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Critical Reviews™ in Oncogenesis
SJR: 0.631 SNIP: 0.503 CiteScore™: 2

ISSN Imprimer: 0893-9675
ISSN En ligne: 2162-6448

Critical Reviews™ in Oncogenesis

DOI: 10.1615/CritRevOncog.2014010630
pages 549-558

Senescence and the Pro-tumorigenic Stroma

Elise Alspach
Department of Cell Biology and Physiology; BRIGHT Institute, Washington University School of Medicine, St. Louis, MO 63110
Yujie Fu
Department of Cell Biology and Physiology, BRIGHT Institute, Washington University School of Medicine, St. Louis, MO 63110
Sheila A. Stewart
Department of Cell Biology and Physiology, BRIGHT Institute, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110

RÉSUMÉ

Hayflick and Moorhead first described senescence in the late 1960's as a permanent growth arrest that primary cells underwent after a defined number of cellular divisions in culture. This observation gave rise to the hypothesis that cells contained an internal counting mechanism that limited cellular division and that this limit was an important barrier to cellular transformation. What began as an in vitro observation has led to an immense body of work that reaches into all fields of biology and is of particular interest in the areas of aging, tissue regeneration, and tumorigenesis. The initially simplistic view that senescence limits cellular division and contributes to aging while stymying tumorigenesis has now evolved into an important and complex biological process that has numerous caveats and often opposing effects on tumorigenesis. In this review, we limit our discussion to the complex role senescence plays in tumorigenesis. Throughout the review we attempt to draw many parallels to other systems including the role senescent cells play in the tumor microenvironment and their significant molecular and phenotypic similarities to cancer associated fibroblasts (CAFs).