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Titlebook: Cancer Genome and Tumor Microenvironment; Andrei Thomas-Tikhonenko Book 2010 Springer-Verlag New York 2010 Chromosom.angiogenesis.cell.gen

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书目名称Cancer Genome and Tumor Microenvironment
编辑Andrei Thomas-Tikhonenko
视频video
概述Reviews how tumor microenvironment and progression are “hard-wired” at the genetic level.Includes supplementary material:
丛书名称Cancer Genetics
图书封面Titlebook: Cancer Genome and Tumor Microenvironment;  Andrei Thomas-Tikhonenko Book 2010 Springer-Verlag New York 2010 Chromosom.angiogenesis.cell.gen
描述.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 profoundly affect tumor milieu. In fact, these non-cell-autonomous changes might be one of the primary reasons such mutations are preserved in late-stage tumors..
出版日期Book 2010
关键词Chromosom; angiogenesis; cell; genes; lymphocytes; lymphoma; melanoma; metastasis; senescence; tumor; tumor pr
版次1
doihttps://doi.org/10.1007/978-1-4419-0711-0
isbn_softcover978-1-4614-2524-3
isbn_ebook978-1-4419-0711-0Series ISSN 2626-1456 Series E-ISSN 2626-1464
issn_series 2626-1456
copyrightSpringer-Verlag New York 2010
The information of publication is updating

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PI3K/AKT Pathway and the Epithelial-Mesenchymal Transitionhibitor .. By some estimates, . carries gain-of-function mutations in 32% of colorectal cancers, 36% of hepatocellular carcinomas, 36% of endometrial carcinomas, 25% of breast carcinomas, 15% of anaplastic oligodendrogliomas, and 5% of medulloblastomas and anaplastic astrocytomas (recently reviewed
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Myc and Control of Tumor Neovascularization control of a heavy chain gene enhancer (Dalla-Favera et al. 1982; Taub et al. 1982). Additionally, double minute chromosomes (dmin) containing amplified copies of the c-Myc gene are commonly detected in acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) (Storlazzi et al. 2004). In par
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Ink4a Locus: Beyond Cell Cycleactivation of p16 include melanoma, adenocarcinoma of the breast, squamous cell carcinomas of the lung, pancreatic adenocarcinomas, and colorectal carcinomas (Baylin et al. 1998; Pollack, Pearson, and Hayward 1996). In pancreatic adenocarcinoma, the frequency of p16 inactivation approaches 100% (Cal
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