[Frontiers in Bioscience, 3, d208-236, February 15, 1998]
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CAVEAT LECTOR




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CELL-CELL COMMUNICATION IN CARCINOGENESIS

James E. Trosko1, Randall J. Ruch2

1Department of Pediatrics and Human Development, Michigan State University, East Lansing, Michigan 48824, 2Department of Pathology, Medical College of Ohio, Toledo, Ohio

Received 2/2/98 Accepted 2/6/98

TABLE OF CONTENTS

1.Abstract
2.Introduction
3.Evolution and cancer
4.Theories of carcinogenesis: Overview
5.Stem cell versus the de-differentiation theories
6.Initiation/promotion/progression theory of carcinogenesis
7.Nature and nurture theory of carcinogenesis
8.Mutation versus the epigenetic theories of carcinogenesis
9.Oncogene and tumor suppressor gene theories
10.Gap junctions - ancient and ubiquitous mediators of cellular homeostasis
11.Structure of gap junctions
12.The connexin multigene family
13.Regulation of connexin gene expression
14.Gap junction formation, control of channel permeability, and mechanisms of disrupted GJIC
15.Multiple functions of GJIC
16.Role of GJIC in regulating cellular proliferation and neoplasia
16.1. Neoplastic cells have fewer gap junctions
16.2. Growth stimuli inhibit GJIC
16.2.1. Carcinogens
16.2.2. Oncogenes
16.2.3. Growth Factors
16.3. Growth inhibitors stimulate GJIC
16.4. Cell cycle-related changes in GJIC
17.Involvement of GJIC in the growth inhibition of neoplastic cells by nontransformed cells
18.Specific disruption and enhancement of GJIC
18.1. Connexin antisense studies
18.2. Connexin gene knockout
18.3. Dominant-negative inhibition of connexin function
18.4. Connexin transfection studies
19.GJIC and other growth control mechanisms
20.Growth regulation mediated by a gap junction signal
21.Modulation of GJIC for cancer therapy
22.Acknowledgment
23.References
24. Entire manuscript

Key words: Connexins; Connexons; Gap junctions; Tumor promotion; Carcinogenesis; Stem cells; Intercellular communication; Oncogenes

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