Newly-Found Gene to Improve Cancer Therapies

A gene that was known to be responsible for programmed cell death has recently been proven to play an important role in the destruction of adult stem cells, a finding that carries tremendous implications for existing cancer therapies.

The new research was conducted by investigators at the University of California in San Diego (UCSD), who discovered the secondary function the gene had.

The health, well-being and quality-of-life of cancer patients could arguably be improved considerably, if new therapies based on this gene are developed, ScienceDaily reports.

“During chemotherapy or radiation therapy that kills cancer cells by inducing significant DNA damage in their genomes, one of the main side effects for human cancer patients is the depletion of their own adult stem cells, particularly the ones responsible for making new blood and intestine cells,” says expert Yang Xu.

“So these patients become anemic, lose appetite and a lot of weight,” adds the scientist, who is a professor of biology at UCSD.

“If we can prevent the loss of stem cells during cancer therapy, that would be very beneficial for these patients,” he goes on to say.

Xu is also the leader of the team that conduct the investigation, and which published its discoveries in the latest online issue of the top-rated scientific journal Nature Cell Biology.

In DNA-damaged cells, a tumor suppressor molecule called p53 is used to trigger apoptosis, or programmed cell death. This ensures that the target cells do not multiply further.

The gene called Puma (p53-unregulated modulator of apoptosis) is of paramount importance in this process, but it also makes p53 destroy more and more adult stem cells.

“Since p53 is a critical tumor suppressor, you cannot suppress p53 to prevent the depletion of adult stem cells since it will induce cancer,” Xu explains.

“But you can target Puma to prevent p53-mediated depletion of adult stem cells, because a Puma deficiency does not promote the development of cancer,” he adds further.

“This gives us a nice target for preventing the p53-dependent depletion of adult stem cells in response to DNA damage. If you can suppress Puma function, you can rescue a lot of the adult stem cells that would otherwise be lost after the accumulation of DNA damage such as during cancer therapy,” the expert concludes.