Cancer is so tricky because they are your own cells. So, even when your cells turn cancerous and betray you (et tu, brute?) its hard to fight them, and its hard to recognize which cells are cancerous. This makes it hard to fight cancers, because treatment requires killing the cancerous cells while protecting the normal cells.
There are many established ways to attack cancer: surgery, chemotherapy, radiotherapy, a combination. Then, there are the cool, new, awesome ways to attack cancer - using CAR T cells to detect minute differences between cancerous and normal cells, for example.
Recently a study was posted that shows another cool, new, awesome way to fight cancer - by forcing cancer cells to reveal themselves. By revealing themselves, the immune system is able to say "Hey! You're not normal" (and not "not normal" in like a special, unique way but "not normal" in like bad, bad, bad, you get it).
Chiappinelli et al., found that if you introduce DNMT (DNA methyltransferase) inhibitors to cancer cells you can trigger degradation of those cancer cells. DNA methyltransferases are enzymes that methylate DNA sequences. So, when you introduce a DNMT inhibitor, it was shown that you can reverse some crucial methylation on sequences that code for tumor suppressors, for example.
Furthermore, it was shown that administration of 5-azacytidine (a DNMT inhibitor) can also illicit immune responses in and to cancer cells. 5-azacytidine was observed to induce the expression of surface antigens and their associated proteins. This phenomenon could be exploited by the use of CAR T cells to specifically target the induced antigens on cancer cells.
But, wait! Wait! There's more! 5-azacytidine also has another mechanism. This mechanism induces a cystolic dsRNA sensing pathway that pstimulates a type 1 interferon resone cumulating in the release of chemokine ligand 10 (CXCL10), which serves as a chemoattractant for cytotoxic (or killer) T cells.
The significance of this is this: administration of 5-azacytidine might be all we need to induce cancer cells to reveal themselves by two mechanisms: the induced presence of potentially exploitable surface antigens, and the induced stimulation of a pathway that ends in the release of a substance that attracts killer T cells (which then "kill" the infected cell).
Thus, methods are developing to make cancer cells physically and molecularly different from normal cells.
Neat!
TL;DR: We got 99 problems, and soon, cancer might not be one!
References:
http://www.sciencedirect.com/science/article/pii/S009286741500848X
http://www.jimmunol.org/content/168/7/3195.full.html
This is so interesting! I'm curious if there are limits to what types of cancer cells can be targeted using these new drugs. And if cancers which come to be by specific mutations are more or less susceptible to these treatments. I'm also curious if this process could be used in reverse as a potential treatment for autoimmune disorders. To see if the use of DNMT activators would prevent the activation of the enhanced immune response seen in autoimmune disorders.
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