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|a 9781441907110
|9 978-1-4419-0711-0
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|a 10.1007/978-1-4419-0711-0
|2 doi
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|a 616.994
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|a Cancer Genome and Tumor Microenvironment
|h [electronic resource] /
|c edited by Andrei Thomas-Tikhonenko.
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|a 1st ed. 2010.
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|a New York, NY :
|b Springer New York :
|b Imprint: Springer,
|c 2010.
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|a IX, 480 p. 45 illus., 16 illus. in color.
|b online resource.
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|a text
|b txt
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|a computer
|b c
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|a online resource
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|a text file
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|a Cancer Genetics,
|x 2626-1464
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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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|a Cancer.
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|a Oncology.
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|a Cancer Biology.
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|a Oncology.
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|a Thomas-Tikhonenko, Andrei.
|e editor.
|4 edt
|4 http://id.loc.gov/vocabulary/relators/edt
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|a SpringerLink (Online service)
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|t Springer Nature eBook
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|i Printed edition:
|z 9781441907127
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|i Printed edition:
|z 9781461425243
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|i Printed edition:
|z 9781441907103
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|a Cancer Genetics,
|x 2626-1464
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|u https://doi.uam.elogim.com/10.1007/978-1-4419-0711-0
|z Texto Completo
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|a ZDB-2-SBL
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|a ZDB-2-SXB
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|a Biomedical and Life Sciences (SpringerNature-11642)
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|a Biomedical and Life Sciences (R0) (SpringerNature-43708)
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