Saturday, February 23, 2013

Epigenetics: Cancer Development Redefined

The Scientist & The Daily Beast.

When working with thyroid cancer, Dr.Stephen Baylin discovered certain enzymes and calcitonin that worked well as a biomarker for tumor recognition. Most tumors secrete calcitonin so researchers started looking at methylation in the 1980s , since methylation is responsible for random gene expression. Methylation is simply the addition of a methyl group on the outside of the DNA. To put it simply, it’s the same information held, but different casing. What they found was that methylation was being gained in certain tumors at hundreds of chromosomal regions on different genes. Thus begun his quest to understand the pile up of DNA methylation. It took his team 10 years to figure out that these densely methylated genes code for tumor suppression. Their first discovery was the p16 gene and a nucleoside analog called 5-azacytidine which disables an enzyme that normally methylates DNA residues. By removing the enzyme, gene expression can continue. They also discovered a DNA repair gene called MLH1 that is often muffled by methylation. This methylation pins down genes that are necessary to drive cell differentiation. This keeps tumor cells impressionable. Stem cell cancer cells were found to be just as treatable with 5-azacytide than any other variation of cancer. Most other therapies do not differentiate between cells and can harm healthy ones. Baylin also worked at USC identifying the MGMT DNA repair gene , which is silenced in many cancer patients. This can lead to higher cell damage. When cancer reoccurs in patients they shown a drastic amount of genetic mutations at multiple gene sites. Cancer is such a virulent disease that if you block a single protein pathway , but if you can slow the progression of the disease, more realistic results can occur like slowing tumor growth or early detection.

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