Cancer can arise through de-differentiation?

Tumor suppressor pulls double shift as reprogramming watchdog, Press Release, Salk Institute for Biological Studies, August 9, 2009. Excerpts:

A collaborative study by researchers at the Salk Institute for Biological Studies uncovered that the tumor suppressor p53, which made its name as "guardian of the genome," not only stops cells that could become cancerous in their tracks but also controls somatic cell reprogramming.

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"There's been a decade-old idea that cancer arises through the de-differentiation of fully committed and specialized cells but eventually it was discarded in favor of the currently fashionable cancer stem cell theory," says [Geoffrey] Wahl. "Now, that we know that p53 prevents de-differentiation, I believe it is time to reconsider the possibility that reprogramming plays a role in the development of cancer since virtually all cancer cells lose p53 function in one way or another."

See also: Cancer, stem cells linked in Salk study by Bradley J Fikes, North County Times, August 9, 2009. Excerpts:

A widely accepted theory of how cancer arises has been challenged by a study led by scientists at the Salk Institute.

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When the p53 gene is removed, normal cells can be reprogrammed into stem cells with a tenfold greater success rate, the study found.

If the link is confirmed by other researchers, it would undermine a popular hypothesis that cancers arise from "cancer stem cells," caused by genetic changes in stem cells, [Juan Carlos Izpisúa] Belmonte said. Instead, he suggested, cancer could begin when normal cells spontaneously reprogram themselves, for reasons yet unknown, beginning the process that results in a cancerous tumor.

Based on this publication: Linking the p53 tumour suppressor pathway to somatic cell reprogramming by Teruhisa Kawamura and 7 co-authors, including Geoffrey M Wahl and Juan Carlos Izpisúa Belmonte, Nature 2009(Aug 9) [Epub ahead of print][PubMed Citation].