Paradoxical down-regulation of p16(INK4a) mRNA with advancing age in Acute Myeloid Leukemia

Aging is generally considered to be the consequence of stem cell attrition caused by the activity of tumor suppressor pathways that censor potentially malignant clones by eliciting apoptosis or senescence. An important effector of aging is the cyclindependent kinase inhibitor p16(INK4a), which is al...

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Detalles Bibliográficos
Autores principales: de Jonge, Hendrik J.M., Woolthuis, Carolien M., de Bont, Eveline S.J.M., Huls, Gerwin
Formato: Texto
Lenguaje:English
Publicado: Impact Journals LLC 2009
Materias:
Research Perspective
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2815746/
https://www.ncbi.nlm.nih.gov/pubmed/20157576
Descripción
Sumario:Aging is generally considered to be the consequence of stem cell attrition caused by the activity of tumor suppressor pathways that censor potentially malignant clones by eliciting apoptosis or senescence. An important effector of aging is the cyclindependent kinase inhibitor p16(INK4a), which is also a known suppressor of cancer. The expression of p16(INK4a) is very low or absent in young organisms but increases with advancing age. We recently showed that, unlike healthy cells, acute myeloid leukemia (AML) derived blasts show a down-regulation of p16(INK4a) mRNA with increasing age. Based on this observation we hypothesize that suppression of defense mechanisms which protect older cells against cellular and DNA damage might facilitate oncogenesis in older individuals.

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