Oncogenes and tumor suppressor genes had been traditionally studied in the context of cell proliferation, differentiation, senescence, and survival, four relatively cell-autonomous processes. Consequently, in the late ’80s-early ’90s, neoplastic growth was described largely as an imbalance between net cell accumulation and loss, brought about through mutations in cancer genes. In the last ten years, a more holistic understanding of cancer has slowly emerged, stressing the importance of interactions between neoplastic and various stromal components: extracellular matrix, basement membranes, fibroblasts, endothelial cells of blood and lymphatic vessels, tumor-infiltrating lymphocytes, etc. The commonly held view is that changes in tumor microenvironment are “soft-wired”,i.e., epigenetic in nature and often reversible. Yet, there exists a large body of evidence suggesting that well-known mutations in cancer genes profoundlyaffect tumor milieu. In fact, these non-cell-autonomous changes might be one of the primary reasons such mutations are preserved in late-stage tumors. INDICE: Part One: Opening remarks. 1. Hardwiring tumor progression. Part Two: Breaking away: Epithelial-mesenchymal transition. 2. I3K/AKT pathway and the epithelial-mesenchymal transition. 3. Loss of cadherin-catenin adhesion system in invasive cancer cells. 4. Rho GTPases in regulation of cancer cell motility, invasion, and microenvironment. 5. Merlin/NF2 tumor suppressor and Ezrin-Radixin-Moesin (ERM) proteins in cancer development and progression. Part Three: Coming up for air: Hypoxia and Angiogenesis. 6. von Hippel–Lindau tumor suppressor, hypoxia-induced factor-1, and tumor vascularization. 7. RAS oncogenes and tumor-vascular interface. 8. Myc and control of tumor neovascularization. 9. p53 and angiogenesis. 10. Ink4a locus: beyond cell cycle. Part Four: Gaining new ground: Metastasis and stromal cell interactions. 11. NM23 as a metastasis inhibitor. 12. HGF/c-MET signaling in advanced cancers. 13. Contribution of ADAMs and ADAMTSs to tumor expansion and metastasis. 14. Stromal cells ; tumor milieu: PDGF et al. 15. Tgf-beta signaling alterations in neoplastic and stromal cells. Part Five: Getting attention: Immune recognition and inflammation. 16. Genetic Instability and Chronic Inflammation in Gastrointestinal Cancers. 17. Immunoglobulin gene rearrangements, oncogenic translocations, B-cell receptor signaling, and B-lymphomagenesis. 18. Modulation of Philadelphia chromosome-positive hematological malignancies by bone marrow microenvironment. Part6: Putting it all together. 19. Melanoma: mutations in multiple pathways at the tumor-stroma interface. 20. Cooperation and Cancer.
- ISBN: 978-1-4419-0710-3
- Editorial: Springer
- Encuadernacion: Cartoné
- Páginas: 392
- Fecha Publicación: 01/10/2009
- Nº Volúmenes: 1
- Idioma: Inglés