Chemical carcinogen induction of skin tumors in mice was investigated to determine (i) if tumor induction efficacy was modified by single gene mutations, (ii) if the histologic types of the tumors varied with these mutations, and (iii) if a novel papillomavirus was involved as a cocarcinogen. A two-
Morphological and carbogen-based functional MRI of a chemically induced liver tumor model in mice
✍ Scribed by Carole D. Thomas; Evelyne Chenu; Christine Walczak; Marie-José Plessis; François Perin; Andreas Volk
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 1016 KB
- Volume
- 50
- Category
- Article
- ISSN
- 0740-3194
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✦ Synopsis
Abstract
A multifocal mouse liver tumor model chemically induced with 5,9‐dimethyl‐7H‐dibenzo[c,g]carbazole was investigated by respiratory‐triggered morphological and functional MRI (fMRI) at 4.7 Tesla. The model is characterized by the presence of two tumor types: hypovascular cholangioma and vascularized hepatocellular carcinoma (HCC). Growth curves measured by 3D‐MRI showed limited growth of cholangiomas and rapid growth of HCCs after a latency of about 25 weeks. Functional imaging based on T‐weighted fast gradient‐echo MRI and carbogen breathing was optimized for liver imaging in mice. A response to carbogen was observed in HCCs but not in cholangiomas. Transversal analysis (50 HCCs) of signal change upon carbogen revealed four different types of response patterns: 1) signal increase upon carbogen administration (74%); 2) small or insignificant signal change (10%), 3) transient signal decrease and delayed increase (8%), and 4) signal decrease (8%). Longitudinal follow‐up of a subgroup (N = 17) showed that an initially observed type 1 response, attesting to the presence of a functional vasculature, remained stable for at least 3 weeks in 14 HCCs. A switch from a type 1 response to another response type may be useful for demonstrating, in a noninvasive manner, a disturbance of tumor vasculature induced by anti‐vascular or anti‐angiogenic therapy. Magn Reson Med 50:522–530, 2003. © 2003 Wiley‐Liss, Inc.
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