Wednesday, March 12, 2014

Brain Cancer & The Action Of Stopping PLD

By Rob Sutter


There could be a number of reasons as to why brain cancer could come about. It is apparent that enzymes could play a great role on the matter but what does this entail specifically? Keep in mind the presence of glioblastoma, which is regarded as the most serious type of cancer in this regard. It's likely to assume that as long as an enzyme is stopped in its tracks, matters will be made better, so what will play into this process to make it most effective?

Futurity put forth a report that spoke about a method that could help for this purpose. The report in question referred to it as a "backdoor" approach in order to help brain cancer and one of its potential triggers. It's possible that an enzyme related to glioblastoma can be stopped, which is a great point to consider when looking at organizations like Voices against Brain Cancer. Not all of the details are clear, though, which is why a learning experience is more than helpful here.

The enzyme in particular that was looked at was given the name of phospholipase D, though it isn't relevant to brain cancer alone. In fact, it is one that has been focused on while focusing on cancers the likes of breast and gastric. It's apparent that PLD has been given a tremendous amount of focus but another point to take into account is how it was able to regulate Akt. For those who are unaware, Akt is an enzyme that also plays into the growth of cancer.

The way that this was focused on, though, was during a study with mice, each of them afflicted with glioblastoma. It sounds like the blocking of Akt is a positive one but the truth of the matter is that going about such an action can create strong actions within the body. For example, the body can trigger an exaggerated immune response in addition to diabetic symptoms. It's clear that the focus brought on this enzyme is one that has to be done with the utmost care.

According to Professor Craig Lindsley, as the article stated, it is possible to modulate the one isoform associated with Akt without bringing harm to the patient. Without Akt being activated in the body, the cancerous cells in the body die, which does not negatively impact the patient in question in any way. This is especially vital in this field of research. As long as the implications do not long-lasting results, I do not think that anyone can argue with the level of potential seen here.




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