[Frontiers in Bioscience, 3, d672-683, July 1, 1998]
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CAVEAT LECTOR




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PLASTICITY OF CD44S EXPRESSION DURING PROGRESSION AND METASTASIS OF FIBROSARCOMA IN AN ANIMAL MODEL SYSTEM

Lloyd A. Culp1 and Priit Kogerman2

1 Department of Molecular Biology and Microbiology, Case Western Reserve University School of Medicine Cleveland, OH 44106, USA 2 Karolinska Institutet, Department of Biosciences, Novum, S-141 57, Huddinge, Sweden

Received 4/27/98 Accepted 5/15/98

TABLE OF CONTENTS

1. Abstract
2. Introduction and background
2.1 CD44 in primary tumors
2.2 CD44 correlates with metastasis
2.3 Parallels with lymphocyte homing
3. CD44s and growth regulation in the 3T3/oncogene system
3.1 CD44 levels in oncogene transformants and tumors
3.2 CD44 modulation in nonmetastatic systems
4. CD44s overexpression: acquisition of metastatic potential
4.1 Three cell systems under study--transfection of human CD44s gene
4.2 CD44s as HUSI progresses and metastasizes
4.3 Counter-selection model of progression
4.4 CD44s as revertant or 3T3 transfectants progress and metastasize
4.5 In vivo analyses of CD44s levels
5. CD44s gene hypermethylation: mechanism of expression modulation
6. Functions for CD44s in metastatic spread
6.1 Earliest events analyzed with experimental metastasis model
6.2 Lung colonization results
6.3 Hyaluronan binding properties during early events of metastasis
6.4 Analyses of various tumor classes
6.5 Mixtures of two different CD44s classes
7. Perspectives for future mechanistic studies
7.1 Evaluating other connective tissue cell types
7.2 Modulating DNA hypermethylation in vivo
7.3 Suitable orthotopic model of fibrosarcoma
7.4 Significance of HA binding
7.5 Can these results be extrapolated to carcinoma systems?
8. Acknowledgements
9. References
10. Entire manuscript

Key words: CD44, Fibrosarcoma, Tumor, Tumor progression, Oncogene, Metastasis, Vasculature

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