Different accumulation of cisplatin, oxaliplatin and JM216 in sensitive and cisplatin-resistant human cervical tumour cells

Martelli, Laura; Mario, F. Di; Ragazzi, Eugenio; Apostoli, P; Leone, Roberto; Perego, Paola; Fumagalli, Guido Francesco

doi:10.1016/j.bcp.2006.06.008

Cited by 35 publications

(31 citation statements)

References 21 publications

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“…Consequently, a circumvention of the reduced influx should result in a diminution of resistance [13,14]. In both the ovarian carcinoma and the ileocecal colorectal adenocarcinoma cell line pair 7 was able to bypass the reduced influx in the resistant cell line.…”

Section: Resistancementioning

confidence: 99%

“…It has been suggested that increasing lipophilicity may help overcome accumulation defects and consequently enhance cytotoxicity in resistant cell lines [13]. Moreover, lipophilicity was shown to correlate with cytotoxic activity [14][15][16].…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, lipophilicity was shown to correlate with cytotoxic activity [14][15][16]. In other studies a strong relationship between intracellular platinum concentrations and lipophilicity of platinum complexes was demonstrated [13,[17][18][19]. Most of the reported investigations have been carried out with platinum(IV) complexes or with a panel of structurally very different platinum complexes.…”

Section: Introductionmentioning

confidence: 99%

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Enhancing lipophilicity as a strategy to overcome resistance against platinum complexes?

Buss

Garmann

Galanski

et al. 2011

Journal of Inorganic Biochemistry

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Section: Resistancementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Enhancing lipophilicity as a strategy to overcome resistance against platinum complexes?

Buss

Garmann

Galanski

et al. 2011

Journal of Inorganic Biochemistry

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“…In vitro studies have shown antineoplastic activity of satraplatin and its active metabolites against several human cancer cell lines, including prostate (15,16), ovarian (8, 16 -18), cervical (19,20), and lung (16,21) cancers. In two independent experiments using the National Cancer Institute antitumor drug screen panel representing leukemia, small cell lung cancer, non -small cell lung cancer (NSCLC), central nervous system tumors, melanoma, colon, renal, and ovarian cancer cell lines, incubation with satraplatin for 48 hours induced growth inhibition of all 52 tested tumor cell lines in the first experiment and all 58 tested tumor cell lines in the second experiment (16).…”

Section: Preclinical Antineoplastic Activitymentioning

confidence: 99%

Current Status and Future Prospects for Satraplatin, an Oral Platinum Analogue

Choy

Park

Yao

2008

Clinical Cancer Research

200

156

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Platinum drugs are major chemotherapeutic agents that are used alone or in combination with other systemic agents and/or radiation therapy in the management of many human malignancies. All three platinum drugs approved by the Food and Drug Administration, cisplatin, carboplatin, and oxaliplatin, are administrated intravenously. Satraplatin is the first orally administered platinum drug under active clinical investigation. Satraplatin and its major metabolite, JM118, have shown antineoplastic activity in in vitro, in vivo, and in clinical settings. Use of satraplatin as an alternative platinum cytotoxic agent is particularly attractive because of the convenience of administration, milder toxicity profile, lack of cross-resistance with cisplatin, theoretical advantage as a radiosensitizer, and activity in cancers historically nonresponsive to platinum drugs. The most mature clinical data for satraplatin come from the recently completed phase III trial that investigated the efficacy of satraplatin and prednisone on hormone-refractory prostate cancer patients who had failed a course of other chemotherapy agents. Preliminary reports show that the combination is statistically superior to placebo and prednisone in multiple end points, including progressionfree survival, prostate-specific antigen response, objective tumor response, pain response, and duration of pain response. The difference in overall survival, however, did not reach statistical significance.

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“…Satraplatin unlike other approved platinum-based compounds (cisplatin, carboplatin, and oxaliplatin) is administrated orally, whereas the others are administrated intravenously [13]. This compound was considered a probable chemotherapeutic agent because it demonstrated a greater extent of cell killing in cisplatin-resistant cancers [14]. Satraplatin also demonstrated clinical activity against various mammalian cancers including prostate [15,16], ovarian [12], cervical, and lung [17] cancers.…”

Section: Introductionmentioning

confidence: 99%

<i>In Vitro</i> Investigation of DNA Damage Induced by the DNA Cross-Linking Agents Oxaliplatin and Satraplatin in Lymphocytes of Colorectal Cancer Patients

Alotaibi¹,

Baumgartner²,

Najafzadeh³

et al. 2012

JCT

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Exposure to toxic chemicals, especially chemotherapeutic drugs, may induce several DNA lesions, including DNA interstrand crosslinks. These crosslinks are considered toxic lesions to the dividing cells since they can induce mutations, chromosomal rearrangements, and cell death. Many DNA interstrand crosslinks lesions can be generated by platinum-based chemotherapeutic agents. Satraplatin is a novel orally administered platinum-based chemotherapeutic agent. In the present study, we investigated DNA interstrand crosslinks lesions induced by oxaliplatin and satraplatin in lymphocytes obtained from colorectal cancer patients and healthy volunteers. Satraplatin demonstrated an increase in interstrand crosslinks in a dose-dependent manner in the Comet assay (p < 0.001). In addition, satraplatin and oxaliplatin increased significantly the number of sister chromatid exchanges up to 8.5-fold and 5.1-fold (p < 0.001) respectively, when treated with 2 µM concentration in comparison to untreated colorectal cancer cells. Further, the γH2AX foci formation was investigated by an immunofluorescence assay with oxaliplatin and satraplatin. The γH2AX foci formation rate was increased by approximately 9-fold when lymphocytes were treated with 2 μM oxaliplatin. Satraplatin was found to significantly induce the number of γH2AX foci by 8.5-fold and 11-fold with both 0.2 μM and 2.0 μM, respectively, compared to the control volunteers that may indicate the repair system in cancer cells experiences a loss of ability to cope with the repair of DSBs. In conclusion, oxaliplatin and satraplatin effectively induced DNA interstrand crosslinks in lymphocytes obtained from colorectal cancer patients and healthy volunteers in vitro. Here, to the best of our knowledge we report for the first time evidence of DNA double strand breaks formation as a possible molecular mechanism of action for satraplatin.

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Different accumulation of cisplatin, oxaliplatin and JM216 in sensitive and cisplatin-resistant human cervical tumour cells

Cited by 35 publications

References 21 publications

Enhancing lipophilicity as a strategy to overcome resistance against platinum complexes?

Enhancing lipophilicity as a strategy to overcome resistance against platinum complexes?

Current Status and Future Prospects for Satraplatin, an Oral Platinum Analogue

<i>In Vitro</i> Investigation of DNA Damage Induced by the DNA Cross-Linking Agents Oxaliplatin and Satraplatin in Lymphocytes of Colorectal Cancer Patients

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Different accumulation of cisplatin, oxaliplatin and JM216 in sensitive and cisplatin-resistant human cervical tumour cells

Cited by 35 publications

References 21 publications

Enhancing lipophilicity as a strategy to overcome resistance against platinum complexes?

Enhancing lipophilicity as a strategy to overcome resistance against platinum complexes?

Current Status and Future Prospects for Satraplatin, an Oral Platinum Analogue

&lt;i&gt;In Vitro&lt;/i&gt; Investigation of DNA Damage Induced by the DNA Cross-Linking Agents Oxaliplatin and Satraplatin in Lymphocytes of Colorectal Cancer Patients

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<i>In Vitro</i> Investigation of DNA Damage Induced by the DNA Cross-Linking Agents Oxaliplatin and Satraplatin in Lymphocytes of Colorectal Cancer Patients