Hardwiring Tumor Progression

Chapter
Part of the Cancer Genetics book series (CANGENETICS)

Abstract

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 1980s–mid-1990s, neoplastic growth was described largely as a net imbalance between cell accumulation and loss, brought about through mutations in cancer genes (Evan and Littlewood, 1998). In the last 10 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. (Hanahan and Weinberg, 2000). Nevertheless, the commonly held view is that changes in tumor microenvironment are “softwired,” 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. This book will review how tumor microenvironment and progression can be “hardwired,” i.e., genetically controlled.

Keywords

Lymphoma Tyrosine Leukemia Myeloma Boris 

References

  1. Evan G, Littlewood T (1998) A matter of life and cell death. Science 281:1317–1322PubMedCrossRefGoogle Scholar
  2. Hanahan D, Weinberg RA (2000) The hallmarks of cancer. Cell 100:57–70PubMedCrossRefGoogle Scholar
  3. Land H, Parada LF, Weinberg RA (1983) Tumorigenic conversion of primary embryo fibroblasts requires at least two cooperating oncogenes. Nature 304:596–602PubMedCrossRefGoogle Scholar
  4. Vogelstein B, Kinzler KW (2004) Cancer genes and the pathways they control. Nat Med 10:789–799PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC 2010

Authors and Affiliations

  1. 1.D516H Abramson Research CenterUniversity of Pennsylvania and the Children’s Hospital of PhiladelphiaPhiladelphiaUSA

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