. and Shimada, K.: "Heterogeneous methylation and deletion patterns of the INK4a/ARF locus within prostate carcinomas"Am. J. Pathol.. 160. 1207-1214 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Konishi, N., Nakamura, M., Kishi, M., Nishimine, M., Ishida, E. and Shimada, K.: "DNA hypermethylation status of multiple genes in prostate adenocarcinomas"Jpn. J. Cancer Res.. 93. 767-773 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Shimada, K., Nakamura, M., Ishida, E., Kishi, M., Yonehara, S., Konishi, N.: "Contributions of mitogen-activated protein kinase and nuclear factor kappa B to N-(4-hydroxyphenyl) retinamide-induced apoptosis in prostate cancer cells"Mol. Carcinogenesis. 35. 127-137 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Shimada, K., Nakamura, M., Ishida, E., Kishi, M., Yonehara, S. and Konishi, N.: "Phosphorylation of Fas-associated death domain contributes to enhancement of etoposide-induced apoptosis in prostate cancer cells"Jpn. J. Cancer Res.. 93. 1164-1174 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Shimada, K., Nakamura, M., Ishida, E., Kishi, M., Yonehara, S. and Konishi, N.: "c-Jun NH2-terminal kinase-dependent Fas activation contributes to etoposide-induced apoptosis in p53-mutated prostate cancer cells"Prostate. in press.

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Konishi, N.: "Heterogenous methylation and deletion patterns of the INK4a/ARF locus within prostate carcinomas"Am. J. Pathol.. 160. 1207-1214 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Konishi, N.: "DNA hypermethylation status of multiple genes in prostate adenocarcinomas"Jpn. J. Cancer Res.. 93. 767-773 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Shimada, K.: "Contributions of mitogenactivated protein kinase and nuclear factor kappa B to N-(4-hvdroxyphenyl) retiramide-induced apoptosis in prostate cancer cells"Mol. Carcinog.. 35. 127-137 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Shimada, K.: "Phosphorylation of Fas-associated death domain contributes to enhancement of etoposide-induced apoptosiss in prostate cancer cells"Jpn. J. Cancer Res.. 93. 1164-1174 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Shimada, K.: "c-Jun NH2-terminal kinase-dependent Fas activation contributes to etoposide-induced apoptosis in p53-mutated prostate cancer cells"The Prostate. (in press).

    • Related Report
      2002 Annual Research Report
  • [Publications] Nakamura, M.: "Novel tumor suppressor loci on 6q22-23 in primary central nervous system, lymphomas"Cancer Res.. (in press).

    • Related Report
      2002 Annual Research Report
  • [Publications] Konishi, N., Nakamura, M., et al.: "Specific genetic alterations in rat renal cell carcinomas induced by N-ethyl-N-hydroxyethylnitrosamine"Toxicol. Pathol. 29. 232-236 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] Nakamura, M., Konishi, N., et al.: "Frequent alterations of the p14^<ARF> and p16^<INK4a> genes in primary central nervous system lymphomas"Cancer Res.. 61. 6335-6339 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] Cho, M., Konishi, N., et al.: "Hypomethylation of the MN/CA9 promoter and upregulated MN/CA9 expression in human renal cell carcinoma"Br. J. Cancer. 85. 563-567 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] Kawada, Y., Konishi, N., et al.: "Aberrations of p14^<ARF> and p16<INK4a> genes in renal cell carcinomas"Jpn. J. Cancer Res.. 92. 1293-1299 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] Konishi, N., Nakamura, M., et al.: "Heterogeneous methylation and deletion patterns of the INK4a/ARF locus within prostate carcinomas"Am. J. Pathol. (In press). (2002)

    • Related Report
      2001 Annual Research Report
  • [Publications] Matsumoto K.,Konishi,N., et al.: "ELISA for a complexed antigen with a monoclonal antibody blocking reaction with the free antigen."J.Immunological Methods. 234. 99-106 (2000)

    • Related Report
      2000 Annual Research Report
  • [Publications] Nishimine,M.,Konishi,N., et al.: "Epigenetic alterations in methylation in oral squamous cell carcinoma cell lines detected by two-dimensional gel electrophoresis."Int.J.Oncology. 17. 743-747 (2000)

    • Related Report
      2000 Annual Research Report
  • [Publications] 小西登: "前立腺癌の病理から何を学ぶか。全摘標本の組織学的検索"泌尿器外科. 13・2. 143-146 (2000)

    • Related Report
      2000 Annual Research Report
  • [Publications] 小西登: "前立腺癌の病理から何を学ぶか。T1c症例の病理学的実態"泌尿器外科. 13・2. 171-173 (2000)

    • Related Report
      2000 Annual Research Report

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Published: 2000-04-01   Modified: 2016-04-21  

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