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  • Tracking down bowel cancer stem cells - Cancer Research UK - Science blog
    Next the scientists knocked out APC in normal bowel lining cells and found that tumours also developed but much less readily or frequently than those from the stem cells The results suggest that the stem cells are much more likely to give rise to cancer that the lining cells The scientists also found that the stem cell derived cancers produced bulk cancer cells similar to bowel lining cells supporting the classic cancer stem cell concept So we now know that stem cells are likely to be the fuel for bowel cancers at least in mice But does it hold true for humans too Similarities and differences Obviously it s virtually impossible to do genetic engineering experiments directly in humans But we do know that the mouse system the team was using is a very good model for the development of human bowel cancer There s one key difference though Experiments with mice have shown that their bowel cells only need one or two major gene faults to push them down the cancer path whereas human bowel cells need several more But these results suggest that stem cells are on the brink and need only a relatively small genetic push whether that s one fault or several compared with other cells in the bowel More experiments need to be done before we know for sure whether stem cells play a vital role in human bowel cancer For now these results are a promising step in the right direction and a confirmation that the stem cell theory may well hold true for at least one type of cancer If we can understand more about the molecular pathways that control cancer we can start to design new more effective ways to prevent and treat the disease Click on the player below to hear Dr Sansom talking about his work in a short audio clip Audio clip Adobe Flash Player version 9 or above is required to play this audio clip Download the latest version here You also need to have JavaScript enabled in your browser Link to download 1 5Mb 3min10 Kat Share this article More on this topic Tags Bowel cancer Cancer in the news Cancer Research UK funded research Cancer type Research and trials Stem cells Comments Click here to cancel reply Mike March 6 2009 I would be interested to know which chemo D Casemore had to remove multi secondaries as I have had two secondary events both removed by surgery as the chemo didn t seem to work D Casemore February 10 2009 I had ca colon removed a year ago picked up through ve occult blood test I seemed generally in good health at the time Chemo was successful in removing multiple secondaries in the liver CEA is 1 My delight in the outcome is now somewhat tempered by this news although I d rather know than not Is there any info on the frequency of recurrence Valerie Thomson February 10 2009 I had bowel cancer three and

    Original URL path: http://scienceblog.cancerresearchuk.org/2008/12/17/tracking-down-bowel-cancer-stem-cells/ (2016-02-11)
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  • ASCO 2011 – the challenge and promise of the genomic era - Cancer Research UK - Science blog
    to hear the very latest results from trials of new treatments and learn more about hot topics such as personalised medicine or new DNA sequencing technologies In his welcome speech outgoing ASCO president Dr George Sledge discussed the challenges ahead as we enter what he termed an era of genomics In the not too distant future according to Dr Sledge fast and cheap technologies will be used to map each patient s genetic make up compare it with that of their cancer and highlight all the faults in their DNA that affect how their cancer responds to treatment While this information has the power to transform treatment for patients around the world there are still huge challenges ahead for scientists and doctors As the costs of analysing or sequencing DNA plummet doctors need to find ways to start translating this new genetic knowledge in a way that s useful and beneficial for patients Dr Sledge gave a recent example of how new sequencing technology transformed the care of a difficult to diagnose patient with acute promyelocytic leukemia Scientists at Washington University used whole genome sequencing to help understand the patient s cancer and within seven weeks they had enough information to guide the doctor s decision and change the course of treatment sparing the patient an unecessary bone marrow transplant Stupid versus smart cancers Different types of cancer have different numbers and types of DNA faults and this can vary widely between cancers with lung cancer and melanoma for example typically having many thousands more faults than other cancer types Dr Sledge described cancers as being either stupid or smart The stupid tumours are those that have a single predominant fault or mutation that drives the disease and a small total number of different faults in the cancer cells These cancers for example many cases of chronic myeloid leukaemia can be treated with a single drug glivec and resistance to treatment is rare However the smart tumours have a huge spectrum of faults that fuel the disease It s unlikely that doctors will be able to target them with a single drug or treatment and resistance is more common An example of this is non small cell lung cancer which can develop resistance to many different drugs And it now seems that smokers s cancers are particularly smart lung cancers in smokers usually have many more gene faults in their tumour compared with non smokers and so tend to have an even poorer response to treatment The Red Queen principle In Alice in Wonderland the Red Queen says to Alice it takes all the running you can do to stay in the same place Dr Sledge used this quote to highlight the shear effort that will be required to tackle the complexity of these smart tumours For these cancers there will be no magic bullet but rather a magic shotgun that is able to fire at multiple targets The approaches needed to tackle these smart cancers are varie d and

    Original URL path: http://scienceblog.cancerresearchuk.org/2011/06/08/asco-2011-the-challenge-and-promise-of-the-genomic-era/ (2016-02-11)
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  • Guarding the genome – p53 and Cep63 - Cancer Research UK - Science blog
    cancer P53 and cancer But this protection isn t infallible in the late 80s scientists found that many human cancers have a damaged version of p53 meaning that the loss of its protective power is an important and possibly fundamental step towards developing the disease So understanding more about exactly how p53 works is a pressing concern for many cancer researchers Professor Sir David Lane Cancer Research UK s Chief Scientist is probably the world s leading authority on p53 and played a fundamental role in its discovery back in 1982 Lane along with colleagues in Dundee and Singapore has now made another important discovery published in the journal Genes Development showing how p53 is controlled in response to DNA damage P53 not one but many Professor Lane and his team had previously discovered that there are in fact several different versions or isoforms of p53 within each of our cells and that different cells at different stages of development have different amounts of each isoform This posed a question what exactly did each of these isoforms do Professor Lane s latest research has started to answer this puzzle Delta113 p53 Delta113 p53 is an isoform of p53 that which has previously been found in high levels in certain human breast cancers This is a bit of a paradox normally cancer cells lack p53 How could this isoform be involved in cancer To find out more the researchers studied the protein in zebrafish whose p53 is very similar to the human version To make their studies easier they used a genetic trick to engineer the fish so that their p53 proteins glowed green when they were activated Firstly they showed that zebrafish engineered to lack normal p53 but not delta113 p53 were unable to activate delta113 p53 when their DNA was damaged This showed that the two isoforms were somehow affecting each others behaviour They then found that fish that lacked the delta113 isoform died when they were exposed to relatively low levels of radiation which wouldn t normally be enough to kill normal fish They then showed precisely how at a molecular level the delta113 isoform blocked normal p53 from causing the cells to commit suicide It seems the isoform switches on a protein called bcl2L which prevents cell death What does it mean Given their results Professor Lane and his team think that the delta113 p53 isoform helps healthy cells to maintain the fine balance between life and death They propose that if the cell s DNA suffers relatively minor damage p53 is switched on and its levels in the cell start to rise But p53 also activates its own isoform delta113 p53 preventing the cell from dying straight away as a result of relatively trivial damage On the flip side the scientists suggest that if the DNA damage is too severe then p53 levels soar over riding the restraining effect of the delta113 isoform and triggering cell suicide This multi layered control mechanism gives normal cells exquisite

    Original URL path: http://scienceblog.cancerresearchuk.org/2009/02/09/guarding-the-genome-%E2%80%93-p53-and-cep63/ (2016-02-11)
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  • The shape of things to come? - Cancer Research UK - Science blog
    Some of these have a walk on part Others are virtually extras But there are some that can be thought of as the big stars of the field the George Clooney or Nicole Kidman of cell division if you like One of these is called p53 and often billed as the guardian of the genome But despite years of research we re still a long way from knowing exactly how p53 works A paper published last week in top science journal PNAS is helping change all that Researchers are working out the protein s exact 3D structure and aim to use this knowledge to find out more about this reclusive superstar and what makes it tick Scientists have been fascinated by p53 since its discovery in 1979 thanks in part to top Cancer Research UK scientist Professor Sir David Lane who helped to track it down It seems that in healthy cells p53 plays the role of a detective tracking down DNA damage If it finds any it springs into action kicking off a cascade of events which can either halt the cell s ability to divide or even cause it to commit suicide This appears to be one of evolution s most important anti cancer mechanisms protecting us from the disease by neutralising potentially dodgy cells And one of the most exciting findings in recent cancer research was that p53 is faulty in the majority of human cancers This failure allows cancer cells which are riddled with DNA damage that p53 would normally spot to cheat death and multiply out of control So scientists think that if we could develop treatments based on reactivating p53 this might be a good way to treat most cases of cancer But so far this has proved impossible to achieve partly because we have a relatively limited understanding of the exact way p53 recognises damage and alerts the rest of the cell Last week scientists came a little closer to understanding this mysterious molecule after an international collaboration of researchers managed to figure out p53 s 3 D structure and see exactly how it sticks to DNA The team was led by Professor Sir Alan Fersht at the University of Cambridge and you can see a representation of the fruits of their labour in the picture below Certain important parts of p53 are coloured red green and blue while DNA is a rather fetching shade of purple Now this may not sound terribly exciting unless you re a structural biologist of course but it has taken many years and much frustration to get to this point Despite figuring out the structure of small parts of p53 one at a time no one has been able to work out the whole shape of the molecule until now Previous efforts have been hampered by the fact that the protein is quite unstable and tends to break down or fall apart easily And there are quite a few parts of the protein shown in grey in

    Original URL path: http://scienceblog.cancerresearchuk.org/2007/08/07/the-shape-of-things-to-come/ (2016-02-11)
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  • Positive early results for experimental melanoma drug - Cancer Research UK - Science blog
    work The drug is designed to target BRAF a molecule that is faulty in more than half of all melanomas and some other types of cancer as well As we wrote about recently in our High Impact Science strand Cancer Research UK helped to fund the work that led to the discovery that BRAF is faulty in many cancers And we continue to support research and drug development work based on this finding But the current research from which the news stories originate comes from researchers in the United States Importantly the patients in this trial were all selected because they had faulty BRAF genes in their tumours So discovering that the BRAF blocking drug works in so many of them is an important proof of the principle and shows that targeted cancer therapies may well live up to their promise And we can expect to see more trials like this selecting patients based on their cancer s individual gene profile in the future When will PLX4032 be available for patients There is still a long way to go before this drug is widely available for cancer patients Larger trials must be done to confirm that PLX4032 is safe and effective The researchers are now planning another small study involving 90 patients starting late in 2009 and they hope to begin a much larger trial with hundreds of patients within the next year If the results from these larger trials are positive then there are regulatory hurdles to be cleared before the drug can be marketed worldwide but it s speculation to say when this might happen As we ve mentioned before the road for a new cancer drug can be long For example the discovery of the prostate cancer drug abiraterone was first made in 1995 yet despite the success of smaller studies we are still waiting for the results of large scale trials So although it may be some years before we see the drug or others like it in widespread use today s results are still an exciting announcement as it shows that cancer researchers around the world are making progress in beating cancer Kat If you are concerned about cancer please contact our information nurses on 0207 061 8355 or freephone 0808 800 4040 weekdays 9 5pm or by email Further reading About melanoma What s new in melanoma High Impact Science Finding faults in BRAF Drug shrinks skin tumours NHS Choices blog Share this article More on this topic Tags Cancer in the news Research and trials Skin cancer Treatment Comments Click here to cancel reply Ben Rowe November 20 2009 Hi Everyone My Father has a melignant melenoma that has spread to his lungs He is about to start chemo this week to try and keep it at bay I was wondering if you know of this drug being trialed outside of the US Naturally we would fly him where ever we could in the world from New Zealand to see if he had

    Original URL path: http://scienceblog.cancerresearchuk.org/2009/09/23/positive-early-results-for-experimental-melanoma-drug/ (2016-02-11)
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  • More good progress for experimental cancer drug - Cancer Research UK - Science blog
    Manage your research grant Manage your grant online Guide to managing a grant online Notify us of new publications Update your profile How we deliver research Our research strategy Our institutes Our centres Our research partnerships More Drug discovery and development Recently funded awards Researcher case studies ABOUT US What we do We beat cancer We fundraise We develop policy Our organisation Our strategy Our Trustees CEO and Executive Board Annual report and accounts Annual review Current jobs Graduates and interns Your development Benefits Cancer news Science blog Latest press releases Latest news reports Search all news More Contact Us Press office Publications HOME ABOUT CANCER SUPPORT US NEWS RESOURCES FUNDING RESEARCH ABOUT US You are here Home border 0 Support us Home About us Cancer news Science blog More good progress for experimental cancer drug More good progress for experimental cancer drug Category Science blog August 26 2010 Henry Scowcroft New results for PLX4032 are promising Last September we covered results from a small trial of an experimental drug called PLX4032 which has been developed to treat patients whose cancers are caused by a faulty version of a gene called BRAF Today yet more encouraging results were announced in the New England Journal of Medicine which were reported widely in the media The trial was very small and carried out in two stages The first stage involved 55 patients and was simply to find the most suitable dose In the second stage 32 patients whose cancers were caused by BRAF mutations were given the drug at this dose Of these 26 patients tumours shrank by 30 per cent or more and in two of these patients the cancers disappeared completely We discussed this with one of our leading skin cancer scientists Professor Richard Marais who was part of a team that discovered the underlying genetic fault in BRAF that PLX4032 is designed to target He said These results are extremely exciting This is the first time in over 30 years that this level of response has been seen in melanoma patients in any clinical trial While these results are very promising there is still work to be done Although patients initially respond they can often relapse during treatment so now we need to learn how to get longer lasting responses in these patients This last point is crucial There s no hard evidence yet that the drug actually prolongs patients lives The trial has only demonstrated that it can cause tumours to shrink Although several patients cancers eventually became resistant to the drug we need more research to work out how best to use this addition to the doctor s toolbox before we can be certain that this is going to save lives But for now the results of these small early trials show great promise and we ll be keeping an eye on what happens next Henry Reference Flaherty K et al 2010 Inhibition of Mutated Activated BRAF in Metastatic Melanoma New England Journal of Medicine 363 9

    Original URL path: http://scienceblog.cancerresearchuk.org/2010/08/26/more-good-progress-for-experimental-cancer-drug/ (2016-02-11)
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  • Introducing our new arrivals - Cancer Research UK - Science blog
    RESEARCHERS Our funding schemes Biomarker Project Awards Career Development Fellowship Grand Challenge award View all schemes and deadlines Applying for funding Start your application online Guide to filling in your application form How to make a successful application Funding committees Manage your research grant Manage your grant online Guide to managing a grant online Notify us of new publications Update your profile How we deliver research Our research strategy Our institutes Our centres Our research partnerships More Drug discovery and development Recently funded awards Researcher case studies ABOUT US What we do We beat cancer We fundraise We develop policy Our organisation Our strategy Our Trustees CEO and Executive Board Annual report and accounts Annual review Current jobs Graduates and interns Your development Benefits Cancer news Science blog Latest press releases Latest news reports Search all news More Contact Us Press office Publications HOME ABOUT CANCER SUPPORT US NEWS RESOURCES FUNDING RESEARCH ABOUT US You are here Home border 0 Support us Home About us Cancer news Science blog Introducing our new arrivals Introducing our new arrivals Category Science blog September 12 2013 Safia Danovi The Cancer Research UK family just got a little bigger And we d like to share our happy news with you Labour pains began a few months ago when one of our funding committees the Training and Career Development Board was tasked with trawling through nearly one hundred grant applications to find the UK s brightest and most creative scientific minds And after four exhausting days 12 fledgling scientists were delivered to the cancer research community nine boys and three girls collective weight approximately 1818lb 13oz Cancer Research UK and the little ones are all doing well The below slideshow gives some details about their work This slideshow requires JavaScript Investing in new talent maintains a flow of new ideas and keeps cancer research fresh and invigorated Like all our researchers our new arrivals carry the hopes of hundreds of thousands of cancer patients on their shoulders To meet this incredible challenge we ve invested over 8m towards helping them so that they can help all of us We d like to welcome them to the family and we wish them success in their research Share this article More on this topic Tags Cancer Research UK funded research Treatment Comments Click here to cancel reply RobbieW September 13 2013 I wish them the best of luck Have you told them about your policy on e cigs though Probably the biggest public health prize in a generation with the potential to almost eliminate smoking related cancers Do your new starts know that CRUK support a policy which is essentailly a de facto ban Careful new starts being associatsed with CRUK and their repidly diminising reputation may be harmful to your career Rebecca September 12 2013 Go for it and all the best of luck you clever lot xxx Older Comments Newer Comments Popular posts Most read today Most discussed Don t believe the hype 10 persistent

    Original URL path: http://scienceblog.cancerresearchuk.org/2013/09/12/introducing-our-new-arrivals/ (2016-02-11)
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  • A home from home – how cancer cells spread to new organs - Cancer Research UK - Science blog
    there was nothing random about the choice of secondary organ at all some organs were simply more hospitable than others So what makes these particular organs so special The short answer is that we don t really know but research in this area has unearthed some fascinating findings Finding the local hotspots Incredibly some research suggests that growing tumours send chemical messages to the lung a common site of metastasis effectively phoning ahead to ensure that preparations for the arrival of the first tumour cells are in place The researchers also found that lungs responded with the help of cells called myeloid cells by kick starting inflammation which wandering tumour cells find irresistible Myeloid cells also collaborate with local tissue to carve out cosy pockets in which incoming cancer cells can lodge These early changes in secondary organs which occur before tumour cells arrive create what scientists call the pre metastatic niche a relatively new concept in biology It s a far cry from the random model of metastasis that Paget challenged because it s based on the idea that the primary tumour controls where its seedlings go But what happens when the pre metastatic niche opens for business Rooms available the metastatic niche The pre metastatic niche prepares for the arrival of tumour cells When the first tumour cells arrive the pre metastatic niche becomes the metastatic niche and its role in determining tumour cell fate becomes more crucial than ever before Research suggests that other local cell types such as fibroblasts and endothelial cells make sticky glue like molecules to help tumour cells attach to their new surroundings Researchers also think myeloid cells help protect tumour cells from patrolling immune cells We don t completely understand how they do this but there s some evidence that they produce molecules which dampen the immune system allowing tumour cells to rest and recuperate undetected In other words when tumour cells arrive secondary organs work hard to keep them there and keep them safe Chatting to the locals But docking safely to the target organ is the easy bit the real challenge is learning to adapt and thrive in a foreign environment Yet again success depends on productive interactions with the local community For starters tumour cells have to quash the urge to self destruct that usually comes with being alone in a foreign land But again welcome signals from its new environment are thought to help soothe and reassure Local tissue is also a handy source of growth factors molecules that cells depend on to grow and thrive These are invaluable as tumour cells get to work on the crucial task of building their own blood supply and forming colonies of their own Making the hospitable inhospitable In the future we could stop metastasis from happening Research is always a voyage into the unknown and the best studies often throw up more questions than answers We ve still got big questions to address We need to understand how target organs

    Original URL path: http://scienceblog.cancerresearchuk.org/2013/06/04/a-home-from-home-how-cancer-cells-spread-to-new-organs/ (2016-02-11)
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