Aging, Nutrient Signaling, Hematopoietic Senescence, and Cancer

Priya Balasubramanian; Valter D.  Longo

doi:10.1615/CritRevOncog.2013010596

Critical Reviews™ in Oncogenesis

Editor en Jefe: Benjamin Bonavida (open in a new tab)

Publicado 4 números por año

ISSN Imprimir: 0893-9675

ISSN En Línea: 2162-6448

Indexed in

Aging, Nutrient Signaling, Hematopoietic Senescence, and Cancer

Volumen 18, Edición 6, 2013, pp. 559-571

DOI: 10.1615/CritRevOncog.2013010596

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Priya Balasubramanian
Andrus Gerontology Center, University of Southern California, 3715 McClintock Avenue, Los Angeles, California 90089-0191, USA

Valter D. Longo
Andrus Gerontology Center, the Molecular and Computational Biology Department, and the Norris Cancer Center, University of Southern California, 3715 McClintock Avenue, Los Angeles, California 90089-0191, USA

SINOPSIS

It is well known that cancer is one of the main causes of mortality in the aged population. Recent studies suggest that oncogenic pathways, such as the insulin-like growth factor-1 (IGF-I), Ras, and Akt/PKB, can contribute to both aging and cancer not only by promoting growth and preventing apoptosis, but also by promoting DNA damage and genomic instability. Epidemiological studies suggest that the chronic, low-grade inflammation that accompanies aging also contributes to tissue damage and tumor progression. Coupled with the accumulation of senescent cells and declining immune function, this leads to the generation and survival of cancer cells, possibly explaining why advanced age is the primary risk factor for cancer.

PALABRAS CLAVE: aging, cancer, inflammation, immunosenescence, hematopoietic stem cells

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