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?

According to a Futurity article, it appears as though this will be the case. A new "backdoor" approach has been seen in order to help this form of brain cancer. Basically, it will be able to halt an enzyme that is responsible for the progression of glioblastoma, which is reason enough for organizations along the lines of Voices against Brain Cancer to bring their focus on it. What are the specifics behind this, though, and how was the study carried through? The details are quite interesting, to say the least.

The enzyme that was focused on was referred to as phospholipase D, though it's not just in the realm of brain cancer that this has been seen. Other types of cancers like breast and gastric have been correlated to it as well, so it goes without saying that it has seen a great deal of attention in the way of science. PLD is also responsible for the regulation of Akt, another enzyme that is integral to cancer growth. There are many more details than I would have expected to uncover before reading this report.

PLD was given a tremendous amount of focus during a study with mice, each of the subjects afflicted with glioblastoma. One would assume that simply locking Akt would aid the problem but, as the article detailed, it is a course of action that stands a great chance of creating strong actions in the body. An exaggerated immune response, for example, could come to the surface. This subject deserves focus, without question, but care is another element that shouldn't be ignored.

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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