The small news story last week about scientists led by Zheng Cui, M.D., at Wake Forest University piqued our curiosity: The scientists had discovered a cancer-resistant mouse and were curious and perspicacious enough to study him further and discover that the resistance was genetic and inheritable. Could this really have some application for human beings?
“You never know where science will take you,” warned Mark Willingham, M.D., one of Dr. Cui’s colleagues and a professor of pathology at Wake Forest (who emphasized that it was Dr. Cui’s insight and leadership that made the discoveries possible). “But this is exciting and very promising.”
There are several reasons this discovery might help human beings. Mouse and human immune systems are fairly similar, and the gene mutation that leads to this powerful resistance to cancer is a dominant rather than a recessive trait, requiring only one copy to work. The cancer-suppression qualities did not affect the mouse’s health or lifespan (it lived 26 months, two months beyond normal life expectancy, and reproduced normally). All 700 of the direct and indirect offspring have the cancer resistance trait.
Since the human genome project has identified all the elements of both the human and mouse genotype, when scientists identify the gene that was mutated to produce cancer resistance (which could take a while) it should be possible to identify an analogous human gene. From there it is possible — not inevitable, but possible — that treatments could be developed to improve cancer resistance in people.
“It’s a good thing nature never read our textbooks,” Dr. Willingham said. This cancer-resistant trait occurs not in the T-cells or B-cells of the immune system, but in the “innate” immune system that normally fights off what we might consider minor problems, like infection in a cut — where almost none of the researchers expected it. And it works in mice previously bred with defects in their T-cell-B-cell immune systems.
Simply boosting the immune system with drugs or vitamins apparently won’t do the trick here and might even do harm. Boosting the immune system can throw it out of whack and bring on auto-immune diseases such as lupus, scleroderma and (some scientists believe) Type 1 Diabetes. Researchers will have to discover the specific mechanisms through which this resistance works first.
This discovery also validates the rare phenomenon of spontaneous regression of advanced cancer and might help to explain how and why cancers become more common as people and animals age. There are two basic theories: that cancerous cells mutate frequently until one of them gets us, or that there are natural cancer-fighting mechanisms in the body that wear out as we age. This discovery provides support — not proof but support — for the second theory, known as “immune surveillance.”
Of course, what works in mice might not work in humans and the scientists are years from knowing this for sure. But even if this discovery doesn’t lead to a surefire treatment or something like a “vaccine” for cancer, it adds to human knowledge about the genetics of cancer. However it all turns out, Dr. Cui and his team at Wake Forest — who are reaching out aggressively to other organizations that can help with the next phases — deserve congratulations and thanks.