Episode 95      32 min 16 sec
Personalized Medicine: Treatments Tailored to Your Unique Genetic Profile

Assoc Prof Melissa Southey and Prof Dan Roden discuss how advances in genetics research are making it possible to develop customized medications and treatments -- in particular for cancer and cardiac arrhythmia  -- based on one's own genetic profile. With science host Dr Shane Huntington.

"We are now poised in an era of individual genomes and individual proteomes and understanding more about what it is that makes us individuals; to use that information to better tailor therapies." -- Prof Dan Roden




           



Assoc Prof Melissa Southey
Assoc Prof Melissa Southey

Assoc Prof Melissa Southey heads a laboratory that conducts population-based studies of the genetic epidemiology of breast, pediatric, prostate and colorectal cancer. Her research will provide definitive information about cancer susceptibility genes and may identify further susceptibility genes that impact on clinical genetics services worldwide. This will have immediate and significant impact on the clinical management of all individuals and families with early-onset and miltiple-cases of cancer and may provide additional target information for future treatment strategies and drug development.

Prof Dan Roden
Prof Dan Roden

Prof Dan Roden is Assistant Vice-Chancellor for Personalized Medicine at Vanderbilt University Medical Center.

Dan is also Professor of Medicine and Pharmacology and the William Stokes Professor of Experimental Therapeutics at Vanderbilt University.

Prof Roden's research specialization is the mechanisms and treatment of cardiac arrhythmias.

Credits

Host: Dr Shane Huntington
Producers: Kelvin Param, Eric van Bemmel
Associate Producer: Dr Christine Bailey
Series Creators: Eric van Bemmel and Kelvin Param
Audio Engineer: Gavin Nebauer

View Tags  click a tag to find other episodes associated with it.

 Download mp3 (31.1 MB)

Personalized medicine: treatments tailored to your unique genetic profile

VOICEOVER 
Welcome to Up Close, the research, opinion and analysis podcast from the University of Melbourne, Australia. 
 
SHANE HUNTINGTON 
Hello and welcome to Up Close. I’m Dr Shane Huntington. The single most significant change in healthcare in the next decade will be the movement from one size fits all medical towards medicine that is specific to the individual. The use of genetic information that recognises our differences will enable doctors to tailor treatments to our individual needs. There are substantial technical and ethical difficulties to overcome and many industries will be transformed in the process. To discuss the fascinating concepts surrounding personalised medicine my guests today on Up Close are Associate Professor Melissa Southey, the Head of the Epidemiological Laboratory within the Department of Pathology at the University of Melbourne, and Professor Dan Roden who joins us online from Nashville, Tennessee.  Professor Roden is the Assistant Vice Chancellor of Personalized Medicine at Vanderbilt University Medical Centre. Welcome to Up Close Melissa and Dan.
 
MELISSA SOUTHEY
Thank you, Shane.
 
DAN RODEN
You’re welcome, thank you for having us.
 
SHANE HUNTINGTON
Dan, let me start with you with regards to personalised medicine. Before we get into that particular topic could you describe for us the way in which patients are currently treated?
 
DAN RODEN
I think that’s a useful starting point for this kind of discussion. We’ve come a long way in the last several decades in terms of not only developing new therapeutics but understanding how to evaluate them in patients. The standard tool that we use in medicine to evaluate therapies is the randomised clinical trial. In that approach large groups of patients are generally split into two and randomly assigned to treatment A or treatment B. At the end of the day we can decide if treatment A is better than treatment B. That kind of approach has dramatically changed the way I which we approach problems like high cholesterol, high blood pressure and breast cancer. The problem it seems to me is that when we look at results of the large randomised clinical trials what we’re able to say is that in a population of X 1,000 patients or X 10,000 patients this treatment, on average, is superior to that treatment. If you knew nothing more about patients you would be a fool not to choose the better of the two treatments across populations. What we have now is an increasing body of information that allows us to say that in a specific individual this treatment is more likely to work than that treatment because of particular pharmacokinetic features or particular features about the patient, notably genetic features but many other features perhaps. That runs counter to our ideas about large randomised clinical trials. I don’t want people to walk away from this discussion saying that I think randomised clinical trials are a bad thing. If we knew nothing else we’ve made huge advances using that tool. I think we are now poised in an era of individual genomes and individual proteomes and understanding more about what it is that makes us individuals to use that information to better tailor therapies. The challenge is going to be to try to decide who should get which therapies of course.
 
SHANE HUNTINGTON
Dan, can I ask you with your local general practitioner how do they go about essentially looking at a patient and determining what the problem is? Is there a personalised element there or is it all sort of one size fits all?
 
DAN RODEN
So a patient will go to their physician for a general check up or perhaps for a specific problem, let’s take high blood pressure. When a physician sees a patient with high blood pressure the first thing that you want to do is to make sure that the diagnosis is correct. Usually it is. Then you decide on which therapy. Now there are guidelines in our country and worldwide that tell us which therapies work better than others as starting therapies. There’s a lot of controversy around those guidelines despite the fact that there are many, many large clinical trials supporting one or the other. But in our environment an ordinary question or an ordinary factor that would go into deciding the initial therapy for high blood pressure would be a person’s racial background. White people respond better to certain medications than do patients of African origin. Conversely patients of African origin often respond better to certain kinds of therapy that would not be first line therapy in white people. So we do, even now and in the absence of very sophisticated genetic testing take personal characteristics into account when we’re treating a patient. A cancer doctor will approach a patient and in the absence of anything else will say, well this person got breast cancer when they were post-menopausal, this person got breast cancer when they were pre‑menopausal. Those are different diseases. So they get different therapies. We are more sophisticated now in the cancer space, and Melissa will tell us more about that I’m sure. But right now a general practitioner or a primary care doctor would take those kinds of characteristics into account when prescribing therapy for common diseases. If somebody is prescribed ten different medications for a variety of illnesses, the likelihood that they’re going to be compliant with a complex medical regimen is small. So we have to figure out a way of deciding which of those ten medications is most likely to benefit that patient and simplify the regimens. So that’s another form of personalised medicine. I believe pretty strongly that when we talk about personalising medicine we’re talking about the patient across the desk from the doctor. Using everything that you can know about that patient from their intellectual capabilities, their socio economic environment, their genome, their specific molecular diagnosis of their disease and so on. I think that personalising means really personalising.
 
SHANE HUNTINGTON
When we think about the individual patient and we look forward say ten years as to what personalised medicine will hopefully look like.  How much do the genetics of the patient come into those decisions that will be made about the medicines and the treatments that are given to them?
 
DAN RODEN
That’s a great question. I mean if you read the popular press the answer is 100 per cent. I don’t think that’s likely to be the answer. There are medications that we will continue to use where we will not have any genetic worries or genetic input. There are other medications that we may decide not to continue to use because there is such genetic variability. Once we identify the fact that response to a medication varies on the basis of genetics, we’re faced with three options. One is to ignore those data and that’s what’s done largely these days. The second is to genotype patients before we prescribe that medicine and then choose whether to prescribe that medicine or to adjust the dose based on genetics. The third option is to pick some other medicine for that particular indication. So it is possible that as we get smarter and smarter about the genetics of drug response what we will see is more and more people switching to drugs where they think there is no genetic input into the response. The fact is that when you look at drug responses across large populations you always find people who respond well and people who appear to derive no benefit or worse yet have severe or not so severe adverse effects. It seems to me switching from one medicine to another to avoid that kind of problem is a bit like the ostrich burying your head in the sand. There always is going to be variability in response to drug therapy until we tailor the specific drug to the specific patient’s disease mechanism and to their particular genetics that determine dose correctly. Ten years from now there will be some drugs where I believe that we will be using genetic information. Whether that’s genetic information that you’re born with or genetics of the tumour or the infectious disease that you’re being treated for remains to be seen.
 
SHANE HUNTINGTON
Dan, when it comes to the personalisation of the use of drugs in particular patients, do we have enough information genetically to start doing that now or do we need much larger genetic sample sets in order to know what sort of drug works best on what type of genetic profile?
 
DAN RODEN
For some drugs we have a lot of information now and for other drugs we’re just beginning to scratch the surface. The way it works is that if there are genetic variants that have very strong effects by themselves on drug response in many cases we know about them. Of course in the cases where we don’t know about them I can’t say anything at all. But we do have many examples now of drugs where there are variants in single genes that really drive a lot of the variability and response that we see. That database exists now and I would say that there are several dozen drugs or drug gene combinations for which such data are available. As I said before the fact of the matter is that there is substantial variability in response to drug therapies across the board. Whether we’re talking about cancer, hypertension, asthma or high cholesterol. The extent to which you get the target effect varies across the population substantially. The risks, even the small risks associated with many of the therapies, small but spectacular risks have yet to be understood at a genetic level. So we’re now working on the problem of understanding those specific genes or the specific combination of genetic variance that drive variability of response to common therapies. My suspicion is some of that will come from variability in the actual molecular basis of the diseases that we’re treating. Other parts will come from variability in the way in which the drugs interact with those disease pathways. For some drugs with large effects we know the answer. For other drugs with large effects we don’t yet know the answer because we don’t know that they’re large effects of single gene variants. For others we’re still working on the problem of multiple genetic influences.
 
SHANE HUNTINGTON
Dan, are there particular ethical barriers that we’re going to have to address over the next ten years in order for personalised medicine to really come to the forefront?
 
DAN RODEN
The answer to  that question is yes. When it comes to the idea of starting to use genetic information in clinical decision-making I think people get a little nervous. There are a lot of misconceptions out there about what it is that your genetic profile does or doesn’t define for you. The vision that we and many other have that large chunks of genomic information will be embedded in the medical record makes people very nervous. You know how will that be used by insurance companies? How will that be used by police agencies, by people who are interested in segregating populations into various groups of any kind at all? Part of that is a real concern and part of it is the problem that people have this view that genetics are highly, highly deterministic. I think that what we’re understanding now is that with few exceptions most genetic variants just change the probability of something happening. Many of them change the probabilities by not all that much. The other part of genetic medicine that I think people haven’t gotten their heads around yet, and I think will present ethical issues, is this business of whole genome sequencing. That is upon us. It is possible now to sequence a whole genome for less than $10,000 and that price is going to continue to plummet over the next half decade. The problem is that we’re going to find that people have many rare variants. Variants that they and their immediate family members share and perhaps are not seen in anyone else. Those kinds of variants, in some context, if they’re in certain genes might mean something to a naïve reader. So for example I study ion channels. I study cardiac arrhythmias. There are certain mutations, rare variants in ion channel genes that predispose people to serious arrhythmias. We’re coming up against the problem now that with genetic testing we find people with rare variants in those selfsame genes. Those people may or may not be at increased risk, we often don’t know. But we’re opening this floodgate of large numbers of patients who are going to see that they have variants in genes and the problem is we don’t have the knowledge base to understand what those variants might do to them, to their clinical phenotypes. That’s an area which I think we’re still going to have to struggle with as we start to sequence more and more individuals.
 
SHANE HUNTINGTON
You're listening to Up Close coming to you from the University of Melbourne, Australia. Today we’re talking about personalised medicine with Professor Dan Roden and Assistant Professor Melissa Southey. Dan, you mentioned a moment ago the area of cardiac arrhythmias. This is an area your work is focused on in many regards.  Can you describe for us what cardiac arrhythmia is and what it does to the patient?
 
DAN RODEN
Your heart beats normally 60 to 100 times a minute in a very organised sequence. There is an electrical system within the heart that controls the orderly activation and then recovery from that activation of heart cells. Any disturbance of that ordinary sequence can result in a heart rate that is too fast. A heart rate that is too slow or sometimes a heart rhythm in which certain parts of the heart are activated normally and other parts of the heart are not activated normally. That is the connections across parts of the heart are not maintained. So the symptoms that people get in general with abnormal heart rhythms range from nothing to a sense of about to lose consciousness and actually fainting spells. Interestingly people would say a common reason for fainting would be that your heart would stop for a couple of seconds. It’s true that if your heart stops for a couple of seconds you will faint. But we don’t actually in my world get terribly concerned about that. But what we are more concerned about is when the heart beats very, very rapidly. Occasionally the heart can beat so rapidly that it doesn’t have time to fill in between beats. When it doesn’t have time to fill it has no blood to pump out. So loss of consciousness under that condition is also a very common symptom. It’s that kind of abnormally fast heart rhythm that can kill people. In our country somewhere between a quarter of a million and half a million adults die suddenly every year.  It is the commonest cause of death among adults in the United States, something like 10 per cent to 20 per cent of all death is sudden death. We are not sure what the triggers for sudden death are. Very often we think the trigger is an occlusion in a coronary artery, that is the early stage of a heart attack. In other cases there is nothing wrong with the coronary arteries and the person is fine one instant and dead the next. That’s one extreme and that’s a huge problem. The other common arrhythmia problem that we’re interested in studying is a problem called atrial fibrillation. I can’t speak for Australia but in the United States In the year 2010 there are somewhere between two and five million patients with atrial fibrillation. This is an abnormality of heart rhythm that is not severely as severe as one that can kill you. But in atrial fibrillation the upper chambers of the heart, the atria beat very, very rapidly. They conduct those impulses occasionally to the lower chambers of the heart. So when you feel the pulse of a patient with atrial fibrillation it’s often irregular and often quite fast. The symptoms range again from nothing to a sense that the heart is beating irregularly to a sense of breathlessness particularly on exertion. In atrial fibrillation there is the extra added feature that the part of the heart that is in this abnormal rhythm this fibrillation can actually predispose it to the creation of blood clots. What I tell my patients is, I don’t care if you make a blood clot in your heart but I care deeply if that blood clot decides to go travelling somewhere else. Unfortunately one of the places those blood clots like to travel is to the brain. So atrial fibrillation related stroke is a pretty common problem. Atrial fibrillation and sudden death due to very rapid heart rhythms or common abnormalities of heart rhythm, occasionally patients have very slow rhythms and we do treat those with pacemakers in general. But the first two atrial fibrillation and sudden death are the ones where we’re focusing a large amount of our attention. They are really quite nice data now that say that one of the risk factors is if you have a family member that is affected. So if your parents have atrial fibrillation, you’re more likely to have atrial fibrillation. There are other risk factors. High blood pressure diabetes, those are risk factors. But interestingly family history is also a risk factor. For sudden death it turns out that there is the same story. That there are risk factors, advanced heart disease is a commonly invoked risk factor. But having a parent die suddenly increases your risk of dying suddenly, probably two fold. If you are unfortunate to have had both parents die suddenly your risk of dying suddenly, in one study, is increased nine fold. What that tells us is that there is probably something in your genes that predisposes you to having these abnormal rhythms. Now of course you don’t have the abnormal rhythms on the day you are born. So it is almost certainly an interaction between your genetic makeup and other factors that come along to increase the risk of atrial fibrillation or of sudden death and ultimately culminate in the actual abnormal rhythm. That is not very different from the way we think about a lot of genetics.  Genetics for type 2 diabetes, genetics for breast cancer, genetics for Alzheimer’s Disease. So there’s clearly a genetic story and groups that we work with are defining what the places in the genome are that predispose patients to sudden death or atrial fibrillation. The conventional wisdom, the wisdom to which I subscribe is that risk will be a combination of three things. Very common genetic variants, that is a variant that there are three of us on this phone call one us might have and the other two might now. Or one of us might be homozygous or one of us might be heterozygous and one of us might be homozygous for the wild type allele. Those are common variants. They increase risk a little bit. Weird genetic variants that might increase risk a lot but they are not very common so they don’t influence population and then what happens to us in our environments.
 
SHANE HUNTINGTON
Dan, can you say a little bit about the current treatments for these conditions and how you expect those to change as personalised medicine comes more and more into the fold over the next decade?
 
DAN RODEN
The thing that has revolutionised therapy for sudden cardiac death is the development of the implantable cardio defibrillator device. This is an extension of pacemaker technology that basically sits in the chest and monitors the heart rhythm on a beat to beat basis. When the heart rate gets very, very fast and disorganised, the machine will recognise that, charge itself up and deliver what we call a defibrillating shock to shock the rhythm back to normal. These are lifesaving devices. The question is who should get them. When they were first developed the criteria were you had to have survived a cardiac arrest or two. That is you had to be in a place where somebody would have resuscitated you and then you could get one of these devices. Then the criteria moved to you had to have survived one cardiac arrest. We are now pretty good at identifying patients with heart disease who are at risk for having a cardiac arrest. So it’s pretty standard to implant these devices, at least in the United States, in patients who have not yet had a cardiac arrest but who for some reason have such advanced heart disease that we think they are at risk. It’s a huge financial burden but it clearly saves lives. The way in which genetic information that predisposes to risk might affect the way we practice medicine could be to identify a group of people who meet ordinary criteria for defibrillator replacement but who are not as at high risk as we think. Or to identify patients who are still healthy but who for some reason we think are at excessive risk. Now I am very, very hesitant to think of a scenario where we would start to do genetic testing for common variation and then implant cardio defibrillator devices. I think that’s just very, very farfetched. But we could for example if we understood why certain genetic variants predispose to sudden death develop new drug therapies that would reduce the risk.
 
SHANE HUNTINGTON
You're listening to Up Close coming to you from the University of Melbourne, Australia. Today we’re talking about personalised medicine with Professor Dan Roden and Assistant Professor Melissa Southey. Melissa, now your lab is focused on genetic epidemiology. Can you tell us a bit about what your research is about?
MELISSA SOUTHEY
My research is really focused on looking at the population. So we’ve invested a lot of time, nearly 20 years collecting population based studies. So recruiting people from the community in various differently designed studies so that we can answer some of these questions that Dan has raised in the last few minutes. It is about trying to understand how genetics can relate to first determining a person’s susceptibility to a disease and hopefully moving through into determining perhaps a person’s best treatment for a disease.
 
SHANE HUNTINGTON
Are you just selecting people from the population who already have difficulties or a problem or the onset of disease or is it just a completely random sample?
 
MELISSA SOUTHEY
We’re doing both. We’re doing a very large number of studies. Some are recruiting people that have been diagnosed with for instance cancer. Case control family studies where we recruit people that are affected and their families so we can understand. Of course in a genetic study it is very important to have the whole family involved. Other studies like the Melbourne Collaborative Cohort Study where we’ve recruited 40,000 people in Melbourne who are unaffected at the time of recruitment and we’ve followed them through their life since their recruitment for the last 20years. To look at not just their underlying genetic composition but also the sorts of diseases that they’ve come across in their life course.
 
SHANE HUNTINGTON
I’m assuming there is an interplay between our genes and the environment in which we live and how the two things collectively affect us. Can you tell us how that works?.  What do you see in your studies?
 
MELISSA SOUTHEY
It’s really a very challenging area. Our work really to date has been focused on some of the key genetic variants that we know change a person’s individual risk quite predominantly and quite significantly. Again this goes back to some of the interesting themes that Dan talked about. I use the word individual, but in fact what our risk estimates are doing at the moment is talking about an average. So looking at a community of people or a group of people with certain genetic variants we know what their average risk is. But we certainly are getting very close to what their individual risk might be. In the last few year’s there’s been several studies that have shown that an individuals’ risk can be modified by large numbers of things. It was really interesting the common themes between Dan’s discussion and the cancer theme specifically. We do know that there are some very, very rare mutations that increase an individual’s risk significantly. But in the last few years via some very large international consortiums we now are showing evidence that this risk can be modified by other genetic factors. The environmental question that is really the next frontier. It’s very challenging in the context of cancer to try and have a good measure of what environmental variations are and how that affects an individual’s risk in a composite way with their genetic makeup.
 
SHANE HUNTINGTON
Do you have a feeling at this point for just how much the environment matters relative to genetics or is that still sort of a long way off?
 
MELISSA SOUTHEY
Perhaps in some contexts environment is a big player. I think smoking would perhaps be one area where people are fairly familiar with the risks associated with smoking. Other perhaps more subtle environmental exposures and in the context of breast cancers the use of oral contraception is really quite unclear what the effect of that is against your genetic makeup. It may be different for some people depending on their genetic makeup.
 
SHANE HUNTINGTON
Specifically in your lab you’ve been looking at the breast, paediatric, prostate and colorectal cancers. I guess that’s’ quite a wide range. What sorts of things have the studies shown so far in terms of these statistical answers that we’re getting?
 
MELISSA SOUTHEY
General the themes are all common cancers, that’s their unifying bridge between the studies that we’re conducting. It’s interesting the genetic component of diseases as far as we know it now was actually quite different. For breast cancer about 15 years ago in the mid-1990s, the first breast cancer susceptibility genes were cloned and identified by our studies of extremely unusual families. Families where there was an incredible number of breast cancers in the pedigrees. Some of them more than 50 cases of breast cancer. They were really extraordinary families. But those studies of extraordinary families led the way to describe these genes. Then we were able to translate that information into what it meant in the population. What it means in the population is that these genetic variants in these two breast cancer susceptibility genes are extremely rare. They account for a very, very small amount of the breast cancer that we see in the community, and indeed a very small amount of breast cancer that we see in families that have multiple cases of breast cancer. That really left us with a very large amount of breast cancer yet to be explained. In recent years we have begun via very large international collaborations that have involved 50,000 cases of breast cancer and 50,000 controls to identify more common genetic variants that have a very small effect on breast cancer risk. So in breast cancer we have very, very rare variants in some genes that predispose people to quite elevated risk of breast cancer, and other genetic variants that are very common that probably interplay with the very rare variants and how exactly they do that. They at least modify it in some way in some instances. But in other cases for instance prostate cancer we really haven’t had those breakthrough events to describe prostate cancer predisposition genes like we have for breast cancer. So that field has moved on and we now have a very large collection of common variants that we know influence risk to a very small degree. In paediatric cancer it’s really been a very different story. Each cancer some type perhaps has a very specific explanation but again we only know some of those explanations. There’s a huge field and years of work probably ahead of us to describe the genetic predisposition of genes involved in some of the smaller groups of paediatric cancer.
 
SHANE HUNTINGTON
Melissa, when we have a gene that we know makes us susceptible, what causes it to essentially start causing the problem? Do we have an idea in any of these areas what that trigger is?
 
MELISSA SOUTHEY
At least as far as our modelling of the underlying biological pathways that might lead to cancer development, and perhaps if I go back to the examples of the breast cancer predisposition genes Brc1 and BRCA2. We have considered those as classical tumour suppressor genes. So an individual might inherit a mutation from one parent but the other parent will provide them with an intact gene. So that individual grows up with one or more gene and their biological function is quite normal for a large amount of time. They can go through life without ever developing cancer. In fact we know that’s the most likely outcome for individuals who inherit such a mutation. But for some mutations and perhaps applying the classic Knudson hypothesis. During the course of life the other gene might acquire another mutation. So this individual then in some cells has a mutation in both genes. Usually these tumour suppressor genes have some fundamental function in a cell such that when this function is not operating properly the cell’s function is disturbed such that cancer progression is initiated.
 
SHANE HUNTINGTON
In our general population how prevalent are these genes that are potentially problematic? Are they sort of in almost everyone and they’re just not switching on in most people or is that there are very few?
 
MELISSA SOUTHEY
No, the data that we have strongly suggests that these genetic variants are extremely rare. Even in families that have a lot of breast cancer in them, they are extremely rare. There are probably a number of genes that we haven’t identified yet that could explain some of these other cancer family syndromes, but they are extremely rare. It’s a real puzzle at the moment and one of our frontiers in our research to try and identify the other genes that are involved in predisposing some families to breast cancer development and other cancer development.
 
SHANE HUNTINGTON
When we look at a specific area like breast cancer and we look at something I know you work on which is mammographic density, which I will get you to describe in a moment. Does this allow us a very solid predictor of cancer? Are we able to make that very distinct link between the sort of measurement of this density level in the breast and the cancer that is coming forward? I will get you to explain mammographic density first.
 
MELISSA SOUTHEY
Really our understanding of mammographic density is really in its infancy. But it’s one of the strongest risk factors for breast cancer. In our attempts to try and predict an individual’s risk of breast cancer it’s a very important factor. We have been at the situation really where everyone has been at population risk and a few individuals where we’ve been able to identify the very rare risk factors that increase an individual’s risk have been able to be pulled out. But really we think along the spectrum we have a lot of work to do. I think in the future it offers a lot of potential to modify some of our screening programs to target people at much higher risk and to alleviate other people at much lower risk from the screening programs. We have published a paper in 2010, which was the first paper to demonstrate that some of mammographic density is determined by genetic factors. In fact some of those genetic factors are factors that we know about in terms of breast cancer risk. So it’s interesting to try unravel mammographic density in the context of breast cancer risk because clearly it interplays with some of the genetics that we already understand in terms of breast cancer risk as a whole in the population level.
 
SHANE HUNTINGTON
Melissa, just finally how does the data that you’re collecting at the moment lead into the type of personalised medicine that we heard Dan speaking about earlier in the program?
 
MELISSA SOUTHEY
It has extremely complementary themes. Many of the things that Dan discussed are certainly relevant to the work that we do. We’re a little bit more focused at prevention and early detection. Using genetic information to identify people who are at particularly elevated risk of a disease. Being able to tailor screening or perhaps even prevention programs to prevent the onset of disease in individuals at highest risk. But also to identify people at this higher risk to be very alert to disease like in the context of breast cancer.  To provide them with breast screening protocols that are appropriate for their underlying genetic predispositions to detect disease at an early stage. Dan’s discussions were really interesting about using genetics for best treatment and certainly genetics is going to have a play from prevention to treatment.
 
SHANE HUNTINGTON
Melissa and Dan thank you very much for being our guests on Up Close today.
 
MELISSA SOUTHEY
Thank you, Shane.
 
DAN RODEN
You’re welcome. Thank you for having us.
 
SHANE HUNTINGTON
Relevant links, a full transcript and more information on this episode can be found on our website at http://upclose.unimelb.edu.au. Up Close is brought to you by Marketing and Communications of the University of Melbourne, Australia. Our producers for this episode were Kelvin Param and Eric Van Bemmel, with audio engineering by Gavin Nebauer. Melbourne University Up Close is created by Eric van Bemmel and Kelvin Param. I'm Dr Shane Huntington. Until next time, goodbye.
 
VOICEOVER
You’ve been listening to Up Close.  For more information visit upclose.u-n-i-m-e-l-b.edu.au.  Copyright 2010, The University of Melbourne.

show transcript | print transcript | download pdf