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L. Martelli, F. Di Mario, E. Ragazzi, P. Apostoli, R. Leone, P. Perego and G. Fumagalli, “Different Accumulation of Cisplatin, Oxaliplatin and JM216 in Sensitive and Cisplatin-Resistant Human Cervical Tumour Cells,” Biochemical Pharmacology, Vol. 72, No.6 , 2006, pp. 693-700. doi:10.1016/j.bcp.2006.06.008

has been cited by the following article:

• TITLE: In Vitro Investigation of DNA Damage Induced by the DNA Cross-Linking Agents Oxaliplatin and Satraplatin in Lymphocytes of Colorectal Cancer Patients

  AUTHORS: Amal Alotaibi, Adolf Baumgartner, Mojgan Najafzadeh, Eduardo Cemeli, Diana Anderson

  KEYWORDS: DNA Interstrand Crosslinks; Oxaliplatin; Satraplatin; γH2AX Foci Formation

  JOURNAL NAME: Journal of Cancer Therapy, Vol.3 No.1, February 17, 2012

  ABSTRACT: 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 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.