A new research reveals for the first time one of the mechanisms by which malignant melanoma, the most deadly form of skin cancer, grows and spreads. This discovery may lead to another crucial weapon in the rather small arsenal of treatments available for this dangerous disease and offer the first hope for a new melanoma treatment target in decades.
Study proves a role for an important gene called PTEN and suggests that PTEN dysfunction may be responsible in 30 percent to 60 percent of melanomas. //
The process leading to the formation of melanoma begins when a cell growing in the top-most layer of the skin is damaged, such as through severe sunburn. The damaged cells act as a melanoma trigger and, at first, the body's natural defense system is often able to fight them. But as they multiply, the melanoma cells develop new strategies to evade the body's immune system. The changes that occur in these cells are difficult to pinpoint and therefore, little is known about how and where they occur.
This study reveals PTEN as a target gene that is altered, enabling melanoma cells to form tumors. In non-cancerous cells, PTEN normally starts a chain reaction ensuring that malfunctioning and damaged cells are killed. In contrast, abnormal cancerous cells gain the ability to switch off PTEN, allowing the dysfunctional cells to survive and thrive. Accumulation of multiple changes like this in melanoma cells results in the development of a faster growing and more aggressive tumor.
A technique called chromosome transfer technology was used to transfer an entire chromosome 10 - about 5 percent of the genome - from healthy cells into the abnormal melanoma cells. The introduction of chromosome 10, which contains the PTEN gene, temporarily switched off the tumor cell growth in mice and allowed apoptosis, or cell death normally occurring in non-cancerous cells, to resume. Apoptosis made the cells behave more like normal cells, thereby clearing away the dysfunctiona
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