Contagious Cancer: Genome Study Reveals How Tasmanian Devil Cancer Has Spread

tasmanian_devil_cancer_genome Image courtesy of Save the Tasmanian Devil Program

A killer cancer that is threatening to wipe Tasmanian devils off the map for good has been spreading from an original infected female 15 years ago via live cancer cells, according to evidence from genome sequences of the cancer and the animal, published online Thursday in Cell. Finding out how this happened could help save this species from extinction and it could also prepare researchers for the unlikely event that a contagious cancer ever appeared in humans.

The facial cancer, which is spread through bites, has plagued this animal’s precarious population for more than a decade. Tasmanian devils (Sarcophilus harrisii) are the largest surviving carnivorous marsupials and live on Australia’s island state Tasmania. [Read more about this scourge in "The Devil's Cancer," from Scientific American's June 2011 issue.] All of the tumors afflicting the animals today contain cells from one original devil, genetic sequences show. “I call her the immortal devil,” Elizabeth Murchison, a researcher at the Wellcome Trust Sanger Institute and co-author of the new paper, said in a prepared statement. “Her cells are living on long after she died.”

An earlier version of the Tasmanian devil genome was published last year in Proceedings of the National Academy of Sciences and revealed some secrets about why the cancer hasn’t killed off the species already. One of the two devils sequenced, named Cedric, showed resistance to at least two strains of the cancer, although he later succumbed to a third.

“The Tasmanian devil cancer is the only cancer that is threatening an entire species with extinction,” Murchison said. After the first tumor appears on the doomed animals face, it will likely die within three months.

But by turning to genetics, researchers and conservationists hope to be able to find clues to at least slow the cancer’s spread. The researchers studied tumors from 104 tumors collected from Tasmanian devils from various locations on the island and found that there were separate geographic groups of cancer types but that all of them contained cells from the original female. “Sequencing the genome of this cancer has allowed us to catalogue the mutations that caused this cancer to arise and to persist,” Murchison said. More detailed genetic details could point the way to targeted cancer drugs. It might also suggest how the cancer is able to sneak past the immune system and start its explosive growth so quickly.

“Tracing the evolutionary history and spread of this cancer helps us to understand not only what caused this disease but also to predict how it might behave in the future,” David Bentley, chief scientist at Illumina Cambridge, Ltd. and study co-author, said in a prepared statement.

The Tasmanian devil’s cancer has more than 17,000 mutations. “This is fewer mutations that are found in some human cancers and indicates that cancers do not need to be extremely unstable in order to become contagious,” Bentley said. Only one other type of contagious cancer is known a venereal tumor that infects dogs and wolves. The next step is “to use the genome sequence to understand more about how this cancer became transmissible,” Michael Stratton, director of the Wellcome Trust Sanger Institute and study co-author, said in a prepared statement. “Cancers that transmit through populations are obviously incredibly rare, he said, but we should use the Tasmanian devil example to be prepared in the extremely unlikely event that such an epidemic ever occurs in humans.”

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Aspirin could beat cancer spread: Australian study

Aspirin and other household drugs may inhibit the spread of cancer because they help shut down the chemical "highways" which feed tumours, Australian researchers said Tuesday.

Scientists at Melbourne's Peter MacCallum Cancer Centre said they have made a biological breakthrough helping explain how lymphatic vessels -- key to the transmission of tumours throughout the body -- respond to cancer.

"We've shown that molecules like the aspirin... could effectively work by reducing the dilation of these major vessels and thereby reducing the capacity of tumours to spread to distant sites," researcher Steven Stacker said.

Doctors have long suspected that non-steroidal anti-inflammatory drugs such as aspirin may help inhibit the spread of cancer but they have been unable to pinpoint exactly how this is done.

By studying cells in lymphatic vessels, the researchers found that a particular gene changed its expression in cancers which spread, but not when the cancer did not spread.

The results published in Cancer Cell journal reveal that the gene is a link between a tumour's growth and the cellular pathway which can cause inflammation and dilation of vessels throughout the body.

Once these lymphatic vessels widen, the capacity for them to act as "supply lines" to tumours and become more effective conduits for the cancer to spread is increased.

But aspirin acts to shut down the dilation of the vessels.

"So it seems like we have found a pivotal junction point in a biochemical sense between all these different contributors," Stacker said.

The discovery could lead to new and improved drugs which could help contain many solid tumours, including breast and prostate cancer, as well as potentially provide an "early warning system" before a tumour begins to spread.

Last year, a study published in medical journal The Lancet found that rates of cancer of the colon, prostate, lung, brain and throat were all reduced by daily aspirin use.

Many doctors recommend regular use of aspirin to lower the risk of heart attack, clot-related strokes and other blood flow problems. A downside of extended daily use is the risk of stomach problems.

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