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Endobronchial photodynamic therapy: Comparison of mTHPC and polyethylene glycol‐derived mTHPC on human tumor xenografts and tumor‐free bronchi of minipigs
Author(s) -
Ris HansBeat,
Hof Vinzenz Im,
Stewart Charles M.,
Mettler D.,
Altermatt HansJörg
Publication year - 1998
Publication title -
lasers in surgery and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.888
H-Index - 112
eISSN - 1096-9101
pISSN - 0196-8092
DOI - 10.1002/(sici)1096-9101(1998)23:1<25::aid-lsm4>3.0.co;2-y
Subject(s) - photodynamic therapy , medicine , adenocarcinoma , necrosis , pathology , radiation therapy , cancer research , chemistry , cancer , organic chemistry
Background and Objective Photodynamic therapy (PDT) with mTHPC and polyethylene glycol‐derived mTHPC (pegylated mTHPC) was compared on nude mice bearing human squamous cell carcinoma and adenocarcinoma xenografts. The same treatment regimens were applied to the bronchi of tumor‐free minipigs to assess injury to normal tissue. Study Design/Materials and Methods: Laser light (652 nm, 20 J/cm 2 ) was delivered as surface radiation to the xenografts 4 days after intraperitoneal administration of 0.1 mg/kg mTHPC or an equimolar dose of pegylated mTHPC, respectively. The extent of tumor necrosis was assessed by histomorphometry. Endobronchial PDT was performed on the bronchi of minipigs with the same drug and light doses at drug‐light intervals ranging from 12–96 hr. Results Both sensitizers produced larger necrosis of squamous cell carcinoma and adenocarcinoma xenografts than was observed in untreated controls ( P < 0.005). Pegylated mTHPC led to larger tumor necrosis than mTHPC in squamous cell carcinoma ( P < 0.001), but not in adenocarcinoma xenografts. mTHPC‐PDT resulted in ulceration and necrosis of bronchial mucosa in minipigs at drug‐light intervals ranging from 12–48 hr, which was not observed after use of pegylated mTHPC. Conclusions In this setting, pegylated mTHPC had advantages as a photosensitiser compared to mTHPC. Lasers Surg. Med. 23:25–32, 1998. © 1998 Wiley‐Liss, Inc.