Record Display for the EPA National Library Catalog

RECORD NUMBER: 45 OF 349

OLS Field Name OLS Field Data
Main Title Cancer Genome and Tumor Microenvironment [electronic resource] /
Type EBOOK
Author Thomas-Tikhonenko, Andrei.
Publisher Springer New York,
Year Published 2010
Call Number RC261-271
ISBN 9781441907110
Subjects Medicine. ; Oncology.
Internet Access
Description Access URL
http://dx.doi.org/10.1007/978-1-4419-0711-0
Collation IX, 480p. 58 illus., 29 illus. in color. online resource.
Notes
Due to license restrictions, this resource is available to EPA employees and authorized contractors only
Contents Notes
Opening Remarks -- Hardwiring Tumor Progression -- Breaking Away: Epithelial-Mesenchymal Transition -- PI3K/AKT Pathway and the Epithelial-Mesenchymal Transition -- Loss of Cadherin-Catenin Adhesion System in Invasive Cancer Cells -- Rho GTPases in Regulation of Cancer Cell Motility, Invasion, and Microenvironment -- Merlin/NF2 Tumor Suppressor and Ezrin-Radixin-Moesin (ERM) Proteins in Cancer Development and Progression -- Coming up for Air: Hypoxia and Angiogenesis -- von Hippel-Lindau Tumor Suppressor, Hypoxia-Inducible Factor-1, and Tumor Vascularization -- RAS Oncogenes and Tumor-Vascular Interface -- Myc and Control of Tumor Neovascularization -- p53 and Angiogenesis -- Ink4a Locus: Beyond Cell Cycle -- Gaining New Ground: Metastasis and Stromal Cell Interactions -- Nm23 as a Metastasis Inhibitor -- HGF/c-MET Signaling in Advanced Cancers -- Contribution of ADAMs and ADAMTSs to Tumor Expansion and Metastasis -- Stromal Cells and Tumor Milieu: PDGF et al. -- TGF-? Signaling Alterations in Neoplastic and Stromal Cells -- Getting Attention: Immune Recognition and Inflammation -- Genetic Instability and Chronic Inflammation in Gastrointestinal Cancers -- Immunoglobulin Gene Rearrangements, Oncogenic Translocations, B-Cell Receptor Signaling, and B Lymphomagenesis -- Modulation of Philadelphia Chromosome-Positive Hematological Malignancies by the Bone Marrow Microenvironment -- Putting It All Together -- Melanoma: Mutations in Multiple Pathways at the Tumor-Stroma Interface -- Cooperation and Cancer. 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-mid '90s, neoplastic growth was described largely as a net imbalance between cell accumulation and loss, brought about through mutations in cancer genes. In the last ten years, a more holistic understanding of cancer 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 . Nevertheless, 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 profoundly affect tumor milieu. In fact, these cell-extrinsic changes might be one of the primary reasons such mutations are preserved in late-stage tumors. Cancer Genome and Tumor Microenvironment reviews how tumor microenvironment and progression can be "hard-wired", i.e. genetically controlled.