So I felt as though I was straining away from blogging again (& a sure tale tell sign is when you make of list of things you see & want to blog about, but dismiss it later).
A great article that caught my eye last week. So in my last post I was kind of bashing on bioengineering, but projects like this really perk my interest in the field & give me hope.
Use the common cold virus to target & disrupt cancer cells?
A quick overview: Cancer is a disease associated with uncontrollable cell growth. Unfortunately, these mutant cells metastasize and travel throughout the body, thus taking much needed nutrients & space away from normal, useful, functioning cells.
Right now, as you probably know, there is no widely use method of treating cancer without the destruction of healthy cells. In this article, the mechanism in which cancer cells dodge apoptosis (cell suicide), and therefore multiply uncontrollably, is compared to the mechanism in which an adenovirus causes respiratory infection.
The gene p53 which is commonly referred to as a “tumor supressor” codes for cell death when cells are damaged. In both cancer & the adenovirus infection, p53 is disabled or degraded.
The question now is how can we target cancer cells specifically so we can treat & destroy them without killing a patient’s healthy cells?
Usually adenoviruses produce a protein E1B-55K to break down p53 in a cell & then destroy said cell. But without E1B-55K being released, it is hypothesized the only p53 deficient cells should in the body be cancer cells, thus leaving healthy cells alone when the virus decides to replicate & infect again.
So, in a nutshell, researchers were trying to exploit the fact adenoviruses only infect p53 deficient cells (aka cancer cells).
However, it’s not as easy as it sounds. Adenoviruses also bring along another protein E4-ORF3 to disrupt the integrity of the chromatin in a cell.
According to Estermann, a graduate student working on the project, the binding of E4-ORF3 cause “…parts of chromosomes to condense into so-called heterochromatin, burying the regulatory regions of p53 target genes deep within…with access denied, p53 is powerless to pull the trigger on apoptosis.”
Quick molecular review:
- heterochromatin: very condensed, looks very dark under a scope, may block regions to be expressed because so tightly coiled.
- euchromatin: more loose, lightly stained under a scope, typically expresses genes because more access available to transcribe genes.
However, with further research, scientists hope that by understanding how p53 is inactivated based on these new discoveries, it can help develop a p53 tumor selective oncolytic therapies.
Another article I looked up also wanted to use Salmonella to target cancer cells. I think it’s pretty smart to use viruses & bacteria as a basis of attacking cancer cells. They may seem like very simplistic creatures compared to the complexity of the human body, but clearly they are intelligent enough to survive all these years & procreate in even the most barren environments.