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  • Joining the dots – how lab research can lead to new approaches for treating cancer - Cancer Research UK - Science blog
    how this disease starts as well as finding more effective ways to treat it Cancer Research UK s scientists have a long and distinguished track record in understanding DNA repair One of the world leaders in this field is Professor Steve Jackson at the Gurdon Institute in Cambridge whose work we ve funded for more than a decade Together with postdoctoral researcher Abderrahmane Kaidi he s now managed to join the dots between three previously separate areas of research related to DNA repair Their discovery published in the prestigious journal Nature sheds light on the fundamental mechanisms that detect and repair genetic damage and points towards important new approaches for treatment Let s look at their work in more detail Meet the molecular nurse The key player in this story is a protein called ATM It s a kind of molecular triage nurse that patrols the cell looking out for signs of DNA damage When ATM spots DNA damage it does one of two things if the damage is repairable it tells the cell to stop dividing and calls in emergency crews of repair proteins But if the damage is too bad to be fixed for example in the case of damage caused by radiotherapy or certain cancer drugs then it tells the cell to die instead Because the effects of ATM are so drastic either halting a cell in its tracks or killing it it s very important that it s only activated exactly when needed So there are a lot of control mechanisms that help to make sure that ATM is only switched on at the right time and in the right place But it s still not entirely clear how all these controls work We also know about some other important characters involved in the process of DNA repair These include two proteins called KAT5 and c Abl the latter being the target of the cancer drug imatinib better known as Glivec But what s not been known until now is whether and how these two proteins collaborate with ATM to keep our DNA in tip top shape Through detailed experiments with cancer cells grown in the lab Kaidi discovered a chain of events that links all three proteins together First he found that when DNA damage occurs c Abl switches on KAT5 This activated KAT5 then homes in on the cell s genetic material particularly proteins called histones that package DNA to make up a structure called chromatin which is disrupted when DNA gets damaged Finally the activation and relocation of KAT5 switches on ATM triggering the cell s DNA repair machinery Having discovered how this pathway works Kaidi wondered if it could be switched off So he exposed cancer cells to imatinib which prevents c Abl from switching on other proteins As predicted the drug blocked the DNA repair process from being activated after the cells were exposed to radiation It s all a bit complicated so to explain the process we ve made this

    Original URL path: http://scienceblog.cancerresearchuk.org/2013/05/26/joining-the-dots-how-lab-research-can-lead-to-new-approaches-for-treating-cancer/ (2016-02-11)
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  • Prostate drug decision highlights urgent need for reform - Cancer Research UK - Science blog
    paying for drugs for a small population of patients who are not expected to live for more than 2 years where the drug could extend their lives by at least 3 months This allowed NICE to approve abiraterone given the data available from clinical trials at the time and a deal on price from Janssen Typically NICE allows such End of Life drugs to be approved below a threshold of about 50 000 per QALY read more about what a QALY is here We were pleased to see the drug approved as it makes a real difference and to be completely transparent here we do benefit from this decision Cancer Research UK licensed abiraterone to Janssen and we receive a small royalty from the drug s sales which we reinvest in our research Using it pre chemo Wind forward to January 2013 and a clinical trial called COUGAR 302 showed that giving abiraterone before chemotherapy could be even more beneficial The trial hadn t been running long enough to show for certain how much extra life this would lead to but it did show that the drug could double the time between the hormone therapy failing and the cancer returning from about 8 months to around 16 As a result NICE was asked to look at whether it would be suitable for use at this earlier point in a man s treatment While they looked at the data and talked to Janssen about how best to pay for the drug men were and are still able to get abiraterone on the NHS in England through a mechanism called the Cancer Drugs Fund and elsewhere in the UK via something called an Individual Funding Request This has essentially acted as a way to help patients get treatment while the system works out the numbers says Prof Mason A disappointing decision Today NICE has made its final decision on earlier use of abiraterone and it s a no Why NICE s End of Life criteria have a cut off point says Prof Mason They can only apply for patients who are expected to live for two years or less But Prof Mason says the untreated men on the COUGAR triallived for about 30 months and that s above the threshold for NICE to use End of Life criteria Paradoxically these men are living too long for NICE to approve a drug they could benefit for he says This highlights the inflexibility in the system The drug works but the system s arbitrary built in cut off point coupled to the drug s price means NICE is obliged to say no under its own rules Janssen has pointed out that the system in Scotland uses a cut off of 36 months NICE has replied that the drug is simply too expensive for the benefit it brings and wants Janssen to reconsider how it prices it What next This situation is deeply disappointing and very frustrating for all concerned Janssen has said it will

    Original URL path: http://scienceblog.cancerresearchuk.org/2014/08/15/prostate-drug-decision-highlights-urgent-need-for-reform/ (2016-02-11)
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  • NCRI Cancer Conference 2009 – Bigger benefits from PARP inhibitors - Cancer Research UK - Science blog
    Award from the European Society for Medical Oncology This connection quickly led to early clinical trials of PARP inhibitors in patients with breast and ovarian cancer caused by faulty BRCA genes including one being funded by Cancer Research UK in Newcastle and one run by The Institute of Cancer Research Professor Andrew Tutt from Guy s Hospital in London presented encouraging results from one of these trials later on the same day of the conference His team tested a PARP inhibitor called olaparib in 27 women with advanced disease The majority responded to the drug meaning that their tumours shrank in size and they experienced fewer side effects compared with standard chemotherapies New uses for PARP inhibitors So PARP inhibitors are definitely big news in the research community But cancers caused by inheriting a faulty BRCA gene are relatively rare So what s really exciting is the emerging evidence that they might be effective treatments for other forms of cancer This could dramatically increase the number of people who could benefit from these new drugs Also at the conference was Cancer Research UK funded Dr Ester Hammond from the Gray Institute for Radiation Oncology and Biology in Oxford She presented her research showing that PARP inhibitors might work on cancer cells that have low levels of oxygen This is known as hypoxia found in many different tumours Because hypoxia switches off some of the DNA repair machinery in the cells Dr Hammond thinks that adding PARP inhibitors which block a different part of the repair mechanism acts as a double whammy helping to kill the cells BRCA ness In his talk Professor Ashworth described cancers that have characteristic hallmarks and behave in a similar way to cancers caused by faulty BRCA genes He calls this having BRCA ness But what cancers have this BRCA ness Professor Ashworth s example was a type of breast cancer that doctors describe as triple negative These account for around 15 per cent of all breast cancers are more common in younger women and are often more aggressive and more difficult to treat than other types of the disease So an early clinical trial testing PARP inhibitors in women with this form of the disease has already been carried out in the USA And although it s early days the results are again encouraging and are likely to be followed up in larger trials Professor Ashworth also talked about his experiments on cancer cells grown in the lab with faulty PTEN genes He has found that these are more sensitive to PARP inhibitors than healthy cells similar to cancer cells with faulty BRCA genes although not quite so dramatic As PTEN is often faulty in many different types of cancer this widens the door even further for PARP inhibitors There are now plans afoot to set up clinical trials for people with prostate womb and bowel cancers and melanoma skin cancer who have faulty PTEN genes in their cancers PARP inhibitors in combination So far

    Original URL path: http://scienceblog.cancerresearchuk.org/2009/10/09/ncri-cancer-conference-2009-%e2%80%93-bigger-benefits-from-parp-inhibitors/ (2016-02-11)
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  • Peering behind the pathology lab door: A day in the life of a pathologist - Cancer Research UK - Science blog
    learn how the diagnosis I make down the microscope contributes to care of the patient On the other hand as President my favourite part of the job is talking to members of the College around the country and finding out about their concerns and opinions and representing them at a national and international level to government industry other pathology organisations and the public What are the main challenges On a personal level the main challenge is balancing my two jobs and my family life Professionally the main challenge is that there s insufficient investment in pathology services at a time when the volume and complexity of work is increasing rapidly and targets are being introduced to reduce turnaround times Without reliable IT systems modern equipment and a fully trained workforce pathology services will not be able to keep up with demand What does a typical day look like A typical day starts at 7 30am when I catch up on any emails that have come in while I ve been out of the department on College business I then start reporting cases that have been given to me including bowel cancer screening cases and cervical smears After that I prepare for the MDT meeting reviewing all the slides from cancer cases that have been diagnosed that week In the two hour MDT meeting we discuss all the patients who are being treated that week The surgeon might give the background to the case the radiologist shows the scan and I ll describe the pathology including the presence of any markers that will help decide the best course of treatment There will then be a general discussion with the wider team taking into account the patient s wishes their fitness other health conditions and home circumstances By the end of the discussion a treatment plan will have been put together for discussion with the patient by the surgeon or oncologist After the MDT meeting there ll be a pile of slides on my desk waiting to be reported These will usually include urgent cancer biopsies which need to be reported the same day if possible I work with a great team and I discuss difficult or unusual cases with my colleagues at a multi headed microscope meeting every afternoon We all bring cases to show each other and discuss the best way to proceed with complex cases Finally I usually do a specimen trimming session in the afternoon where I examine large specimens such as colectomies removal of part of the colon or skin cancer excisions that have been sent to the lab for analysis I describe the appearances of the specimen and select small pieces for examination under the microscope the following day If money were no object what would you change about pathology services There are two things I d like to change First would be to introduce a national IT system for pathology Cancer diagnosis increasingly involves tissue being sent from the hospital where the patient is being

    Original URL path: http://scienceblog.cancerresearchuk.org/2015/11/05/peering-behind-the-pathology-lab-door-a-day-in-the-life-of-a-pathologist/ (2016-02-11)
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  • News digest - GPs, cancer survival, herpes virus treatment, smoking statistics… and some terrible puns - Cancer Research UK - Science blog
    this was over optimistic We looked at the study in detail in this blog post Our researchers found that the lower cancer survival in the UK compared to countries with similar health care systems was linked to delays in GPs referring patients for tests BBC reported this as did the Daily Mail the Guardian and many others Here s our in depth analysis Italian researchers suggested that a Mediterranean style diet might halve a woman s risk of womb cancer The Guardian covered this as did the Daily Mail and Mirror But as we said in the press release there s still some way to go to confirm this idea UK researchers uncovered a possible way that breast cancer can spread to the bones which suggests the process can be blocked BBC covered this as did many national papers And here s our take on the story New research showed that because of England s smoking ban 11 000 fewer children now make trips to the hospital each year We talked about this as did the BBC and the Guardian among others But smoking still thrusts over half a million children into poverty According to new research more than half of the 2 3 million children in the UK who live in poverty have a parent who smokes and the addiction places an extra financial burden on the family The Independent and the Daily Mail have more on this story Cancer climbed to second place on the list of the world s biggest killer diseases affecting nearly 15 million each year and killing more than 8 million Heart disease still has the top spot The Week and the Daily Mail have more on this UK researchers are beginning to understand how certain blood cancers come back years after chemotherapy BBC has more details There was coverage of a new study suggesting a link between obesity in teenage boys and a subsequent risk of bowel cancer later in life The BBC and the Guardian have the story Number of the week 11 000 The number of children s hospital visits that England s smoking ban prevents each year A company that manages prescription drug benefits for US employers and insurers has been making deals with pharmaceutical companies to base the prices of some cancer drugs on how well the drug works The Wall Street Journal has the full story Urine for a treat with this next story Popular Science along with the BBC ran a piece about researchers that modified probiotic bacteria the stuff in yogurt to light up when signs of cancer were present in urine But the research was done in mice so there is still a long way to go before there is a urine test for cancer Reuters reported that smokers are more likely to think cancer is a death sentence Younger cancer patients are more willing to try alternative therapies according to a story on Reuters But we recommend they read our blog post on alternative

    Original URL path: http://scienceblog.cancerresearchuk.org/2015/05/30/news-digest-gps-cancer-survival-herpes-virus-treatment-smoking-statistics-and-some-terrible-puns/ (2016-02-11)
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  • Expert opinion: Professor Charlie Swanton – plotting a route through cancer evolution - Cancer Research UK - Science blog
    the number of tumours we ve analysed We ve now read or sequenced the DNA code from multiple biopsies taken from 10 different tumours This is no easy feat but it s confirmed that branched evolution occurs in all tumours it is the norm rather than the exception in these types of kidney cancer We also saw strong evidence for something called parallel evolution Cancer Research UK Can you tell us a little more about that Professor Swanton This is truly fascinating In the case of different species parallel evolution is when two distinct species that share a common ancestor evolve a similar trait Old and new world porcupines are a great example of this Their ancestors were separated when their home continents broke apart yet the old and new world porcupines have evolved strikingly similar spines In kidney cancer we see the same molecules becoming faulty in multiple patients but the faults arise due to different changes within these molecules which are present in distinct regions of the tumour If you look at the numbers the probability of this happening by chance is very very small It s fascinating and seems to show that one way or other these kidney cancers are inactivating the same handful of molecules If we can understand more about this and find out what the early events are in the tumour then we might be able to predict the cancer s next evolutionary move That s the hope it s very exciting as it shows us there is actually order in these chaotic tumours Cancer Research UK Are there any other patterns emerging Professor Swanton Our lab is very interested in understanding how diversity within tumours occurs And something that s caught our attention recently is a process called genome doubling This is where all the genetic information within the cell becomes duplicated inappropriately meaning a cell is left with double the normal amount of DNA To study this we use bowel cancer cells grown in the lab The majority of these cells contain the correct amount of DNA but around one or two per cent have double the normal amount When we separated these two groups of cells and grew them independently in the lab we found that the cells with the doubled DNA were able to tolerate this added genetic burden and continue to grow Next we followed the cells under the microscope and looked at what happened when they made a mistake when dividing up their DNA during cell division If the cells with the correct amount of DNA made an error they stopped dividing or died The cells with double the amount of DNA were perfectly happy to divide and grow when errors were made This tells us there must be a tolerance mechanism that allows genome doubling to occur and be maintained Finding this mechanism is our next challenge we think this may hold a key to blocking one form of cancer progression We also think that genome doubling

    Original URL path: http://scienceblog.cancerresearchuk.org/2014/02/28/expert-opinion-professor-charlie-swanton-plotting-a-route-through-cancer-evolution/ (2016-02-11)
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  • Expert Opinion – The challenges of lung cancer - Cancer Research UK - Science blog
    you treat cells that have taken one pathway to resistance you may only be killing a small part of the cancer and the rest of the disease will carry on growing So we re looking for ways we can tackle all of the resistant cells at once despite the various pathways driving their resistance Coupled with this is the very physical problem of actually pinning down the genetic mistakes that both cause and drive resistance in lung cancer The technology to map the faults in DNA is readily available and straightforward to use so in theory it is simple to match targeted therapies to the right patient But in practise this is not so straightforward Obviously lung cancer develops in the lungs but it s actually extremely difficult for surgeons to access and take samples biopsies of these tumours This becomes even more of a conundrum when people become resistant to drugs Do we take them back into surgery to collect more samples At this point people are generally more unwell and less fit to cope with the impact of surgery Furthermore as I mentioned earlier different parts of the tumour can develop independently so taking a sample from one tumour site may not reflect the genetic changes that have happened elsewhere And if we aren t able to identify the different genetic faults that are driving the cancer throwing various drugs at it is like playing darts with a blindfold on Fresh ideas One of approach that s generating a lot of excitement and that we re trying here in Leicester is developing ways to monitor cancers using blood tests instead of needing to remove a piece of the tumour itself As the tumour grows some of its cells die and as they do so they release their DNA into the patient s blood So what we re able to do now is get the tumour s DNA profile from a small blood sample We ve just seen some very promising early lab results from a joint project involving a randomised clinical trial with a US pharmaceutical company and it s clear that it could provide an easy way of pinpointing the genetic mistakes causing the development of lung cancer in the first place But importantly it could also allow us to monitor the disease over time detecting break away parts of the tumour as they become drug resistant and working out how they ve achieved it This is the vital information we need to get patients the best targeted treatments both from when they are first diagnosed to when they become resistant to therapy And this is the next quantum leap for us in terms of improving survival rates for lung cancer Spotting it earlier Lastly these new approaches could even have a wider impact by using them to detect lung cancer at an earlier stage At the moment we usually only see lung cancer patients when their cancer is fairly advanced as this is when people start

    Original URL path: http://scienceblog.cancerresearchuk.org/2013/04/04/expert-opinion-the-challenges-of-lung-cancer/ (2016-02-11)
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  • Lifestyle and cancer: against the blame game - Cancer Research UK - Science blog
    when driving which is now enshrined in law and has undoubtedly saved many lives Similarly the overwhelming evidence that smoking causes cancer has gradually percolated into the public mind and has helped make the case for anti smoking legislation in many countries around the world Stricter legislation and taxation along with public health campaigning has helped many thousands of people quit the habit contributing to a drop in smoking related cancers a trend we re determined to see continue High stakes But beyond smoking we know that that it can be hard to get a grip on some of the other preventable causes of cancer It s no wonder stories about diet lifestyle and cancer frequently appear in the media sometimes with conflicting information This coverage gives the incorrect perception that the evidence base shifts drastically from one week to the next and that scientists don t know what they re talking about when it comes to cancer risks This simply isn t true The evidence on lifestyle and cancer has been built through decades of research and has cemented a handful of key lifestyle changes that can reduce the chances of developing cancer Top of the list is to quit smoking and the others are keeping a healthy body weight cutting back on alcohol eating a healthy balanced diet keeping active and staying safe in the sun To take one example from this list there s a huge weight of evidence showing that alcohol can cause seven types of cancer Scientists have been confident about the link between alcohol and cancer since the 1980s pdf Yet and this is crucial only around a third of people know that alcohol increases the risk of cancer To change things in the same way we ve helped reduce smoking rates this gap between what the evidence tells us and what the public understands needs to be closed The stakes are high the latest estimate is that more than 100 000 cancers every year are down to tobacco diet alcohol and obesity This statistic alone tells you why we will continue to bang the drum about lifestyle and cancer Walk through a minefield So we know how to reduce the risk of cancer and can estimate the total proportion of cancers caused by unhealthy living Does this mean we can we spot unhealthy people and say unequivocally that they will develop the disease No Just as it s not possible to say exactly who will crash as a result of risky driving but you can say that such behaviour generally increase the chances of crashing it s not yet possible to categorically pin down specific people who will develop cancer based on their lifestyle Why Because lifestyle isn t the only thing that contributes to cancer Broadly speaking all cancers are caused by faulty or damaged genes And this damage can come from several sources People can inherit these faults from their parents they can accrue by chance over their life or DNA damage can develop as a result of exposure to carcinogens such as tobacco smoke or ultraviolet light from the sun But not every bit of damage to your genes leads to cancer The damage needs to occur in particular genes to do so So just as you might emerge safely from a walk through a minefield there are cases of lifelong heavy smokers living well into their 90s and beyond And such people who survive to a ripe old age despite such unhealthy habits often loom large in popular imagination But these people are the exception to the rule Perhaps they have a particularly robust genome or are just plain lucky This doesn t take away from the fact that smokers are overwhelmingly more likely to develop cancer than non smokers The broader point is that you can control many aspects of your lifestyle but there s not a whole lot you can do to affect chance events or the genetic hand you re dealt by your parents From statistics to the individual Another reason is much geekier and involves a bit of statistical jargon Estimates of how many cancers are caused by lifestyle are calculated by researchers called epidemiologists They look at health patterns across whole populations and try to match different factors such as smoking or weight to the chances of developing a particular disease A common way epidemiologists measure how a lifestyle factor such as smoking contributes to disease is to calculate population attributable fractions These calculations represent the proportion of deaths in the whole population that could be prevented if a cause of death such as smoking were at an ideal safe level in the case of smoking zero tobacco use But by definition these figures don t tell you about specific individuals They are about populations of hundreds thousands or millions of people In other words epidemiologists are excellent at estimating how risky behaviours affect large groups of people but they re no good at predicting what will happen to individuals An ounce of prevention Where does this leave us a charity whose aim is to beat cancer Cancer is not a single disease it s a group of hundreds of different often complex diseases with a range of causes The connection is that all cancers are down to our healthy cells going rogue ignoring the normal rules of meticulously synchronized cell behaviour and dividing out of control Together this group of diseases cause almost 1 in every 4 deaths in the UK The good news is that more people are surviving cancer than ever before and better treatments to kill off these rogue cells will undoubtedly save more lives in the future But treatment is only part of the solution we need other tools in our toolbox to beat the disease And it s indisputable that one of our most powerful tools against cancer is the in depth knowledge we now have about its causes Of course none of us lead a risk free

    Original URL path: http://scienceblog.cancerresearchuk.org/2012/04/11/lifestyle-and-cancer-against-the-blame-game/ (2016-02-11)
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