Bibliothek

X
feed icon rss

Ihre E-Mail wurde erfolgreich gesendet. Bitte prüfen Sie Ihren Maileingang.

Leider ist ein Fehler beim E-Mail-Versand aufgetreten. Bitte versuchen Sie es erneut.

Vorgang fortführen?

Exportieren
Filter
  • 2000-2004  (2)
Datenquelle
Materialart
Erscheinungszeitraum
Jahr
Schlagwörter
  • 1
    Digitale Medien
    Digitale Medien
    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
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: 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.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1046/j.1442-2042.2002.00514.x
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    Artikel (Nationallizenzen)
    Volltext
  • 2
    Digitale Medien
    Digitale Medien
    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
    Schlagwort(e): Bcl-2 ; breast cancer ; chemosensitivity ; HDRA
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: 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.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1023/A:1006474307180
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    Artikel (Nationallizenzen)
    Volltext
Schließen ⊗
Diese Webseite nutzt Cookies und das Analyse-Tool Matomo. Weitere Informationen finden Sie hier...