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Mechanism of gadophrin‐2 accumulation in tumor necrosis
Author(s) -
Hofmann Birte,
Bogdanov Alexei,
Marecos Edgardo,
Ebert Wolfgang,
Semmler Wolfhard,
Weissleder Ralph
Publication year - 1999
Publication title -
journal of magnetic resonance imaging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.563
H-Index - 160
eISSN - 1522-2586
pISSN - 1053-1807
DOI - 10.1002/(sici)1522-2586(199902)9:2<336::aid-jmri28>3.0.co;2-3
Subject(s) - mechanism (biology) , necrosis , pathology , medicine , cancer research , physics , quantum mechanics
Abstract The molecular mechanism by which gadophrin‐2 targets necrotic tumor tissue was investigated. Biodistribution studies and magnetic resonance imaging (MRI) and histologic/autoradiographic correlation were performed in xenograft mouse models bearing human tumors (HT 29, WiDr, LX 1). Binding of gadophrin‐2 to DNA, lipids, or proteins was determined by fluorescence spectrophotometry. Protein binding was determined by dialysis and gel electrophoresis. Accumulation of gadophrin‐2 was low (<0.7% injected dose/g tissue at 24 hours after injection) in viable tumor but higher in necrotic tumor regions and was readily detectable by MRI. Within a given tumor, the agent preferentially localized in the periphery of necrotic areas. Within these regions gadophrin‐2 was bound to interstitial albumin and not other proteins, lipids, or DNA. Tumoral accumulation of gadophrin‐2 most likely occurs through its binding to plasma albumin and subsequent slow extravasation into the tumor interstitium.J. Magn. Reson. Imaging 1999;9:336–341. © 1999 Wiley‐Liss, Inc.