The usual way people think about disease is that it comes from a bacteria or virus and sometimes from an environmental agent.
The cures are most often medicines that help the immune system fight the invading agents or, in the case of the environment, techniques to remove the environmental danger.
Cancer is not like those diseases. Cancer cells are the result of genetic changes in the body.
When Dr. William J. Catalona says, “All prostate cancer is genetic in origin,” he does not mean that all prostate cancer is inherited.
What he and other scientists have come to understand is that the regulation of information from genes affects the production of cancer cells and, in the case of his studies, prostate cancer cells.
Rather than treat the cancer cells themselves – through removal as in a radical prostatectomy or through destruction of cancer cells as in chemotherapy– the search is on to find the causes (the genetic messages) that create the cancer.
Once those message areas are identified for particular types of cancers, the next step is to figure out ways to reverse or alter the messages through drug interventions that stop the creation of the cancer rather than treat the cancer itself.
Genes Regulate Cell Activity
Genes, through their protein messengers, regulate cell activities all the time; it’s just a natural part of living. But when the healthy process of creating cells starts to deteriorate – from causes not yet clear but somehow related to environment, age, ethnicity, diet or other as of yet unknown factors – more errors occur in the messages.
Identifying particular genetic areas with the proteins they produce, especially ones that send unregulated messages producing cancer cells, is extraordinarily complicated and for prostate cancer still very much in the research stage.
Using the Knowledge Now
“Donors giving money to research are impatient. They want to know how far we are from finding a cure for prostate cancer. But we can’t answer that question. What we can say is that we have identified a dozen different chromosome regions associated with prostate cancer that we didn’t know about four years ago.
“A more relevant question to ask now is, ‘How will we use the knowledge from the research as we look for cures?’” Dr. Catalona said.
He explained that as scientists learn more about the proteins that suppress or initiate the production and reproduction of prostate cancer cells, they will be able to test for them, just as men are tested now for PSA (protein specific antigen).
Not only will that information allow for earlier diagnosis but hopefully, doctors will know which proteins are associated with more aggressive cancers and which with less aggressive ones. Treatments will be more effective and will be directed by this new information.
Also, as researchers find the error messages that create too much activity in a cell (called overexpression) or too little activity in a cell (called underexpression), they will find ways to regulate the messages and bring the cell activity back to normal.
Cure Is Ultimate Goal
One model for hope in finding cancer cures is the drug Gleevec which works to turn off protein messages that produce certain leukemia cells. Gleevec was used in clinical studies for prostate cancer treatment, but it did not prove effective.
Avastin, a new drug that has shown good results in treating some colorectal and bone cancers and some Non-Hodgkins lymphomas, is now in Phase II clinical trials for prostate cancer treatment but results have not been reported.
“This trial and error method of finding treatments for prostate cancer is not the best approach. It appears that genetic error messages are specific to specific cancers. While, we all learn from the research of each other, genetic research for prostate cancer needs to be done using prostate cancer tissue,” Catalona said.