An Old Theory Creates New Hope for Cancer
Researchers dicover new type of cell division that may help prevent cancer
-- by Alexia Severson
While testing a theory about cell division and the development of cancer, scientists discovered a new type of cell division that could help prevent the disease from forming in the first place, according to research presented at the American Society for Cell Biology Annual Meeting in San Francisco on Monday.
It takes an estimated 1,013 mitotic cycles—about 25 times the number of stars in our galaxy—to grow a human from a single fertilized egg. This kind of accuracy also counts in mitosis, a type of cell division that results in two daughter cells, each the same as the parent nucleus and a typical stage of ordinary tissue growth.
Scientists based this study on the theory developed in 1914 by the German cell biology pioneer Theodor Boveri, who believed that mistakes while dividing up chromosomes in human cells during the mitotic cell cycle would lead to aneuploidy—too many or too few chromosomes—in the resulting daughter cells. These abnormal cells would lead to out-of-control cell division and, ultimately, cancer.
Over 100 years later, using single-cell videomicroscopy techniques, scientists observed a new type of cell division called "klerokinesis." Researchers believe this type of cell division could be an evolutionary failsafe mechanism that could rescue a range of cell functions during embryonic development, allowing for genetic repair if cell division fails to produce normal cells.
The Expert Take
Study author Mark Burkard, M.D., Ph.D., said his team started the project about two years ago with the goal of making cells that mimic cancer by having too many chromosomes.
“But when we tried to make them, they kept coming back normal,” he said. “When we looked closely, we discovered they were recovering by the new type of cell division.”
Burkard said this type of error in a prior division was thought to lead to abnormal chromosome (DNA) content which could result in a cell turning into cancer. But Burkard and his colleagues discovered that cells can actually protect themselves with this new type of division.
“Human cells can divide in a new and unexpected way,” he said. “This can allow them to recover from an error in a prior division.”
Source and Method
Burkard and his colleagues worked with human retinal pigment epithelial (RPE) cells. The team allowed the PRE cells to undergo karyokinesis, or the orderly separation of chromosomes in mitosis. They blocked cytokinesis, the actual division into two daughter cells.
This process resulted in single cells with two nuclei, termed binucleate, which researchers let go through more mitotic cycles and proliferate, resulting in healthy daughter colonies.
According to the American Cancer Society’s Cancer Facts and Figures 2012, excluding basal and squamous cell skin cancers, an estimated 1,638,910 people in the U.S. will develop some form of cancer in 2012.
This discovery of a new type of cell division opens doors for novel cancer treatments and creates a better understanding of what causes the disease. This study also provides vital information to a theory that was developed over 100 years ago and adds new perspective to cell division and its role in cancer treatment. According to Burkard, if scientists can learn how to promote klerokinesis, they may be able to help prevent cancer.
In an article published in Science in 2007, researchers also examined aneuploidy and the gain of extra chromosomes, except this study focused on cellular physiology and cell division in haploid yeast. Scientists created a collection of haploid yeast strains, bearing an extra copy of one or more of almost all of the yeast chromosomes. Their characterization revealed that aneuploid strains share a number of characteristics. However, these characteristics were observed only in strains carrying additional yeast genes, indicating that they reflect the consequences of additional protein production as well as the resulting imbalances in cellular protein composition.
In another article, published in Current Opinion in Genetics & Development in 2007, authors wrote that aneuploidy is one of the most obvious differences between normal and cancer cells, but that it is undetermined whether aneuploid cells are a cause or consequence of the formation of tumors. But researchers hypothesize that abnormal division of tetraploid cells might facilitate genetic changes that lead to aneuploid cancers.
An article published in 2012 in the Journal of Cell Biology stated that “cellular defects that impair the fidelity of mitosis promote chromosome missegregation and aneuploidy.” Authors also highlighted the fact that mechanisms have been revealed linking abnormal mitosis with the development of DNA damage, how cells respond to such affronts, and the potential impact on tumor formation.