In vitro and in vivo modulation of multi-drug resistance with amiodarone.


:The modulating effect on drug resistance of amiodarone (AM) and its metabolite desethylamiodarone (DEA) was studied in a P-glycoprotein-positive human colon carcinoma cell line COLO 320, and a human small-cell lung carcinoma cell line GLC4 and its adriamycin (Adr)-resistant subline GLC4-Adr (both P-glycoprotein-negative). AM, DEA and verapamil induced an increase in cytotoxicity of Adr, vincristine and etoposide (VP16) in COLO 320 cells, while in the GLC4 and GLC4-Adr cell line no effect was seen. In the COLO 320 cell line, AM caused more intracellular, and especially intranuclear, fluorescence of Adr and more Adr-induced DNA strand breaks as compared to Adr alone. Moreover, an increase in VP16-induced topoisomerase II-DNA complexes was observed when AM was added. Competition between AM and Adr for the same efflux pump was suggested in efflux studies. The colony-forming unit granulocyte macrophage (CFU-GM) assay showed no increase in cytotoxicity of Adr when AM was added. Fourteen patients with Adr-resistant tumors were treated with Adr and AM. In these patients, peak serum levels of AM plus DEA of 10 microM were reached. Patient serum (20%) obtained after the first i.v. AM infusion induced in vitro significantly more cell kill of Adr in COLO 320 cells. Apart from a transient first-degree AV block in one patient, no cardiac toxicity was observed with the combination of Adr and AM. Bone-marrow toxicity was the same as expected from Adr alone in these patients. One of the 13 evaluable patients obtained a partial remission.


Int J Cancer


van der Graaf WT,de Vries EG,Uges DR,Nanninga AG,Meijer C,Vellenga E,Mulder PO,Mulder NH





Has Abstract


1991-06-19 00:00:00












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    abstract::Polymorphism of DNA base excision repair (BER) genes affects DNA repair capacity and may alter sensitivity to platinum-based chemotherapy regimens. This study investigated polymorphisms of OGG1 Ser326Cys, APE1 Asp148Glu APE1-141T/G and XRCC1 Arg399Gln for association with clinical outcome in 235 advanced inoperable no...

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    authors: Peng Y,Li Z,Zhang S,Xiong Y,Cun Y,Qian C,Li M,Ren T,Xia L,Cheng Y,Wang D

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    authors: Zhu JY,Lavrik IN,Mahlknecht U,Giaisi M,Proksch P,Krammer PH,Li-Weber M

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    abstract::Germline variation in the TP53 network genes PRKAG2, PPP2R2B, CCNG1, PIAS1 and YWHAQ was previously suggested to have an impact on drug response in vitro. Here, we investigated the effect on breast cancer survival of germline variation in these genes in 925 Finnish breast cancer patients and further analyzed five sing...

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    authors: Jamshidi M,Schmidt MK,Dörk T,Garcia-Closas M,Heikkinen T,Cornelissen S,van den Broek AJ,Schürmann P,Meyer A,Park-Simon TW,Figueroa J,Sherman M,Lissowska J,Keong GT,Irwanto A,Laakso M,Hautaniemi S,Aittomäki K,Blomqvist

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    pub_type: 杂志文章,随机对照试验


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    journal_title:International journal of cancer

    pub_type: 杂志文章


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    journal_title:International journal of cancer

    pub_type: 杂志文章


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    更新日期:2008-09-15 00:00:00

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    journal_title:International journal of cancer

    pub_type: 杂志文章


    authors: Fleuren ED,O'Toole S,Millar EK,McNeil C,Lopez-Knowles E,Boulghourjian A,Croucher DR,Schramek D,Brummer T,Penninger JM,Sutherland RL,Daly RJ

    更新日期:2010-09-01 00:00:00

  • Interaction of interleukin-11 with cytotoxic therapies in vitro against CEM cells and in vivo against EMT-6 murine mammary carcinoma.

    abstract::Interleukin-11(rhIL-11) is a cytokine that has been shown to enhance the recovery of bone marrow and intestinal crypt cells after cytotoxic insult with radiation or anticancer drugs. The current study examined the effects of rhIL-11 on the response of CEM human lymphoblastic leukemia cells and on the EMT-6 murine mamm...

    journal_title:International journal of cancer

    pub_type: 杂志文章


    authors: Teicher BA,Chen YN,Ara G,Emi Y,Kakeji Y,Maehara Y,Keyes S,Northey D

    更新日期:1996-09-17 00:00:00