Combination Cytotoxic Chemotherapy With Cisplatin or Doxorubicin and Photodynamic Therapy in Murine Tumors1

Nahabedian, Maurice Y.; Cohen, Robert A.; Contino, Michael F.; Terem, Theresa M.; Wright, W. H.; Berns, Michael W.; Wile, Alan G.

doi:10.1093/jnci/80.10.739

Cited by 77 publications

(50 citation statements)

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“…Although combinations of PDT with other treatment modalities, such as X-irradiation (Bellnier & Dougherty, 1986;Winther et al, 1988;Levendag et al, 1989), chemotherapy using adriamycin (Edell & Cortese, 1988), cisplatin or doxorubicin (Nahabedian et al, 1988), hyperthermia by combining PDT with microwave irradiation (Waldow & Dougherty, 1984;Waldow et al, 1987;Levendag et al, 1989) and the use of hypoxic cell sensitisers, e.g.…”

Section: Discussionmentioning

confidence: 99%

“…The typical clinical PDT protocol consists of the systemic administration of 2-5 mg kg-' Photofrin 11 followed 24-72 h later by exposure of malignant lesions to 50-400 J cm-2 visible photoradiation, usually 630 nm laser emission. Utilising these treatment conditions for various types of malignancies, encouraging clinical results have been reported (Kato et al, 1986;Lam et al, 1987;Gilson et al, 1988;Nseyo et al, 1987;McCaughan et al, 1988). Any improvement in the efficacy of PDT should increase its acceptance as a useful cancer treatment.…”

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confidence: 99%

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Increased efficacy of photodynamic therapy of R3230AC mammary adenocarcinoma by intratumoral injection of Photofrin II

Meid²,

Murant³

et al. 1990

Br J Cancer

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Summary Photodynamic therapy consists of the systemic administration of a derivative of haematoporphyrin (Photofrin 11) followed 24-72 h later by exposure of malignant lesions to photoradiation. We investigated the efficacy of this treatment after direct intratumoral injection of Photofrin II. This direct treatment regimen resulted in higher rates of inhibition of mitochondrial cytochrome c oxidase (5.13% J' cmM2 x 10-') and succinate dehydrogenase (3.14% J-' cm-2 X 10-I) in vitro at 2 h after intratumoral injection compared to rates of inhibition obtained after intraperitoneal drug administration: 0.51 and 0.42% J -I cm-2 x 10-', respectively. A significant delay in tumour growth in vivo was observed in animals that received intratumoral injections 2 h before photoradiation compared to animals injected intraperitoneally at either 2 or 24 h before photoradiation. The treatment protocols were compared with control groups, consisting of Photofrin II administration intratumorally or intraperitoneally without photoradiation, or photoradiation in the absence of Photofrin II. These data indicate that the intratumoral injection regimen with Photofrin II enhanced the efficacy of photodynamic therapy. The greater delay in tumour growth observed after intratumoral administration of Photofrin II suggests a mechanism favouring direct cell damage.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Increased efficacy of photodynamic therapy of R3230AC mammary adenocarcinoma by intratumoral injection of Photofrin II

Meid²,

Murant³

et al. 1990

Br J Cancer

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“…The addition of mitomycin C has been shown to enhance the PDT effect (Nahabedian et al, 1988). Recently, it has been reported that loss of MMR is specifically associated with hypersensitivity to mitomycin C (Fiumicino et al, 2000).…”

Section: Molecular and Cellular Pathologymentioning

confidence: 99%

Photodynamic therapy of DNA mismatch repair-deficient and -proficient tumour cells

et al. 2002

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Loss of DNA mismatch repair is a common finding in hereditary nonpolyposis colon cancer as well as in many types of sporadic human tumours. DNA mismatch repair-deficient cells have been reported to be resistant to many chemotherapeutic agents and to radiotherapy, and to have the potential of rapidly acquiring additional mutations leading to tumour progression. Photodynamic therapy is a new treatment modality using light to activate a photosensitiser that preferentially localises in tumour cells. An oxygen dependent photochemical reaction ensues, resulting in selective tumour necrosis. The effect of loss of DNA mismatch repair activity on the sensitivity to photodynamic therapy was tested using pairs of cell lines proficient or deficient in mismatch repair due to loss of either MLH1 or MSH2 protein function. Cells were incubated with the photosensitiser 5,10,15,20-meta-tetra(hydroxyphenyl)chlorin and exposed to laser light at 652 nm with various optical doses ranging from 0 -1 J cm 72 . Cell survival was assessed using the clonogenic assay. Loss of MLH1 or MSH2 function was not associated with resistance to photodynamic therapy. MCF-7 cells repeatedly treated with photodynamic therapy expressed parental levels of MLH1, MSH2, MSH6, and PMS2. DNA mismatch repair-deficient and -proficient cells showed similar subcellular distributions of meta-tetra(hydroxyphenyl)chlorin as analysed by laser scanning and fluorescence microscopy. Therefore, repeated exposure of tumour cells to photodynamic therapy does not seem to result in loss of DNA mismatch repair, and loss of mismatch repair, in turn, does not seem to contribute to resistance to photodynamic therapy. Our results suggest recommending photodynamic therapy as a strategy for circumventing resistance due to loss of DNA mismatch repair.

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“…For example, combinations of chemotherapies using agents with different mechanisms of action (Harris et al, 2005;Shanks et al, 2005); chemotherapy in combination with photodynamic therapy (PDT) (Nahabedian et al, 1988;Jin et al, 1992;Peterson et al, 1995); chemotherapy and immunotherapy (Welt et al, 2003); PDT and radiotherapy (Colasanti et al, 2004); and radioimmunotherapy with radiotherapy (Buchegger et al, 2000) have been studied.…”

Section: Introductionmentioning

confidence: 99%

Enhanced antitumor activity of combinations of free and HPMA copolymer-bound drugs

Hongrapipat

Kopečková

Prakongpan

et al. 2008

International Journal of Pharmaceutics

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The synergism in anticancer effect toward human renal carcinoma A498 cells by binary combinations of free and N-(2-hydroxypropyl)methacrylamide (HPMA) copolymer-bound anticancer drugs, SOS thiophene (SOS), doxorubicin (DOX), and mesochlorin e 6 monoethylenediamine (Mce 6 ), was evaluated. The combination index (CI) analysis was used to quantify the synergism, antagonism, and additive effects. Both free drugs and HPMA copolymer conjugates, when used as single agents or in combination, exhibited cytotoxic activities against A498 cells, as determined using a modified MTT assay. As single agents, SOS and P-GFLG-SOS (HPMA copolymer conjugates containing SOS bound via glycylphenylalanylleucylglycine [GFLG] spacer) were significantly more effective than the other agents evaluated. The synergistic effects ranked in the order SOS+DOX>P-GFLG-DOX +P-GFLG-Mce 6 ≈DOX+Mce 6 >P-GFLG-SOS+P-GFLG-DOX≈SOS+Mce 6 >P-GFLG-SOS+P-GFLG-Mce 6 . The combination of SOS+DOX proved to be synergistic over all cell growth inhibition levels. All other combinations exhibited synergism in a wide range of drug effect levels. The SOS +Mce 6 and P-GFLG-SOS+P-GFLG-Mce 6 combinations displayed synergism up to drug affected fraction (f a ) values of about 0.8 and reached slight antagonism and nearly additivity at f a = 0.95, respectively. However, all other combinations were synergistic up to f a < 0.9 and were additive at higher f a values. The observations that most combinations produced synergistic effects will be important for clinical translation.

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Combination Cytotoxic Chemotherapy With Cisplatin or Doxorubicin and Photodynamic Therapy in Murine Tumors1

Cited by 77 publications

References 0 publications

Increased efficacy of photodynamic therapy of R3230AC mammary adenocarcinoma by intratumoral injection of Photofrin II

Increased efficacy of photodynamic therapy of R3230AC mammary adenocarcinoma by intratumoral injection of Photofrin II

Photodynamic therapy of DNA mismatch repair-deficient and -proficient tumour cells

Enhanced antitumor activity of combinations of free and HPMA copolymer-bound drugs

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