Tumor vascular response to photodynamic therapy and the antivascular agent 5,6-dimethylxanthenone-4-acetic acid: implications for combination therapy - PubMed (original) (raw)
Comparative Study
. 2005 Jun 1;11(11):4241-50.
doi: 10.1158/1078-0432.CCR-04-2703.
Affiliations
- PMID: 15930363
- DOI: 10.1158/1078-0432.CCR-04-2703
Comparative Study
Tumor vascular response to photodynamic therapy and the antivascular agent 5,6-dimethylxanthenone-4-acetic acid: implications for combination therapy
Mukund Seshadri et al. Clin Cancer Res. 2005.
Abstract
Purpose: Photodynamic therapy (PDT) is a clinically approved treatment for a variety of solid malignancies. 5,6-Dimethylxanthenone-4-acetic acid (DMXAA) is a potent vascular targeting agent that has been shown to be effective against a variety of experimental rodent tumors and xenografts and is currently undergoing clinical evaluation. We have previously reported that the activity of PDT against transplanted mouse tumors is selectively enhanced by DMXAA. In the present study, we investigated the in vivo tumor vascular responses to the two treatments given alone and in combination.
Experimental design: Vascular responses to (i) four different PDT regimens using the photosensitizer 2-[1-hexyloxyethyl]-2-devinyl pyropheophorbide-a (HPPH) at two different fluences (128 and 48 J/cm(2)) and fluence rates (112 and 14 mW/cm(2)), (ii) 5-aminolevulinic acid (ALA)-sensitized PDT (135 J/cm(2) at 75 mW/cm(2)), (iii) DMXAA at a high (30 mg/kg) and low dose (25 mg/kg), and (iv) the combination of HPPH-PDT (48 J/cm(2) at 112 mW/cm(2)) and low-dose DMXAA were studied in BALB/c mice bearing Colon-26 tumors.
Results: PDT-induced changes in vascular permeability, determined using noninvasive magnetic resonance imaging with a macromolecular contrast agent, were regimen dependent and did not predict tumor curability. However, a pattern of increasing (4 hours after treatment) and then decreasing (24 hours after) contrast agent concentrations in tumors, seen after high-dose DMXAA or the combination of PDT and low-dose DMXAA, was associated with long-term cure rates of >70%. This pattern was attributed to an initial increase in vessel permeability followed by substantial endothelial cell damage (CD31 immunohistochemistry) and loss of blood flow (fluorescein exclusion assay). Low dose-rate PDT, regardless of the delivered dose, increased the level of magnetic resonance contrast agent in peritumoral tissue, whereas treatment with either DMXAA alone, or PDT and DMXAA in combination resulted in a more selective tumor vascular response.
Conclusions: The observed temporal and spatial differences in the response of tumor vessels to PDT and DMXAA treatments could provide valuable assistance in the optimization of scheduling when combining these therapies. The combination of PDT and DMXAA provides therapeutically synergistic and selective antitumor activity. Clinical evaluation of this combination is warranted.
Similar articles
- The vascular disrupting agent 5,6-dimethylxanthenone-4-acetic acid improves the antitumor efficacy and shortens treatment time associated with Photochlor-sensitized photodynamic therapy in vivo.
Seshadri M, Bellnier DA. Seshadri M, et al. Photochem Photobiol. 2009 Jan-Feb;85(1):50-6. doi: 10.1111/j.1751-1097.2008.00395.x. Epub 2008 Jul 17. Photochem Photobiol. 2009. PMID: 18643909 Free PMC article. - Tumor dose response to the vascular disrupting agent, 5,6-dimethylxanthenone-4-acetic acid, using in vivo magnetic resonance spectroscopy.
McPhail LD, Chung YL, Madhu B, Clark S, Griffiths JR, Kelland LR, Robinson SP. McPhail LD, et al. Clin Cancer Res. 2005 May 15;11(10):3705-13. doi: 10.1158/1078-0432.CCR-04-2504. Clin Cancer Res. 2005. PMID: 15897567 - Vascular-targeting therapies for treatment of malignant disease.
Siemann DW, Chaplin DJ, Horsman MR. Siemann DW, et al. Cancer. 2004 Jun 15;100(12):2491-9. doi: 10.1002/cncr.20299. Cancer. 2004. PMID: 15197790 Review. - Small-molecule cytokine inducers causing tumor necrosis.
Baguley BC. Baguley BC. Curr Opin Investig Drugs. 2001 Jul;2(7):967-75. Curr Opin Investig Drugs. 2001. PMID: 11757800 Review.
Cited by
- Activation of STING by SAMHD1 Deficiency Promotes PANoptosis and Enhances Efficacy of PD-L1 Blockade in Diffuse Large B-cell Lymphoma.
Cai Y, Chen X, Lu T, Fang X, Ding M, Yu Z, Hu S, Liu J, Zhou X, Wang X. Cai Y, et al. Int J Biol Sci. 2023 Aug 28;19(14):4627-4643. doi: 10.7150/ijbs.85236. eCollection 2023. Int J Biol Sci. 2023. PMID: 37781035 Free PMC article. - Lorazepam Stimulates IL6 Production and Is Associated with Poor Survival Outcomes in Pancreatic Cancer.
Cornwell AC, Tisdale AA, Venkat S, Maraszek KE, Alahmari AA, George A, Attwood K, George M, Rempinski D, Franco-Barraza J, Seshadri M, Parker MD, Cortes Gomez E, Fountzilas C, Cukierman E, Steele NG, Feigin ME. Cornwell AC, et al. Clin Cancer Res. 2023 Sep 15;29(18):3793-3812. doi: 10.1158/1078-0432.CCR-23-0547. Clin Cancer Res. 2023. PMID: 37587561 Free PMC article. - Strategies for Improving Photodynamic Therapy Through Pharmacological Modulation of the Immediate Early Stress Response.
de Klerk DJ, de Keijzer MJ, Dias LM, Heemskerk J, de Haan LR, Kleijn TG, Franchi LP, Heger M; Photodynamic Therapy Study Group. de Klerk DJ, et al. Methods Mol Biol. 2022;2451:405-480. doi: 10.1007/978-1-0716-2099-1_20. Methods Mol Biol. 2022. PMID: 35505025 Review. - Regulatory Role of Hexokinase 2 in Modulating Head and Neck Tumorigenesis.
Li WC, Huang CH, Hsieh YT, Chen TY, Cheng LH, Chen CY, Liu CJ, Chen HM, Huang CL, Lo JF, Chang KW. Li WC, et al. Front Oncol. 2020 Mar 3;10:176. doi: 10.3389/fonc.2020.00176. eCollection 2020. Front Oncol. 2020. PMID: 32195170 Free PMC article. - A "Missile-Detonation" Strategy to Precisely Supply and Efficiently Amplify Cerenkov Radiation Energy for Cancer Theranostics.
Yu B, Ni D, Rosenkrans ZT, Barnhart TE, Wei H, Ferreira CA, Lan X, Engle JW, He Q, Yu F, Cai W. Yu B, et al. Adv Mater. 2019 Dec;31(52):e1904894. doi: 10.1002/adma.201904894. Epub 2019 Nov 11. Adv Mater. 2019. PMID: 31709622 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources