Cancer Genome and Tumor Microenvironment [electronic resource] / edited by Andrei Thomas-Tikhonenko.

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Call Number	614.5999
Title	Cancer Genome and Tumor Microenvironment edited by Andrei Thomas-Tikhonenko.
Physical Description	IX, 480 p. 45 illus., 16 illus. in color. online resource.
Series	Cancer Genetics
Contents	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.
Summary	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.
Added Author	Thomas-Tikhonenko, Andrei. editor. SpringerLink (Online service)
Subject	MEDICINE. CANCER RESEARCH. ONCOLOGY. Biomedicine. Cancer Research. Oncology.
Multimedia	http://dx.doi.org/10.1007/978-1-4419-0711-0

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950	Biomedical and Life Sciences (Springer-11642)

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$a 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.

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$a 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.

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Summary	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.
Contents	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.
Subject	MEDICINE. CANCER RESEARCH. ONCOLOGY. Biomedicine. Cancer Research. Oncology.
Multimedia	http://dx.doi.org/10.1007/978-1-4419-0711-0