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Cancer Genome and Tumor Microenvironment [Paperback]

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  • Category: Books (Medical)
  • ISBN-10:  1461425247
  • ISBN-10:  1461425247
  • ISBN-13:  9781461425243
  • ISBN-13:  9781461425243
  • Publisher:  Springer
  • Publisher:  Springer
  • Pages:  480
  • Pages:  480
  • Binding:  Paperback
  • Binding:  Paperback
  • Pub Date:  01-Mar-2012
  • Pub Date:  01-Mar-2012
  • SKU:  1461425247-11-SPRI
  • SKU:  1461425247-11-SPRI
  • Item ID: 100733034
  • List Price: $219.99
  • Seller: ShopSpell
  • Ships in: 5 business days
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  • Delivery by: Jul 13 to Jul 15
  • Notes: Brand New Book. Order Now.

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.

There exists a large body of evidence suggesting that well-known mutations in cancer genes profoundly affect tumor milieu. The reviews in this book explore in detail how tumor microenvironment and progression are hard-wired at the genetic level.

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, endothelialÓ®

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