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The Future of Discovery: A Cancer Biologist’s
Perspective
Sarah Loftus 12.11.11
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At our most recent SciBar (20th October 2011), Professor Russell Stannard discussed whether there would ever be an end to scientific discovery as we now know it. His argument was that our brain evolved to help us find food and a mate and avoid predators, so why should we think that we can answer all questions using “such an imperfect instrument”. Stannard’s discussion took the perspective of a Theoretical Physicist, but the talk and the discussion afterwards got me thinking about the long term future for my own field, Molecular Biology.
Consider the history of cancer research, for example. Cancer is caused by a population of cells that have broken free from the body’s normal cell division surveillance system meaning that they reproduce rapidly and uncontrollably to form tumours. The most commonly-used treatments currently used in the clinic are radiotherapy in conjunction with chemotherapy. The main problem with most chemotherapeutic agents is that they generically target rapidly-dividing cells meaning that as well as cancer cells, healthy but fast dividing cells such as hair follicle cells or cells lining the gut are damaged too. This leads to the familiar side effects of chemotherapy such as hair loss, sickness and diarrhoea. Modern day cancer research therefore aims to find drugs that target only the cancer cells, but in order to do this we need to know exactly what is causing the cancer cells to divide uncontrollably.
All tumour cells are faulty due to a mutation in one of the genes coding for a component of the machinery of a cell that controls its division.On closer examination, it became apparent that every tumour has a different set of mutations making it faulty.This led to the idea of developing patient-tailored therapies involving the identification of the faulty gene for individual patients and then administering a drug that specifically targets the faulty cell component. A successful example of this strategy is the treatment of breast cancer patients with the drug Herceptin. Those treated with this drug have a defect in a gene coding for a protein called HER2, a protein embedded on the surface of breast cancer cells which send signals to components within the cell about how often to divide, how much to grow and whether to migrate.
However, this is a rare example of an effective patient-tailored drug.Cancer research is one of the largest areas of medical research, but despite every cancer-based lab in the world over many decades having the same goal in trying to identify a cure for cancer, the field is just expanding and becoming more complicated with every new discovery.Even if we could identify every function of every cell component and identify a drug that targets it specifically, will we ever live in a society in which we can afford routine genetic analysis of every patient’s tumour? Indeed, we are very much closer to this than we were before the completion of the Human Genome Project in 2003 as we now at least have an idea of how many genes exist in the human genome (much fewer than were originally thought), and whereas sequencing was until recently an extremely labour intensive and expensive feat, it is now becoming increasingly routine. Therefore, perhaps the limiting factor determining whether scientific discovery will continue will be whether advances in technology can continue at the same rate and also whether it can do so at a cost that society can bear. Even if it did, having a great array of drugs to target each and every cell pathway still does not bring us to our goal of curing cancer effectively and without side effects, as we are rapidly assigning more and more roles to each cell component meaning that targeting even a single protein may have multiple effects on a cell, and may, like conventional chemotherapy drugs still have undesired effects on healthy cells.
It is clear now that a single cure-all for cancer is extremely unlikely and we are as yet far from routine prescription of patient-tailored drugs. Despite the complexities however, many new cancer drugs are in clinical trials and the number of effective treatments is growing. We will of course never be completely free from disease as once we cure one disease, others will inevitably appear in their place since we and all other living things around us (such as pathogens) are continually evolving. So long as the technology to aid research progress evolves in parallel with lab-based discovery, perhaps the development of effective new medicines will continue forever. As every researcher will tell you, finding the answer to one question results in the generation of many more questions. I wonder whether our ever widening knowledge and question asking will one day become so complicated that we will lose sight of the questions we originally set out to answer.
At our most recent SciBar (20th October 2011), Professor Russell Stannard discussed whether there would ever be an end to scientific discovery as we now know it. His argument was that our brain evolved to help us find food and a mate and avoid predators, so why should we think that we can answer all questions using “such an imperfect instrument”. Stannard’s discussion took the perspective of a Theoretical Physicist, but the talk and the discussion afterwards got me thinking about the long term future for my own field, Molecular Biology.
Consider the history of cancer research, for example. Cancer is caused by a population of cells that have broken free from the body’s normal cell division surveillance system meaning that they reproduce rapidly and uncontrollably to form tumours. The most commonly-used treatments currently used in the clinic are radiotherapy in conjunction with chemotherapy. The main problem with most chemotherapeutic agents is that they generically target rapidly-dividing cells meaning that as well as cancer cells, healthy but fast dividing cells such as hair follicle cells or cells lining the gut are damaged too. This leads to the familiar side effects of chemotherapy such as hair loss, sickness and diarrhoea. Modern day cancer research therefore aims to find drugs that target only the cancer cells, but in order to do this we need to know exactly what is causing the cancer cells to divide uncontrollably.
All tumour cells are faulty due to a mutation in one of the genes coding for a component of the machinery of a cell that controls its division.On closer examination, it became apparent that every tumour has a different set of mutations making it faulty.This led to the idea of developing patient-tailored therapies involving the identification of the faulty gene for individual patients and then administering a drug that specifically targets the faulty cell component. A successful example of this strategy is the treatment of breast cancer patients with the drug Herceptin. Those treated with this drug have a defect in a gene coding for a protein called HER2, a protein embedded on the surface of breast cancer cells which send signals to components within the cell about how often to divide, how much to grow and whether to migrate.
However, this is a rare example of an effective patient-tailored drug.Cancer research is one of the largest areas of medical research, but despite every cancer-based lab in the world over many decades having the same goal in trying to identify a cure for cancer, the field is just expanding and becoming more complicated with every new discovery.Even if we could identify every function of every cell component and identify a drug that targets it specifically, will we ever live in a society in which we can afford routine genetic analysis of every patient’s tumour? Indeed, we are very much closer to this than we were before the completion of the Human Genome Project in 2003 as we now at least have an idea of how many genes exist in the human genome (much fewer than were originally thought), and whereas sequencing was until recently an extremely labour intensive and expensive feat, it is now becoming increasingly routine. Therefore, perhaps the limiting factor determining whether scientific discovery will continue will be whether advances in technology can continue at the same rate and also whether it can do so at a cost that society can bear. Even if it did, having a great array of drugs to target each and every cell pathway still does not bring us to our goal of curing cancer effectively and without side effects, as we are rapidly assigning more and more roles to each cell component meaning that targeting even a single protein may have multiple effects on a cell, and may, like conventional chemotherapy drugs still have undesired effects on healthy cells.
It is clear now that a single cure-all for cancer is extremely unlikely and we are as yet far from routine prescription of patient-tailored drugs. Despite the complexities however, many new cancer drugs are in clinical trials and the number of effective treatments is growing. We will of course never be completely free from disease as once we cure one disease, others will inevitably appear in their place since we and all other living things around us (such as pathogens) are continually evolving. So long as the technology to aid research progress evolves in parallel with lab-based discovery, perhaps the development of effective new medicines will continue forever. As every researcher will tell you, finding the answer to one question results in the generation of many more questions. I wonder whether our ever widening knowledge and question asking will one day become so complicated that we will lose sight of the questions we originally set out to answer.
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