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  • 1
    Electronic Resource
    Electronic Resource
    Expression and somatic mutation on androgen receptor gene in prostate cancer (2002)
    Melbourne, Australia : Blackwell Science Pty
    International journal of urology 9 (2002), S. 0 
    Details
    ISSN: 1442-2042
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: Lack of androgen receptor (AR) expression or mutation on the AR gene creates the tendency for androgen independence and progression of prostate cancer. However, the association between the progression and AR expression or mutations is still controversial. In this study, we evaluated the prognostic significance of AR expression and mutations in prostate cancers.Methods: Forty-two prostate adenocarcinomas and three lymph node metastatic lesions sampled prior to hormonal therapy were included in this study; AR expression was analyzed immunohistochemically using an antibody against AR and the result was scored as the percentage of AR-positive tumor cells in the total tumor cells. Polymerase chain reaction–single-strand conformational polymorphism (PCR-SSCP) analysis and DNA sequencing were used to detect AR mutations.Results: Our study revealed the average AR expression in the prostate adenocarcinoma was 52.2 ± 27.1%, which was significantly lower than that in the adjacent non-tumorous prostate tissue (68.3 ± 18.3% in average) (P 〈 0.001). A significant correlation was obtained between progression-free survival and AR expression (P 〈 0.01). By SSCP analysis, three silent mutations (T649T, E709E and E711E) were detected in three separate prostate carcinomas.Conclusion : We conclude that AR expression is a useful prognostic indicator for tumor progression. Androgen receptor mutation may be an uncommon molecular event in untreated prostate cancer in Japanese men.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1442-2042.2002.00514.x
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  • 2
    Electronic Resource
    Electronic Resource
    Comparative analysis of clonality and pathology in primary and secondary hyperparathyroidism (1997)
    Springer
    Virchows Archiv 430 (1997), S. 247-251 
    Details
    ISSN: 1432-2307
    Keywords: Parathyroid ; Hyperparathyroidism ; Clonality ; PGK-1 gene ; Pathology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Parathyroid adenoma and hyperplasia are the most common causes for hyperparathyroidism, and distinction between them is controversial based on the current criteria for pathological diagnosis. We studied the clonality of hyperparathyroidism and its correlation with the pathological features, analysing 39 female patients with hyperparathyroidism. Clonality was successfully detected in 12 heterozygous cases by PCR amplification ofPGK-1 gene. The 12 cases yielded 14 hypercellular glands, 8 affected by primary and 6 by secondary hyperparathyroidism. The results revealed that 7 of the 8 glands with primary hyperparathyroidism showed monoclonal proliferation. Only 1 gland pathologically diagnosed as adenoma showed a polyclonal pattern. In the 4 cases with secondary hyperparathyroidism, at least one monoclonal tumour was detected in each case. Our data indicate that monoclonal tumours are more common than expected in both primary and secondary hyperparathyroidism. Monoclonal tumours and polyclonal hyperplasia can co-exist in the same patient. Comparative study of the clonality and the pathological features showed that the clonality was consistent with the diagnosis of parathyroid adenoma, whereas it was in conflict with the diagnosis of hyperplasia with multigland involvement. One of the reasons for this is that we are ignorant of the true natures of hyperparathyroidism with multigland involvement.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01324809
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  • 3
    Electronic Resource
    Electronic Resource
    Expression of Bcl-2 but not Bax or p53 correlates with in vitro resistance to a series of anticancer drugs in breast carcinoma (2000)
    Springer
    Breast cancer research and treatment 61 (2000), S. 211-216 
    Details
    ISSN: 1573-7217
    Keywords: Bcl-2 ; breast cancer ; chemosensitivity ; HDRA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Programmed cell death is an important determinant of the response to chemotherapy. Among the factors controlling this process, a significant role is played by bcl-2, bax and p53. The in vitro chemosensitivity of the 177 breast carcinomas was assessed by the histoculture drug response assay (HDRA) using mitomycin C (MMC), 5-fluorouracil (5-Fu), adriamycin (ADM), cisplatin (CDDP), and cyclophosphamide (CPA). The susceptibility of Bcl-2-negative tumors to all the drugs killing was significantly higher than that of Bcl-2-positive tumors. No relationship between Bax or p53 immunoreactivity and sensitivity for any of anticancer drugs studied was demonstrated. Immunohistochemical results regarding Bcl-2 are promising in the evaluation of the sensitivity of cancer cells to a series of anticancer drugs and might be therapeutically useful as an indicator of response to adjuvant chemotherapy for breast cancer.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006474307180
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