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Intro; Contents; 1: Drosophila Model in Cancer: An Introduction; 1.1 Introduction; 1.1.1 Genetic Tools Available in Drosophila; 1.1.2 The Use of Drosophila to Identify Cancer Related Genes and Pathways; 1.1.3 Drosophila as a "Whole Animal" Model System to Study Human Cancer; 1.1.4 Emerging Concepts from Drosophila Studies in Cancer; 1.1.5 Translational Aspects of Cancer Research in Drosophila; 1.2 Concluding Remarks; References; 2: Using Drosophila Models and Tools to Understand the Mechanisms of Novel Human Cancer Driver Gene Function; 2.1 Introduction
3: Drosophila Models of Cell Polarity and Cell Competition in Tumourigenesis3.1 Cell Competition; 3.2 Cell Polarity Regulator Proteins and Cell Competition; 3.2.1 Scribbled and Discs Large 1; 3.2.1.1 Signalling Pathways Regulating Cell Competition; 3.2.1.2 Systems to Sense Cell Fitness Between Neighbouring Cells; 3.2.1.3 Systems to Eliminate the Loser Cells During Competition; 3.2.2 Lethal (2) Giant Larvae; 3.2.2.1 Elimination of l(2)gl Mutant Clones Is Tissue Dependent; 3.2.2.2 Elimination of l(2)gl Mutant Clones in the Wing Epithelium Is Myc Dependent; 3.2.2.3 Mahjong
3.2.3 Crumbs3.2.3.1 Crumbs Alteration Can Induce Competitor or Super-Competitor Behaviours; 3.2.3.2 The Mechanism of Crb in Cell Competition; 3.2.4 Cell Competition During Cooperative Tumourigenesis; 3.3 Conclusions and Future Directions; References; 4: Two Sides of the Same Coin - Compensatory Proliferation in Regeneration and Cancer; 4.1 Introduction - Caspase-Driven Compensatory Proliferation: Coupling Apoptosis, Regeneration and Cancer; 4.2 Compensatory Proliferation: Studies in Drosophila melanogaster; 4.3 Compensatory Proliferation in Regeneration of Different Model Organisms
4.4 The "Dark Side" of Compensatory Proliferation: Role in Promoting Cancer4.5 Conclusions; References; 5: The Initial Stage of Tumorigenesis in Drosophila Epithelial Tissues; 5.1 Introduction; 5.2 Oncogenic Transformation; 5.3 Competitive Interaction Between Pro-Tumor Cells and Their Neighbors; 5.4 Misoriented Cell Division as an Initiator of Tumorigenesis; 5.5 The Cell Cycle Regulation of the Ovarian Follicle Cells; 5.6 Reintegration of Misplaced Cells as an Error-Correction System; 5.7 Tumorigenesis Induced by Endocytic TSGs Defects; 5.8 Tumor Hotspots, a Tissue-Intrinsic Oncogenic Niche
3: Drosophila Models of Cell Polarity and Cell Competition in Tumourigenesis3.1 Cell Competition; 3.2 Cell Polarity Regulator Proteins and Cell Competition; 3.2.1 Scribbled and Discs Large 1; 3.2.1.1 Signalling Pathways Regulating Cell Competition; 3.2.1.2 Systems to Sense Cell Fitness Between Neighbouring Cells; 3.2.1.3 Systems to Eliminate the Loser Cells During Competition; 3.2.2 Lethal (2) Giant Larvae; 3.2.2.1 Elimination of l(2)gl Mutant Clones Is Tissue Dependent; 3.2.2.2 Elimination of l(2)gl Mutant Clones in the Wing Epithelium Is Myc Dependent; 3.2.2.3 Mahjong
3.2.3 Crumbs3.2.3.1 Crumbs Alteration Can Induce Competitor or Super-Competitor Behaviours; 3.2.3.2 The Mechanism of Crb in Cell Competition; 3.2.4 Cell Competition During Cooperative Tumourigenesis; 3.3 Conclusions and Future Directions; References; 4: Two Sides of the Same Coin - Compensatory Proliferation in Regeneration and Cancer; 4.1 Introduction - Caspase-Driven Compensatory Proliferation: Coupling Apoptosis, Regeneration and Cancer; 4.2 Compensatory Proliferation: Studies in Drosophila melanogaster; 4.3 Compensatory Proliferation in Regeneration of Different Model Organisms
4.4 The "Dark Side" of Compensatory Proliferation: Role in Promoting Cancer4.5 Conclusions; References; 5: The Initial Stage of Tumorigenesis in Drosophila Epithelial Tissues; 5.1 Introduction; 5.2 Oncogenic Transformation; 5.3 Competitive Interaction Between Pro-Tumor Cells and Their Neighbors; 5.4 Misoriented Cell Division as an Initiator of Tumorigenesis; 5.5 The Cell Cycle Regulation of the Ovarian Follicle Cells; 5.6 Reintegration of Misplaced Cells as an Error-Correction System; 5.7 Tumorigenesis Induced by Endocytic TSGs Defects; 5.8 Tumor Hotspots, a Tissue-Intrinsic Oncogenic Niche