Cancer comes in many shapes and forms with a whole host of underlying causes. A few select types are caused by viruses, many have lost the ability to flip the “off” switch of cell division, while others have intentionally disabled the self-destruct button. That’s why cancer is so hard to “cure.” It’s much like the common cold, where there are just so many different varieties that are caused by a dizzying array of small tweaks and malfunctions, it’s nigh impossible to find a silver bullet to treat more than one, let alone a wide array.
One particular root cause of cancer that recently struck the fancy of researchers at the University of Wisconsin was the appearance of too much genetic material. Humans have two sets of chromosomes in each cell nucleus working together to create the molecular engines of life. And just like a poorly written IKEA instruction manual, if there are extra unnecessary instructions, it can cause the production of a piece of junk.
For example, roughly 14 percent of breast cancers and 35 percent of pancreatic cancers have extra sets of chromosomes. In this case, two is company, three is a crowd, and four will fucking kill you.
Well, three probably will too, but that’s beside the point.
To study these subsets of cancers with two extra sets of chromosomes, researchers first set forth to create a plethora of specimens to work with. To do this, they took normal cells on their path of mitosis and simply stopped them from completing their work.
If you recall form middle school, mitosis is the process by which cells divide. The genetic material is duplicated, the two sets move to opposite sides of the enlarging cell, and the whole thing splits down the middle into two daughter cells. Sure, there are a lot more details involved, but this is a blog, not a sixth grade classroom. And I’m definitely not my sixth grade science teacher Mr. Joliff.
One detail that is important to note, however, is how the cell divides. In animal cells, a small pinch appears at the center of the elongated cell containing a ring that eventually contracts to pinch the cell into two. In this experiment, the researchers simply stopped this final, crucial step from happening. The result, they figured, would be a whole bunch of cells with double the amount of genetic material that they could then use to study cancer.
But that’s not what happened.
When they came back, a small but significant number of cells had nonetheless divided into two healthy daughter cells, each with its own nucleus and proper amount of genetic material. Confused, the researchers did what any normal human being would – they put them on tape.
Sure enough, the resulting images showed the cells undergoing a type of cell division that had never been seen before in humans. Dubbed cytofission, the cells managed to pull far enough away from each other that they broke apart and formed new cell walls, even without the help of the pinching ring. Such cell division had been seen before in more primitive forms of life, such as slime molds, but nobody knew we had it in us.
It appears that this is a survival mechanism that we’ve managed to retain during our long course of evolution. When left to their own devices, 90 percent of the mitosis-interrupted cells underwent cytofission and continued on their healthy, normal life cycles.
So the question remaining to the scientists, then, is what stops the rest of the 10 percent from avoiding the problem of having twice as many blueprints in its shop? If they can solve that one, then perhaps they can figure out a way to stop cancers from forming that are a result of having an extra copy of DNA floating about in one’s cells. A lofty goal to be sure, but hey, stranger technologies have started as accidental discoveries in the laboratory.
The paper, “Interphase cytoﬁssion maintains genomic integrity of human cells after failed cytokinesis,” was published in the Proceedings of the National Academy of Sciences by Mark Burkard, assistant professor of hematology-oncology at the University of Wisconsin, and colleagues Alka Choudhary, Robert Lera, Meelissa Martowicz, Kim Oxendine, Jennifer Laffin, and Beth Weaver, all also of the University of Wisconsin.