Human regeneration has to date been the preserve of science fiction. But mammals may have a dormant ability to regrow healthy tissue, research suggests, possibly paving the way for scar-free healing at some point in the future.

Biologists believe that a gene called p21 may hold the key to spontaneous healing, which could allow limited regeneration of the human body, as witnessed in newts, flatworms and the hydra.

It is thought that in mammals this healing potential has been lost through evolution, but may lie dormant in cells and could be reactivated by switching off the p21 gene. Mice engineered in the laboratory to lack the p21 gene, were able to renew surgically removed tissue so that no trace of an injury remained.

Removing p21 causes adult cells to behave like stem cells – those cells in embryos with a "pluripotent" power to become any kind of tissue.

In experiments, mice which were missing the gene had holes punched into their ears (as commonly done to identify lab animals), but after a few weeks all traces of the ear holes had disappeared.

"Much like a newt that has lost a limb, these mice will replace missing or damaged tissue with healthy tissue that lacks any sign of scarring, said Ellen Heber-Katz, a professor at the Wistar Institute in Philadelphia, who led the study.

"While we are just beginning to understand the repercussions of these findings, perhaps one day we'll be able to accelerate healing in humans by temporarily inactivating the p21 gene."

This gene is tightly controlled by another gene, p53, which is a well-known cell division regulator and tumour suppressor. Defective p53 can lead to many types of cancer.

In normal adult cells, p21 acts as an anti-cancer safety mechanism, blocking out cell division in the event of DNA damage, said the biologists. So, mice lacking p21 might be expected to suffer worsening damage to DNA, and eventually cancer.

But, while increased DNA damage was observed in experimental mice, there was no cancer surge, according to a report of the research published in the journal Proceedings of the National Academy of Sciences.

Instead there was an increase in "cell suicide", or apoptosis, a cancer-blocking mechanism that directs dysfunctional cells to kill themselves.

"The combined effects of an increase in highly regenerative cells and apoptosis may allow the cells of these organisms to divide rapidly without going out of control and becoming cancerous," said Prof Heber-Katz.