The effect of cisplatin on the repair of radiation damage in RIF 1 mouse tumours in vivo

Begg, Adrian C.; Bohlken, S.; Bartelink, Harry

doi:10.1016/0167-8140(89)90121-7

Cited by 29 publications

(9 citation statements)

References 27 publications

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“…The early phase of enhancement, when cisplatin was given within a few hours before radiation (Fig. l), was most likely the result of a direct interaction between cisplatin and radiation, which involves an increase in the DNA lesions or inhibition of repair from sublethal radiation damage [12,13,18,19,21]. Regardless of which of these mechanisms may be operating, the enhancement of tumor radioresponse must be acting through reproductive cell death rather than apoptotic cell death.…”

Section: Resultsmentioning

confidence: 96%

Cisplatin‐induced enhancement of radioresponse in a murine mammary carcinoma: Test of a role for apoptosis

Wheeler

Stephens

Milas

et al. 1995

Radation Oncology Invest

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SUMMARYProgrammed cell death or apoptosis has recently been recognized as an important mode of cell death in the response of tumor cells to cytotoxic treatments associated with chemotherapy or radiation therapy (RT). We previously showed that both cisplatin and radiation induced substantial apoptosis in the murine mammary tumor MCA-4 when administered as single agents in vivo. Moreover, the levels of apoptosis correlated with tumor response measured as tumor growth delay. In the current study a role for apoptosis in a combined treatment with cisplatin and radiation was evaluated. Mice bearing MCA-4 tumors were irradiated at different times following an injection with cisplatin, and tumor growth delay was assessed. Apoptosis was scored from histological sections of the tumors. The results showed that whereas the cisplatin sensitized the MCA-4 tumor to a subsequent irradiation in terms of the growth delay, the apoptotic index never rose above the maximum level characteristic of either agent when used singly. Thus, there was no indication that cisplatin sensitized the tumor cells to radiation-induced apoptosis. We conclude that apoptosis is not the only important mechanism for cell killing in tumors following cytotoxic treatment and that tumor response is a complex composite of many different factors.

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Section: Resultsmentioning

confidence: 96%

Cisplatin‐induced enhancement of radioresponse in a murine mammary carcinoma: Test of a role for apoptosis

Wheeler

Stephens

Milas

et al. 1995

Radation Oncology Invest

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“…CP is the most active cytotoxic agent in metastatic and recurrent squamous carcinoma of the cervix (3) . Since CP appears to significantly enhance radiation damage, and may result in a higher level of tumor control, concurrent use of this drug with radiation therapy is an attractive option (18,19) . A number of investigators have examined the combination of 5-FU and CP and have yielded encouraging results, suggesting that the combined treatment may be a useful approach (20)(21)(22) .…”

Section: Discussionmentioning

confidence: 99%

Analysis of thein vitrosynergistic effect of 5-fluorouracil and cisplatin on cervical carcinoma cells

Yim

Lee

et al. 2006

Int J Gynecol Cancer

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5-Fluorouracil (5-FU) is currently being used as an anticancer drug to reduce tumor bulk in order to increase the operability rate and postoperative survival in patients with cervical cancer, which has been combined with cisplatin (CP) because of its superior activities observed in human carcinoma cells. However, the combined anticancer effect of 5-FU and CP in cervical carcinoma cells is poorly understood. Therefore, we conducted a study to investigate whether anticancer drugs 5-FU and CP may exhibit the combined antiproliferative effect in cervical carcinoma cells. Using proteomics analysis, including two-dimensional gel electrophoresis and matrix assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF-MS), we investigated the antiproliferative effect–related proteins after treatment with 5-FU and/or CP. Our experiments showed that the combination of 5-FU and CP engaged both the apoptotic pathways: the membrane death receptor–mediated apoptosis pathway and the mitochondrial apoptotic pathway. Moreover, the combination of 5-FU and CP resulted in remarkable increasing susceptibility to apoptosis. We suggest that the combination of 5-FU and CP suppresses the growth of cervical carcinoma cells by synergistic effect with the induction of apoptosis. In vitro synergistic effect of 5-FU and CP supports the basis of the clinical application of the combination chemotherapy to the patients with cervical cancer.

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“…CP is the most active cytotoxic agent in metastatic and recurrent squamous carcinoma of the cervix (3) . Since CP appears to significantly enhance radiation damage, and may result in a higher level of tumor control, concurrent use of this drug with radiation therapy is an attractive option (18,19) . A number of investigators have examined the combination of 5‐FU and CP and have yielded encouraging results, suggesting that the combined treatment may be a useful approach (20–22) .…”

Section: Discussionmentioning

confidence: 99%

Analysis of the in vitro synergistic effect of 5-fluorouracil and cisplatin on cervical carcinoma cells

Yim

Lee

et al. 2006

Int J Gynecol Cancer

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5-Fluorouracil (5-FU) is currently being used as an anticancer drug to reduce tumor bulk in order to increase the operability rate and postoperative survival in patients with cervical cancer, which has been combined with cisplatin (CP) because of its superior activities observed in human carcinoma cells. However, the combined anticancer effect of 5-FU and CP in cervical carcinoma cells is poorly understood. Therefore, we conducted a study to investigate whether anticancer drugs 5-FU and CP may exhibit the combined antiproliferative effect in cervical carcinoma cells. Using proteomics analysis, including two-dimensional gel electrophoresis and matrix assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF-MS), we investigated the antiproliferative effect-related proteins after treatment with 5-FU and/or CP. Our experiments showed that the combination of 5-FU and CP engaged both the apoptotic pathways: the membrane death receptor-mediated apoptosis pathway and the mitochondrial apoptotic pathway. Moreover, the combination of 5-FU and CP resulted in remarkable increasing susceptibility to apoptosis. We suggest that the combination of 5-FU and CP suppresses the growth of cervical carcinoma cells by synergistic effect with the induction of apoptosis. In vitro synergistic effect of 5-FU and CP supports the basis of the clinical application of the combination chemotherapy to the patients with cervical cancer.

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The effect of cisplatin on the repair of radiation damage in RIF 1 mouse tumours in vivo

Cited by 29 publications

References 27 publications

Cisplatin‐induced enhancement of radioresponse in a murine mammary carcinoma: Test of a role for apoptosis

Cisplatin‐induced enhancement of radioresponse in a murine mammary carcinoma: Test of a role for apoptosis

Analysis of thein vitrosynergistic effect of 5-fluorouracil and cisplatin on cervical carcinoma cells

Analysis of the in vitro synergistic effect of 5-fluorouracil and cisplatin on cervical carcinoma cells

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