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Solving A Cancer Paradox - Why Ageing Cells Turn Into Tumours

  January, 11 2005 9:09
your information resource in human molecular genetics
As we age, the chances of developing tumours increase. While this commonly known characteristic seems to make sense, it is actually a paradoxical observation: ageing cells undergo an irreversible growth arrest but cancer is characterized by uncontrolled cell growth. A report published in Nature Cell Biology by You and colleagues now shows that growth arrest in aging cells might directly lead to cell cancer formation explaining this apparent contradiction.

During the lifetime of a cell, its DNA is constantly damaged by environmental factors like smoking or radiation. This would cause mayhem in our genetic code, leading to a high rate of tumour formation in all of us, if we did not have sophisticated DNA repair systems that can reverse this damage. Nevertheless, some cells struggle to keep up with the ongoing repairs and acquire mutations that can lead to uncontrolled cell growth. To circumvent tumour formation, these cells are normally programmed to commit suicide - a safety mechanism called apoptosis.

You and colleagues have now investigated the human gene Bcl-2, which surprisingly has the ability to both inhibit apoptosis (supporting tumour formation) and induce cell growth arrest (inhibiting tumour formation). They explain this contradiction by showing that the Bcl-2-induced cell growth arrest does not necessarily protect these cells from becoming cancerous, as commonly thought. Rather, it causes inhibition of a DNA repair mechanism called mismatch repair and this subsequently leads to a dramatic accumulation of mutations and carcinogenesis.

This discovery links cell growth arrest - mainly seen in ageing cells - with carcinogenesis and so sheds new light on the development of human cancer.

Author contact:

Ho J. You (Chosun University, Gwangju, Republic of Korea)
Tel: +82 62 230 6337
E-mail: hjyou@chosun.ac.kr

(C) Nature Cell Biology press release.

Message posted by: Trevor M. D'Souza

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