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  • Skin cancer - Cancer Research UK - Science blog
    Fran Balkwill Professor Andrew Biankin See all researchers More Our research history Our research strategy FUNDING FOR 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 Topic Skin cancer Topic Skin cancer The biggest cancer science stories of 2015 Category Science blog December 22 2015 Aine McCarthy We ve enlisted the help of one of our researchers to pick out the biggest cancer research stories of 2015 Read More NCRI cancer conference day 2 big data immunotherapy and prizes Category Science blog November 3 2015 Nick Peel We re back for day two of our highlights from this year s NCRI cancer conference in Liverpool Read More Antioxidants free radicals and melanoma spread what s going on Category Science blog October 16 2015 Emma Smith We explore new research looking at how antioxidants and free radicals might affect the ability of melanoma cells to spread around the body Read More Stopping cancer s scrum for survival Category Science blog September 25 2015 Alan Worsley Our scientists have discovered that similar to a rugby maul cancer cells can ward off tumour killing immune cells through an important cellular signal Read More Expert Opinion Professor Peter Johnson on cancer immunotherapy Category Science blog September 17 2015 Henry Scowcroft We quiz our chief clinician Professor Peter Johnson to get his take on the history of cancer immunotherapy and where the field is heading Read More A legacy of ground breaking research Category Science blog September 9 2015 Nell Barrie Read the inspiring story of how a generous gift left by a couple in their Will is helping our scientists understand how cancers spread Read More Could aspirin boost cancer immunotherapy Category Science blog September 3 2015 Emma Smith We explore new research suggesting that aspirin might help boost the cancer fighting effects of immunotherapy in mice Read More Older Posts Newer Posts Popular posts Most read today Most discussed Don t believe the hype 10 persistent cancer myths debunked How does alcohol cause cancer Processed meat and cancer what you need to know

    Original URL path: http://scienceblog.cancerresearchuk.org/topic/cancer-type/skin-cancer/ (2016-02-11)
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  • Safia Danovi | Cancer Research UK - Science blog
    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 Author Safia Danovi Author Safia Danovi Safia studied biology at UCL and she followed that up with a PhD looking at how cancer cells respond to chemotherapy Her first three years at CRUK were with the science communications team but she s since moved to research funding where she s looking for ways to boost research into cancers of the pancreas lung oesophagus and brain Our new strategy a big step towards putting us all out of jobs Category Science blog April 29 2014 Safia Danovi As we launch our new strategy we catch up with chief scientist Professor Nic Jones and get his take on our plans for the future Read More Introducing our new arrivals Category Science blog September 12 2013 Safia Danovi We welcome the latest group of scientists who ve just been awarded funding from Cancer Research UK Read More A home from home how cancer cells spread to new organs Category Science blog June 4 2013 Safia Danovi This entry is part 5 of 5 in the series MicroenvironmentIn our previous post in this series we talked about how the tumour microenvironment helps tumour cells Read More I want to break free the microenvironment and metastasis Category Science blog February 11 2013 Safia Danovi This entry is part 4 of 5 in the series MicroenvironmentNo man is an island and the same can be said of tumour cells Previous posts in our microenvironment Read More Feeling the heat the link between inflammation and cancer Category Science blog February 1 2013 Safia Danovi This entry is part 3 of 5 in the series MicroenvironmentRegular readers will know that the infrastructure supporting a tumour its microenvironment Read More The queen in the hive scientists find more evidence for cancer stem cells Category Science blog August 3 2012 Safia Danovi Biology has its share of contentious issues and the existence of cancer stem cells treatment resistant cells at the heart of a tumour is certain Read More Hedgehogs flies and skin cancer the story of vismodegib Category Science blog June 7 2012 Safia Danovi This entry is part 11 of 25 in the series Our milestones Professor Phil Ingham s research in fruit flies and fish

    Original URL path: http://scienceblog.cancerresearchuk.org/author/safiadanovi/ (2016-02-11)
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  • Lung cancer evolution – a journey through space and time - Cancer Research UK - Science blog
    to research The search for a smoking gun Swanton s team led by lab researcher Dr Elza de Bruin and biological data expert Nicky McGranahan collected a series of tumours from seven patients with early stage lung cancer who d had surgery aimed at curing them Just as in their kidney cancer study the team analysed and compared DNA from several different regions of each tumour The first two tumours they looked at were from former smokers who d given up at least twenty years beforehand Tobacco causes specific types of damage to DNA Both tumours showed all the characteristic diversity and chaos seen in other cancer types on average only about 70 per cent of a tumour s DNA errors were found throughout the whole tumour the rest being unique to one region or another This implied that the tumour s early life was relatively homogenous with a late explosion of diversity And as expected they saw the tell tale faults known as C to A changes caused by tobacco carcinogens But there was something else going on too The C to A changes were much more likely to be early common errors than to be unique faults confined to specific regions of each tumour These late occurring mutations seemed to be caused by something else DNA editing proteins called APOBEC proteins APOBEC proteins are turning out to be one of the most important DNA damaging forces in a range of cancers says McGranahan Under normal circumstances he explains APOBECs are thought to play a role in protecting us from viruses by damaging their DNA But there s now a wide range of evidence that they get switched on accidentally as cancers develop Although we didn t suspect APOBECs he says we weren t that surprised to find that something other than tobacco was driving cancer development in ex smokers They saw a very similar pattern in another ex smoker s tumour decades of early tobacco damage and a late explosion in APOBEC damage But the big surprise came when they looked at three tumours from people who hadn t given up smoking Weirdly the APOBEC signature was still there It was really quite surprising We expected maybe just to see a long history of tobacco related damage in smokers But just as we saw in the patients who d given up tobacco damage was overtaken by an explosion of APOBEC mutations It s clearly something fundamental driving lung cancer says McGranahan APOBEC s fingerprints were also present in the tumour DNA from the one non smoker on the study which otherwise lacked the smokers tobacco related fingerprint Other implications Our London Research Institute The team made three other important observations First it looked like the cancer fuelling driver mutations in genes like EGFR and ALK against which a new generation of therapies is targeted tended to occur early in a lung cancer s development This contrasts with kidney cancer where similar mutations tended to occur relatively late on This is good news as it suggests that these so called targeted therapies might be more effective in lung cancer particularly if used in combination Second in four of the seven samples it looked like the cancer cells contained not one but two copies of the human genome This seemed to happen before the APOBEC proteins wrought their chaos but after most of the tobacco damage This doubling had previously been seen in other studies but no one knew when in a cancer s development it occurred And third and perhaps most importantly it s more evidence that lung cancers take a very long time to develop maybe more than twenty years Put this all together and it has quite profound implications it might be possible to detect early signs of the disease in the blood long before symptoms develop something that could make an enormous difference to patient outcomes as Professor Jacqui Shaw of Leicester University who studies circulating tumour DNA in breast cancer explains A growing tumour can shed its DNA into a patient s blood as its cells die she says pointing to a research study in 2006 which showed that certain key mutations could be spotted in the blood of people who went on to develop cancer At the moment we don t know enough about whether early lung tumours shed DNA into the bloodstream it s a bit of a black box but it s certainly an idea that s got a huge amount of potential and one we re eager to explore she says Swanton s study gives further impetus to this research Across the pond the US study But as we mentioned earlier Professor Swanton s team weren t the only ones looking at lung cancer A US team led by Professor Andy Futreal had been conducting very similar research Happily Swanton s team s findings agree closely with the US study Across eleven tumour samples Professor Futreal s group found only about three quarters 76 per cent of a tumour s mutations were ubiquitous similar to the 70 per cent Swanton s team found And they also spotted the APOBEC signature at work in the lung cancer genome But because Futreal s team were able to follow up the patients on the study they were also able to tentatively make one extra important observation As of 21 months after having their tumours removed three of the patients cancers have come back And these three patients had the highest degree of overall genetic variation in their tumours This suggests something we ve long suspected in lung cancer says Swanton Heterogeneity the degree of chaos within a tumour could be a really important marker of whether a cancer might come back If we can confirm this we could immediately use it to help these patients by offering them extra treatments like chemo radiotherapy or targeted drugs if appropriate he says Burning questions As with all the best research these studies raise as many questions

    Original URL path: http://scienceblog.cancerresearchuk.org/2014/10/09/lung-cancer-evolution-a-journey-through-space-and-time/ (2016-02-11)
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  • Order from chaos – making sense of bowel cancer’s scrambled DNA - Cancer Research UK - Science blog
    cells and on why and how their chromosome number and structure changes over time Down the microscope The lead researchers in Professor Swanton s team Dr Rebecca Burrell and Dr Sarah McClelland began with a tried and tested technique they looked down a microscope at hundreds of dividing CIN and CIN bowel cancer cells to see if there were any obvious differences between them In particular they were looking for tell tale signs of different types of DNA error that would give clues as to the cause of the instability As the diagram below shows click to enlarge errors occurring during each of the two phases of cell division leave types of damage Errors during DNA copying lead to so called acentric and bridged chromosomes whereas errors during segregation lead to lagging chromosomes Click to enlarge When they studied the cells they saw that those with unstable chromosomes often left chunks of DNA behind as they divided see picture A closer look at these remainder chromosomes revealed that they were usually broken chunks of chromosomes or two chromosomes stuck together in other words acentric and bridged chromosomes Lagging chromosomes were much less common In other words this was clear cut evidence that chromosomal instability was being driven in large part by errors occurring before the chromosomes segregated rather than during division itself This was unexpected and surprising researchers had long suspected that chromosomal instability was caused by defects during segregation Further experiments shed more light on instability s cause unstable cells were copying their DNA extremely slowly suggesting that they were stressed during DNA replication Replication stress is a well known phenomenon to cell biologists If we imagine DNA replication to be like the construction of a new building then replication stress is like the builders running out of bricks or starting building before the foundations are properly laid the building is much more likely to collapse To check that replication stress led to chromosomal instability the researchers used a chemical that interfered with copying DNA managing to flip chromosomally stable cells into a state that looked just like their unstable counterparts Genetic faults But was there order amidst the chaos Was there a particular genetic defect common to CIN cells and absent in CIN cells that could help explain what they were seeing The team then analysed the DNA of CIN bowel cancer cell lines and crucially of similarly unstable tumour samples from cancer patients When they compared this to DNA from CIN stable cancer cells they spotted that a part of one particular chromosome known as chromosome 18q was usually missing in the unstable tumours Loss of this chromosome has been documented in many cancer samples over the years but no one was really sure what its significance was To see whether loss of one or more of the many genes on 18q might cause chromosomal instability they used a technique called RNA interference to painstakingly switch off these genes in stable bowel cancer cells one by one

    Original URL path: http://scienceblog.cancerresearchuk.org/2013/02/27/order-from-chaos-making-sense-of-bowel-cancers-scrambled-dna/ (2016-02-11)
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  • Unpicking the genetic ‘patchwork’ in ovarian cancer - Cancer Research UK - Science blog
    cells grow again after treatment We found that the later drug resistant tumours have a high proportion of cells carrying a faulty version of NF1 But when we looked carefully around five per cent of the cancer cells prior to treatment had it too And it was even there in the original tumour sample from the fallopian tube but only in a few cells This suggests that the genetic seeds of resistance are already present at the very earliest stages of cancer and that the population of cells carrying them expands and grows over time Unfortunately it s very difficult to test patients for these rare gene faults when they re first diagnosed although there is a technique that might help so called liquid biopsies which can detect DNA shed from tumours into the bloodstream and which we ve written more about here Can the early signs that groups of cells carrying particular genes faults are starting to grow be spotted in the blood We want to be able to use this technique to monitor patients in real time as they have their initial treatments and see what is changing in their cancer at a genetic level James tells us Clearly if we could see changes occurring earlier we might be able to do something to make treatment more effective such as switching to a different drug if it looks like the cancer is becoming resistant But we need to be able to pick up on these changes quickly while there s still a chance to make a difference At the moment it s not possible to measure the amount of heterogeneity and put a precise prediction on survival but James is hopeful that he ll get there While we ve shown that there definitely is a relationship between the amount of heterogeneity and survival we can t put precise numbers on it yet as we don t have enough data he says But I think this kind of approach will eventually allow us to make those correlations High grade serous ovarian cancer is a disease where there are extraordinary genetic changes and it s very complex to figure it all out Now we need to work out ways we can do this on a larger scale over hundreds of patients We did this study looking at a lot of samples from a few patients but we want to know if we can develop methods where we just need a couple of samples from many women From patchwork to plan From a scientific point of view this is fascinating But what we really need to do is turn it into more effective treatments This is still very much a work in progress and something that the Cambridge team is now turning its attention to although there are a few exciting ideas in the pipeline James says We need to be thinking about how we schedule chemotherapy and other treatments to make it very unfavourable for these resistant cells to grow we need to make life very uncomfortable for them He thinks it s important to look at the ways doctors give drugs to patients and whether tweaking the dosing or timing could be beneficial for patients with lots of heterogeneity in their cancer Is it such a good idea to give big doses of drugs every few weeks or might it be better to give smaller doses more regularly James asks We need to think about how to schedule chemotherapy in different ways whether we can use the immune system to tackle cancer as well as drugs and even if we can alter the evolution of the disease in the body Research like this is enabling scientists to reveal the genetic landscape of cancer within the body for the first time and it should lead to urgently needed improvements in the way that women are treated for ovarian cancer And by agreeing to take part in studies like James s it s these women who will ultimately lead to advances for future patients I m not sure how much they know about tumour heterogeneity he says They just want something to make the cancer go away and make them feel better But they all really want to help our research Kat References Cooke S L et al 2010 Genomic analysis of genetic heterogeneity and evolution in high grade serous ovarian carcinoma Oncogene PMID http www ncbi nlm nih gov pubmed 20581869 Schwarz R F et al 2015 Spatial and Temporal Heterogeneity in High Grade Serous Ovarian Cancer A Phylogenetic Analysis PLoS medicine PMID http www ncbi nlm nih gov pubmed 25710373 Quilt image by Natasha2006 from Wikimedia Commons Public domain Share this article More on this topic Tags Cancer genes Cancer Research UK funded research Chemotherapy Ovarian cancer Research and trials Comments Click here to cancel reply Kat Arney May 8 2015 Hi The majority of cervical cancer cases are linked to HPV an infection passed on by skin to skin contact including through sex The evidence shows that if a woman has never been sexually active then her risk of developing cervical cancer is very low indeed although it s not possible to say that it s an absolutely zero risk If you re worried about anything please do go and talk to your doctor as we can t give medical advice on the blog Best wishes Kat Letlole Gontse May 2 2015 Hi From the symptoms that I read I can t find anything to do with having cervical cancer if you are not sexually active Does it mean that you can t have cervical cancer Kat Arney April 27 2015 Hi Nuala Thanks so much for your feedback glad you found it interesting Best wishes Kat Gaughan Nuala April 25 2015 I found this information very clear and informative and the quilt image very helpful to a non medical person given the concept of a quilt where each piece could have a distinct image Nuala gaughan Kat

    Original URL path: http://scienceblog.cancerresearchuk.org/2015/03/12/unpicking-the-genetic-patchwork-in-ovarian-cancer/ (2016-02-11)
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  • Translating breast cancer’s life history - Cancer Research UK - Science blog
    in the DNA code in other words to look at the letters either side of each spelling mistake to see if patterns emerged And they did The researchers identified five clear signatures each corresponding to a different biological process at work as the tumour developed And they then looked for and found the same signatures at work in a further twenty tumours They also spotted an entirely new and perplexing phenomenon which they termed kataegis after the Greek for thunderstorm where specific regions of the tumour s DNA had mutated extraordinarily rapidly at a particular time in its history But what was causing these signatures Detailing the damage The researchers discovered thunderstorms in the genome The researchers compared what they d seen to what s currently known about DNA error and repair pathways to see if they could work out what was going on But they could only definitively link one of the five observed signatures to a process known to be involved in cancer the conversion of a modified version of a DNA letter called cytosine a C in the DNA code to thymine a T when the C comes before a G a guanine They have their suspicions about what might be behind the other four and excitingly one of the prime suspects is a process we ve blogged about before but this is the starting point for a very exciting period of research Knowing the precise molecular forces at work as a cancer develops is exactly the sort of intelligence that could transform our ability to fight cancer But the researchers didn t stop there Their second analysis tried to find out when particular mutations arose in a cancer s history It s all in the timing If tumours contain genetically different populations of cells that evolved from a common ancestor then each sample from a tumour should give a slightly different set of results when it s DNA is analysed So measuring how often different genes are mutated in different samples mapping these gene mutations to different regions of chromosomes and applying some pretty sophisticated maths to the results should allow a tumour s genetic past to be reconstructed And so again the researchers started off with data from the single tumour they d analysed 188 times but now they looked at how often each mutation or DNA rearrangements occurred in each of the 188 analyses And again the researchers turned to sophisticated computer algorithms this time to look for patterns to help them reconstruct the tumour s family tree And just as before they repeated their analysis in twenty other tumours testing and confirming their findings As anticipated each tumour seemed to be made up of different populations subclones of cells each stemming from a common ancestor unique to each patient and yet each subtly different They also found that each tumour had a dominant population of cells making up at least half of the tumour And they were able to get a sense of

    Original URL path: http://scienceblog.cancerresearchuk.org/2012/05/22/translating-breast-cancers-life-history/ (2016-02-11)
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  • Migration, settlement, and more migration: how prostate cancers spread - Cancer Research UK - Science blog
    his original prostate tumour and from the sites to which it later spread 51 samples in all It s the first time multiple different metastatic prostate cancer samples from the same individuals have been analysed in such detail Armed with this wealth of DNA data they turned to a series of sophisticated computer tools to map out each patient s prostate cancer s ancestral history showing how each cancer had evolved and spread beyond the prostate And this analysis has revealed three important things We are family First the different secondary tumours from each man s cancer all tended to share a very similar set of ancestral DNA errors although these differed from patient to patient In other words all the secondary colonies had the same founders from the same ancestral site in the man s prostate This suggests that even though prostate cancers may begin independently in different parts of the prostate gland from different sets of genetic changes only one or a few of these founder clones manages to migrate and settle elsewhere Gaining this ability to go on the move is a relatively rare event and not common to all cancer cells in the prostate most stay put Although this is based on results from only 10 men the researchers found the same process at work in all of them And a further study from some of the same team also published today adds further weight to these results again they see just one or a few or the tribes of cells in the prostate spreading then gaining footholds in other places The next finding relates to the mechanics of how prostate cancer spreads Current thinking about cancer spread holds that after a tumour arises genetic changes occur that allow its cells to start moving round the body Once they find a suitable location they settle down forming secondary tumours that stay put in their new home But for prostate cancer at least the ICGC team s results suggest otherwise In each patient the secondary tumours were more closely related to each other than to the primary tumour This suggests that as the diagram below shows once the first few first cancer cells escape from the prostate they build a new settlement carry on growing and evolving and then spread further afield The researchers third observation raises some important questions about how prostate cancer cells colonise new locations in the body Although all the cells in a secondary tumour shared a common ancestor in at least half of the 10 men studied each secondary was made up from several different less related groups of cancer cells This is fascinating and suggests that they came from different places and somehow met up in their new location Whether this is coincidence for example there s something in their genetic wiring that independently attracts them to the same place or whether the groups of cells somehow communicate and cooperate to form a new tumour is still unknown Close relations As

    Original URL path: http://scienceblog.cancerresearchuk.org/2015/04/01/migration-settlement-and-more-migration-how-prostate-cancers-spread/ (2016-02-11)
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  • Finding faults in the BRAF gene - Cancer Research UK - Science blog
    and what did they find The scientists started by taking DNA from 15 samples of cancers 6 breast cancers one small cell lung cancer 6 non small cell lung cancer one malignant melanoma and one mesothelioma a type of lung cancer Crucially the researchers also had access to healthy cells from the original patients as well They compared the DNA sequence of the BRAF gene in the samples and found three important occasions where the sequence in the cancer cells differed from that of the healthy cells by just one DNA letter base pair The BRAF gene is faulty in more than half of all melanoma skin cancer Thinking that these differences could be important in cancer the researchers widened their study to look at DNA taken from 530 samples of cancer cells that had been grown in the lab called cell lines They found faults in BRAF in 43 of the cancer cell lines including 20 out of 34 melanoma samples and 7 out of 40 bowel cancer samples as well as a smaller proportion of other cancer types All the BRAF faults they had identified were clustered around two particular points within the gene They homed in on these regions using a further 378 tumour samples from patients with a range of different cancer types The results were striking faults in BRAF were found in over two thirds of the melanoma samples and a smaller proportion of bowel and ovarian cancers The final part of the puzzle was to figure out how the faults in BRAF might lead to cancer Usually faults in genes mean that the protein they produce is faulty and doesn t work properly But in this case the scientists discovered that the BRAF faults they identified actually send the gene into overdrive This means that it sends too many signals telling the cell to divide a direct link to cancer In fact one specific fault can increase the activity of BRAF by up to five hundred times fuelling the runaway growth of cancer cells What impact has this work had At the end of their paper the researchers themselves noted The high frequency of BRAF mutations in melanoma and the relative lack of effective therapies for advanced stages of this disease suggest that inhibition of BRAF activity may be an important new strategy for the treatment of metastatic melanoma In other words designing drugs that specifically block BRAF could lead to urgently needed treatments for malignant melanoma once it has spread Researchers suggest that around 5 000 people die every year from different cancers with BRAF faults and around 7 out of ten melanomas are caused by BRAF faults so the stakes are high To this end Cancer Research UK has continued to fund research into BRAF In 2004 a team at the Institute of Cancer Research led by Professor Richard Marais analysed the structure of overactive BRAF from cancer cells and compared it with BRAF taken from healthy cells press release They found

    Original URL path: http://scienceblog.cancerresearchuk.org/2009/08/24/high-impact-science-%E2%80%93-finding-faults-in-braf/ (2016-02-11)
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