It has been known for decades that tumors develop when there is a mutation in an individual gene(s). By knowing the type of mutation, scientists can predict the kind of cancer one may develop. However, this theory does not tell the whole story. There are some types of brain cancers where no gene mutation is found, and for years, scientists have been trying to figure out the reason. Why would cells under normal control suddenly start to become cancerous and spread?
New Boston Study Could Be HUGE Breakthrough
Now a study from Boston may provide more clues. The results reported in the Journal Nature reveal that in some brain cancers, there is a disruption in the 3-Dimensional structure and organization of DNA groups that may be the cause. As a result, two different gene groups that are usually separated like “gated” communities, suddenly merge. When this merger occurs, the dormant (sleepy) growth gene suddenly awakens and takes off by multiplying uncontrollably.
This type of phenomenon has never before been recognized in cancer cells but is probably not unique to brain cancers. The researchers in Boston mention that this discovery could help make a significant breakthrough in treatment; by developing medications that can restore the wall/partition separating the DNA sections.
Glioma Brain Tumors: Making Positive Progress
This news will be most welcome by patients with one of the most common type of malignant brain tumors known as gliomas. Each year in the US, nearly 18,000 cases are diagnosed, and the most aggressive of the gliomas is the glioblastoma, which kills most of those affected within 18 months. The lower grade gliomas tend to grow slowly and survival times are much longer. However, little progress has been made in the treatment of gliomas over the past three decades. Even though surgery, radiation, and chemotherapy are used aggressively, these tumors are resistant and often recur.
The other feature that the researchers noted was that in about 80% of cases of gliomas, a common gene with no relevance to cancer was frequently mutated. The gene, isocitrate dehydrogenase, is known to play a role in energy production, and yet it was elevated in many gliomas. The question was why was this gene mutated?
What the researchers noted was with the mutation of the gene, the cancer cells became tagged with methyl groups. It is now believed that it is these methyl group tags that play a role in the disruption of the 3D structure of DNA. Typically, human DNA is tightly packed and forms thousands of independent loops like separate “gated” communities. The walls between the loops are made of a protein called CTCF. It is now believed that the extra methyl tags have the ability to remove the CTCF walls and allow the neighborhood DNA communities to merge.
The Goal: Detect and Eliminate Methyl Groups!
So is there a way to stop this extra methylation? Yes, these Boston scientists have already started to look at drugs that can dissolve the methyl groups. One old cancer drug that was studied is 5-Azacytidine. This agent is known to dissolve methyl groups, and it did turn the growth gene off by dissolving the methyl groups in cancer cells grown in the laboratory.
It is anticipated that by treating glioma patients with drugs like 5-azacytidine one may prevent the extra methyl groups and restore DNA loops. It is hoped that this discovery may also apply to the treatment of many other cancers with a high number of methylated tags on their DNA.
The only thing needed now is a cost efficient and easy method of detecting methyl tags in DNA. In the meantime, search for drugs that can prevent methylation of DNA has gained renewed interest.