000 04172nam a22004455i 4500
001 978-1-4419-0711-0
003 DE-He213
005 20140220084503.0
007 cr nn 008mamaa
008 110414s2010 xxu| s |||| 0|eng d
020 _a9781441907110
_9978-1-4419-0711-0
024 7 _a10.1007/978-1-4419-0711-0
_2doi
050 4 _aRC261-271
072 7 _aMJCL
_2bicssc
072 7 _aMED062000
_2bisacsh
082 0 4 _a614.5999
_223
100 1 _aThomas-Tikhonenko, Andrei.
_eeditor.
245 1 0 _aCancer Genome and Tumor Microenvironment
_h[electronic resource] /
_cedited by Andrei Thomas-Tikhonenko.
264 1 _aNew York, NY :
_bSpringer New York,
_c2010.
300 _aIX, 480p. 58 illus., 29 illus. in color.
_bonline resource.
336 _atext
_btxt
_2rdacontent
337 _acomputer
_bc
_2rdamedia
338 _aonline resource
_bcr
_2rdacarrier
347 _atext file
_bPDF
_2rda
490 1 _aCancer Genetics
505 0 _aOpening 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.
520 _aOncogenes 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.
650 0 _aMedicine.
650 0 _aOncology.
650 1 4 _aBiomedicine.
650 2 4 _aCancer Research.
650 2 4 _aOncology.
710 2 _aSpringerLink (Online service)
773 0 _tSpringer eBooks
776 0 8 _iPrinted edition:
_z9781441907103
830 0 _aCancer Genetics
856 4 0 _uhttp://dx.doi.org/10.1007/978-1-4419-0711-0
912 _aZDB-2-SBL
999 _c110240
_d110240