Two articles today provide good examples of the way in which cancer research benefits all fields of medicine. Effectively fighting cancer requires detailed knowledge of biochemical and genetic mechanisms and the ability to manipulate cellular processes - one could argue that all of the effort prior to the 1990s went into developing the tools to make the tools to do the work. Only with comparatively recent capacities in genetics and bioinformatics has real progress been made in understanding cancer and developing cures. This work brings very real benefits to all other areas of medicine - knowing how cells work is revolutionizing the way in which new medicine is created.
While mutations in Rb, are linked to several types of cancer including the childhood disease retinoblastoma, Rb normally keeps cell division in check. That means Rb is a tumor suppressor gene, which keeps cells from growing out of control. Scientists believe that Rb is linked to two key processes that frequently malfunction when cancer begins - proliferation (cell growth), and apoptosis (cell death).
Knowing how Rb functions in normal cells could clue scientists in to the gene's behavior as a tumor suppressor and why it mutates. It could also ultimately help scientists understand how other types of cancer progress.
"Cancer cells are altered in so many different ways that it's hard to conduct controlled experiments with them," Leone said. "That's why we need to figure out what Rb normally does, as opposed to studying a mutated version of the gene in a cancer cell. This may also help us uncover the mechanisms that cause mutations in other tumor-suppressing genes."
"Virtually all cancer cells acquire the ability to change their genomic structure," said Saunders. "Researchers in the field are looking for single events that can cause multiple mutational changes to the genome, and this research is an example of that."
Before a normal cell divides, its chromosomes are duplicated and then pulled apart by a structure called a spindle, so that the two daughter cells each will have the same number of chromosomes.
At the end of a normal spindle is the spindle pole, also called the centrosome, which pulls the chromosomes outward. Cancer cells often have extra centrosomes. When a cell has more than two centrosomes, sometimes--but not always--the spindles will have more than one pole and cell division won't work correctly, leading to the swapping of genetic material, uncontrolled cell division, and the formation of tumors.
Why this doesn't always happen when there are too many centrosomes was the focus of the Pitt researchers' investigation. They found that as long as the extra centrosomes "cluster" together, the spindles will form normally, with two ends, and the cells will divide normally. "No one else appreciated that that was required, or what the mechanism was that separated them," said Saunders.
Investigating the mechanism by which this occurs, the researchers found that in cultured oral cancer cells a protein called dynein is missing from the spindle, and the centrosomes no longer cluster together.
Furthermore, the researchers discovered that in some types of tumors, dynein is inhibited by the overexpression of another protein called NuMA. Excess NuMA seems to prevent dynein from binding to the spindle. When they reduced the level of NuMA in cultured cancer cells, the dynein returned to the spindles, and the spindles were no longer multipolar.
"This finding suggests that a possible treatment for some types of cancer could be a drug that inhibits NuMA."
This sort of detailed knowledge of cellular processes will invariably prove useful to other scientists in other fields of medicine. There is no useless piece of the puzzle when it comes to understanding how our bodies work. Curing cancer is a very necessary part of the march towards longer, healthier lives - but the knowledge acquired while doing it will be essential to more directed attempts to extend the healthy human life span.