Off the wire
Results of FINA Diving World Series 2017 Beijing  • Russian scientists successfully test cancer-killing drug in space  • Hong Kong stocks close 0.74 pct lower  • Malaysia issues arrest warrant for Air Koryo staff over airport killing  • Top news items in major Kenyan media outlets  • Foreign exchange rates in India  • Hormone predicts death, problems in heart patients: New Zealand scientists  • U.S. bentonite eyes East Asia for kitty litter market  • Police seize arms, ammunition from vehicle in N. Afghan province  • 2nd LD-Writethru: Caixin service PMI slips to 52.6  
You are here:   Home

Gene engineering improves chemotherapy for cancer patients: New Zealand scientists

Xinhua, March 3, 2017 Adjust font size:

New Zealand scientists claimed on Friday that they had engineered enzymes that could help make chemotherapy more effective for cancer patients.

The "artificial forms of evolution" were being used to improve the ability of microbes to attack tumors, research leader Associate Professor David Ackerley, of Victoria University's biotechnology program, said.

This underpinned the development of a new form of chemotherapy that exclusively targeted cancer cells, he said.

A key goal of this chemotherapy was a more targeted treatment method that resulted in fewer side effects for cancer patients.

To achieve this goal, Ackerley and his team engineered enzymes that could transform a relatively safe and non-toxic compound (a "pro-drug") into a drug that was highly toxic to cancer cells.

The genes encoding the enzymes were delivered to cancer cells using viruses or bacteria that were only able to replicate in tumors.

The team worked with a pro-drug called PR-104A, which was developed by scientists at the University of Auckland.

"The enzyme we started with was moderately active with PR-104A. However, this was purely by chance - nature has never evolved enzymes to recognize these very artificial types of molecules," said Ackerley.

"We reasoned that by mimicking evolution in the laboratory - by introducing random mutations into the gene encoding our target enzyme, then selecting the tiny minority of variants where chance mutations had improved activity - we might eventually achieve a more specialized enzyme that could more effectively activate PR-104A."

The artificially evolved enzyme proved significantly better at activating PR-104A within living cells.

The team was collaborating with groups at the University of Nottingham in Britain and Maastricht University in the Netherlands to progress the therapy into clinical trials in cancer patients. Endit