What kind of technologies will create personalised care, then? There are a few different options put forward by the all-Nobel laureate panel, which includes Peter Agre, Ferid Murad and Martin Evans, as well as Ciechanover. They say the future of medicine will include: Advances in cellular-based therapies, genome-based tailored treatments, and antibody therapies.
“We are not satisfied with current medicine,” says Ciechanover. He thinks it’s too general and not targeted enough. In breast cancer, for instance, the drug Herceptin, which is an antibody, works for people who are HER2 mutant positive. If the mutant is negative, it won’t work.
Evans says that the new thing in cellular-based therapies will be using pluripotent cells to treat specific cells. These can be cultured in the lab and selected as they develop into a wide variety of cell types for repairs. “This opens up regenerative medicine,” he says. For example, people with burns or open wounds can be treated with a spray of their own cells disaggregated into a suspension. “The site they have to grow, is the best site to grow them”, Evans asserts. Or you can grow more skin in culture to transplant. This is an alternative to traditional grafts.
Celular therapies also open the way for bone marrow transplantation using the patient’s own cells that have been purified in the lab. In this way, cells can be a kind of pharmacology and the possibility to personalise medicine. “cell transplantation therapies need to be personalised,” says Evans.
Ciechanover says that: “We are developing techniques for genetic profiles through to proteins.” However, Agre plays the ‘naysayer’ on genome-based therapy. He says: “We have the genome, but we are still waiting for major breakthroughs”. You can learn more from family histories at the moment, for example getting information about the history of breast cancer in a family.
But will this new personalised vision for medicine be available to people in poor countries? Over 1 billion people in developing countries are living in extreme poverty and earn less than a dollar a day.
Ciechanover says “It will almost certainly going to be very expensive” to achieve a new kind of healthcare. In particular, antibody therapies are more expensive than small molecule drugs. But Murad says that advances in biomedicine “will permit us to develop agents which are more selective, much more efficacious, possibly less toxicity and maybe the costs are going to be the same.” This considers the fact that people will not be treated with medicines they won’t respond to.
Another bioethical dilemma is whether the pharmaceutical industry is going to deliver what is needed, with their profit motivations? The panel debate whether the cost of new therapies will do down as the quantity of production goes up. There is some cynicism over how industry set the prices drugs according to what they can get away with rather than what is dictated by supply and demand. Murad says he has worked in industry in the past, and he thinks that “we are being hoodwinked by industry for the sake of income and profit.”
There is also the issue of bacterial antibiotic resistance, which is a huge challenge for treating malaria and TB, for example. Agre is concerned that antibiotic resistance is spreading “astonishingly fast.” Even if new medicines, such as antibiotics developed that comply with our new understanding of the structure of the ribosome, are cheap enough to be used in developing countries, then Agre has misgivings over how these medicines will be handled by policymakers. He says: “Intelligent use of these medicines will be very important.” But he says antibiotics have been ‘abused’ in the past: “If the new antibiotics are put in animal feed, then their long-term usefulness will decline.”
Evans points out this is a problem with worldwide regulations to prevent this happening. “Bacterial resistance is on an international level,” he says, but the mechanisms are not sufficient to regulate the worldwide use of medication.
See the talk in full below:
Updated:2/07/11 to change ‘EGFR’ to ‘HER2’ in the paragraph about Herceptin. HER2 is EGFR type 2, so although EGFR is what Ciechanover says (27.45) for clarity it has been changed.