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Cancer DNA repair

Scientists Gain Insight Into 'Cancer Paradox'

13 years, 5 months ago

618  0
Posted on Dec 28, 2004, 4 a.m. By Bill Freeman

A team of Korean scientists have found a way to solve the cancer paradox of why aging cells with reduced ability to proliferate are susceptible to cancer, characterized by uncontrolled cell growth. The team, led by Chosun University professor You Ho-jin, yesterday said that growth arrest in aging cells might directly lead to the formation of cell cancer, explaining the contradiction.

A team of Korean scientists have found a way to solve the cancer paradox of why aging cells with reduced ability to proliferate are susceptible to cancer, characterized by uncontrolled cell growth.

The team, led by Chosun University professor You Ho-jin, yesterday said that growth arrest in aging cells might directly lead to the formation of cell cancer, explaining the contradiction.

``We have proved that the slowed growth seen in aging cells does not necessarily protect these cells from becoming cancerous, contrary to general belief. Our findings will redirect the research tailored to fight cancer,'' You said.

As people age, the chance of developing tumors increases, especially from the late 40s.

Although this has been empirically recognized, doctors have failed to prove it scientifically because aging cells lose the ability to divide but cancer cells suffer divisions that become out of control.

In order to solve the cancer riddle, You's team investigated the human gene Bcl-2, which causes the arrest of growth or aging of cells, and learned the Bcl-2-induced cell growth slowdown does not protect these cells from shifting to explosive cell growth.

Instead, Bcl-2 barred the DNA repair mechanism, depriving the human body of a significant tool in countering mutations, dramatically heightening the likelihood of tumors appearing.

``Up until now, scientists have suspected cells accumulate mutations when they are young and become tumors when they are old. But we have learned aged cells suffer abrupt mutations due to a lack of DNA repair,'' You said.

During the lifetime of a cell, its DNA suffers constant damage through both normal metabolic activities and environmental factors like smoking or radiation.

These may cause structural mayhem to the DNA molecule and change the way a cell reads information encoded in its genes, posing a serious threat to the body.

To straighten things up, the human body has a two-phase self-repair mechanism. The first is a DNA repair system, which reverses the damage. But some cells struggle to keep up with ongoing repairs and acquire further mutations.

To protect the human body from the strain, human bodies rely on a last resort, called apoptosis, which means irreparably damaged DNA commits suicide as it is programmed to do.

It has been widely known that the Bcl-2 inhibits apoptosis, but You was the first to discover that the gene is directly associated with both aging and cancer through its role of attenuating the DNA repair system.

``Anti-cancer research will shift its focus toward finding substances that can protect the DNA repair mechanism, thus preventing tumors from occurring,'' You predicted.

His medical breakthrough will be printed in the next edition of Nature Cell Biology, a renowned science journal.

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