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  1. Article: Direct effects of bisphosphonates on breast cancer cells.

    Senaratne, Siddhika G / Colston, Kay W

    Breast cancer research : BCR

    2001  Volume 4, Issue 1, Page(s) 18–23

    Abstract: In addition to inhibiting bone resorption, bisphosphonates have also been shown to exhibit antitumour effects. In vitro, bisphosphonates inhibit proliferation and induce apoptosis in cultured human breast cancer cells. In addition, bisphosphonate ... ...

    Abstract In addition to inhibiting bone resorption, bisphosphonates have also been shown to exhibit antitumour effects. In vitro, bisphosphonates inhibit proliferation and induce apoptosis in cultured human breast cancer cells. In addition, bisphosphonate treatment interferes with breast cancer cell adhesion to bone matrix, and inhibits cell migration and invasion. The combination of bisphosphonates with other anticancer drugs such as the taxoids markedly enhances these effects. These newly recognized direct actions of bisphosphonates on breast cancer cells indicate that these agents may have a greater role to play in treatment of patients suffering from cancers with a propensity to metastasize to bone.
    MeSH term(s) Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Apoptosis/drug effects ; Breast Neoplasms/prevention & control ; Cell Adhesion/drug effects ; Diphosphonates/pharmacology ; Diphosphonates/therapeutic use ; Female ; Humans ; Tumor Cells, Cultured/drug effects
    Chemical Substances Antineoplastic Agents ; Diphosphonates
    Language English
    Publishing date 2001-11-14
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2015059-3
    ISSN 1465-5411
    ISSN 1465-5411
    DOI 10.1186/bcr412
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5494: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article: Induction of apoptosis in breast cancer cells by apomine is mediated by caspase and p38 mitogen activated protein kinase activation.

    Lowe, Lorraine C / Senaratne, Siddhika G / Colston, Kay W

    Biochemical and biophysical research communications

    2005  Volume 329, Issue 2, Page(s) 772–779

    Abstract: The 1,1-bisphosphonate ester family member apomine (SR-45023A) is known to have anti-tumour activity in various cancer cell types. The aims of this study were to determine the effect of apomine on the growth of two breast cancer cell lines, MCF-7 and MDA- ...

    Abstract The 1,1-bisphosphonate ester family member apomine (SR-45023A) is known to have anti-tumour activity in various cancer cell types. The aims of this study were to determine the effect of apomine on the growth of two breast cancer cell lines, MCF-7 and MDA-MB-231, to ascertain whether any growth inhibitory effects found were due to induction of apoptosis, and to investigate the mechanism of action of apomine. Apomine caused significant growth inhibition of both cell lines after 72h of treatment. Apomine-induced growth inhibition was associated with caspase and p38 MAPK activation and DNA fragmentation. Apomine had no effect on Ras localisation, nor did addition of mevalonate to treatment media prevent apomine-induced apoptosis. We conclude that apomine induces apoptosis in breast cancer cells, an effect that is independent of oestrogen receptor status and is not via inhibition of the mevalonate pathway. Our study suggests apomine is a potential anti-neoplastic drug in breast cancer treatment.
    MeSH term(s) Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Breast Neoplasms/enzymology ; Caspases/metabolism ; Cell Line, Tumor ; Cell Proliferation/drug effects ; DNA Damage/drug effects ; Diphosphonates/pharmacology ; Dose-Response Relationship, Drug ; Enzyme Activation/drug effects ; Humans ; p38 Mitogen-Activated Protein Kinases/metabolism
    Chemical Substances Antineoplastic Agents ; Diphosphonates ; apomine ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Caspases (EC 3.4.22.-)
    Language English
    Publishing date 2005-04-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 205723-2
    ISSN 0006-291X ; 0006-291X
    ISSN (online) 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2005.02.032
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 116: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article: Nitrogen containing bisphosphonates induce apoptosis and inhibit the mevalonate pathway, impairing Ras membrane localization in prostate cancer cells.

    Oades, Grenville M / Senaratne, Siddhika G / Clarke, Ian A / Kirby, Roger S / Colston, Kay W

    The Journal of urology

    2003  Volume 170, Issue 1, Page(s) 246–252

    Abstract: Purpose: Metastasis to bone is an important cause of morbidity in advanced prostate cancer. Despite the typically sclerotic nature of prostatic bone metastases osteolysis has a significant role in the pathogenesis of this disease. The nitrogen ... ...

    Abstract Purpose: Metastasis to bone is an important cause of morbidity in advanced prostate cancer. Despite the typically sclerotic nature of prostatic bone metastases osteolysis has a significant role in the pathogenesis of this disease. The nitrogen containing bisphosphonates (N-BPs), such as pamidronate and zoledronic acid, have greatly enhanced potency for inhibiting bone resorption and inducing apoptosis in osteoclasts. We investigated the effects of N-BPs on prostate cancer cells.
    Materials and methods: Cell viability was determined with an MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymeyhoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) dye reduction assay. Cell cycle analysis, DNA fragmentation and caspase 3 activity were assessed using flow cytometry. Ras, Bcl-2 and Bax were quantified by Western blotting.
    Results: Pamidronate and zoledronic acid decreased cell viability in the 3 human cell lines DU145, PC3 and LNCaP. These effects were associated with changes in cell cycle distribution, induction of DNA fragmentation and a decrease in the Bcl-2-to-Bax ratio, which are features of apoptotic cell death. Pre-incubation with caspase inhibitors attenuated the effects of zoledronic acid and caspase 3 activity was demonstrated in treated DU145 cells. Zoledronic acid induced loss of cell viability in DU145 cells was prevented by co-treatment with farnesol, suggesting that N-BPs cause inhibition of the mevalonate pathway and Ras prenylation. A decrease in active, membrane bound Ras in zoledronic acid treated DU145 cells was shown by Western blot analysis.
    Conclusions: N-BPs induce apoptosis in prostate cancer via a caspase dependent mechanism. They have effects on protein prenylation via inhibition of the mevalonate pathway and impair membrane localization of Ras in prostate cancer cells.
    MeSH term(s) Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Blotting, Western ; Caspase 3 ; Caspases/metabolism ; Cell Membrane/metabolism ; Cell Survival/drug effects ; DNA Fragmentation/drug effects ; Diphosphonates/pharmacology ; Humans ; Imidazoles/pharmacology ; Male ; Mevalonic Acid/antagonists & inhibitors ; Mevalonic Acid/metabolism ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/physiopathology ; Protein Prenylation/drug effects ; ras Proteins/metabolism
    Chemical Substances Antineoplastic Agents ; Diphosphonates ; Imidazoles ; zoledronic acid (6XC1PAD3KF) ; CASP3 protein, human (EC 3.4.22.-) ; Caspase 3 (EC 3.4.22.-) ; Caspases (EC 3.4.22.-) ; ras Proteins (EC 3.6.5.2) ; pamidronate (OYY3447OMC) ; Mevalonic Acid (S5UOB36OCZ)
    Language English
    Publishing date 2003-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3176-8
    ISSN 1527-3792 ; 0022-5347
    ISSN (online) 1527-3792
    ISSN 0022-5347
    DOI 10.1097/01.ju.0000070685.34760.5f
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ui VI Zs.91: Show issues Location:
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    Zs.MO 331: Show issues

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