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  • Solving a breast cancer mystery – why do ‘double-positive’ women do better? - Cancer Research UK - Science blog
    lab for a short time Remarkably the team saw exactly the same effect adding progesterone at the same time as oestrogen slowed down the rate tumours grew They also saw exactly the same phenomenon in mice transplanted with human breast cancer cells oestrogen fuelled tumours growth but progesterone put the brakes back on The final and most crucial experiment was to see if their findings had any potential implications for treating breast cancer Again working with mice transplanted with tumour samples and given oestrogen the researchers used the standard treatment for hormone responsive breast cancer tamoxifen which slowed down tumour growth But when they gave the mice tamoxifen AND progesterone the tumours grew even more slowly Changing the way breast cancer is treated Dr Carroll s research is a big step forward in understanding the role of progesterone receptor in breast cancer Until now its presence was simply considered an indication of how good a woman s chances of surviving were But Dr Carroll s study findings reveal that the receptor itself is the direct reason why these women have a better outlook Understanding the progesterone receptor s role as a molecular handbrake on oestrogen fuelled growth could also explain the observation that breast cancers frequently evolve to get rid of their progesterone receptors this is an advantage to cancer helping it grow quicker This new research offers a unique opportunity to exploit the braking action of the receptor with hormone therapy to improve breast cancer outcomes According to Dr Carroll this is precisely what needs to be done and the next steps are obvious The results are pretty clear and potentially have direct benefits for many women with breast cancer he told us We re already discussing a clinical trial to test whether giving women with ER PR double positive breast cancer progesterone alongside oestrogen blocking drugs helps more women survive this disease If proven successful they suggest that it could benefit up to half of women diagnosed with the disease It s even possible that Professor Tilley s new technique of growing tumour tissue samples in the lab could form the basis of a test to help doctors identify who might benefit from this combination of treatments The pioneering technology we used in this study could be used as a simple way to see if adding progesterone to oestrogen blocking drugs further slows tumour growth Tilley predicts This potential new dual therapy is still a way off there s a lot of clinical research ahead before we know for sure that giving progesterone to women with double positive breast cancer will definitely help them But it s an elegant and exciting demonstration of how hard graft in laboratories around the world is continuing to make strides against a disease that despite undoubted progress still claims the lives of nearly 12 000 UK women each year Emma Note In the light of media coverage of this story this morning we want to clear up an important point the effects observed in this study were from using progesterone itself Many contraceptives and certain forms of HRT contain derivatives of progesterone e g medroxyprogesterone acetate MPA these seem to act differently So headlines claiming that a hormone found in The Pill slows growth of tumours are slightly inaccurate Reference Mohammed H et al Progesterone receptor modulates estrogen receptor α action in breast cancer Nature 2015 DOI 10 1038 nature14583 Share this article More on this topic Tags Breast cancer Cancer biology Cancer in the news Hormones Research and trials Comments Click here to cancel reply Emma Smith November 26 2015 Really sorry to hear about your breast cancer diagnosis Ritika Dr Carroll s research showed that progesterone could actually help slow the growth of breast cancer but it s early days yet If you have questions about your treatment you can call our cancer information nurses Monday to Friday 9 5 on 0808 800 4040 Emma Ritika November 25 2015 Hi I was diagonosed with ER PR Breast cancer 2 yrs back How effective is tamoxifen in such case as what I would really need is something to stop progesterone from going wrong Emma November 13 2015 Hi Susan We re really sorry to hear about your breast cancer diagnosis The research described in this article shows that progesterone slows the growth of double positive breast cancers in mice but we are still a way off knowing if the same is true in women with breast cancer Furthermore there s also no information on how creams might compare to other ways of taking progesterone Until we know more we recommend you talk to your doctor before using any hormone treatments You can also call our cancer information nurses Monday to Friday 9 5 on 0808 800 4040 Susan November 12 2015 I have just been diagnosed with an ER PR positive receptors breast tumour and found your research article interesting I have used natural compounded by a pharmacist progesterone cream for a number of years to control unbearable body soaking hot flashes I did not want to use HRT due to obvious concerns The cream eventually evened out my postmenopausal heat flashing problems so much so that I had planned to remain on the small amount I use each day with a 7 day break Now after my diagnosis I stopped using the cream a couple of weeks ago afraid that somehow this cream may have been involved However could the reverse be true that the natural progesterone cream was actually giving the PR receptor the ability to fight the ER cells from being able to speed up their growth Could this also go along with the research that looked at the fact that premenopausal women who had breast surgery at the point when their own progesterone was high faired better as far as recurrences were concerned Perhaps there is a case for my staying on the natural progesterone cream Emma October 9 2015 Hi Nina Sorry for the slow reply

    Original URL path: http://scienceblog.cancerresearchuk.org/2015/07/08/solving-a-breast-cancer-mystery-why-do-double-positive-women-do-better/ (2016-02-11)
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  • Prostate cancer: researchers begin to unpick drug resistance - Cancer Research UK - Science blog
    a blood test to tell which men are most likely to benefit from them in the first place Variations on a theme The discovery centres on the presence in the bloodstream of so called splice variants of the androgen receptor molecule These are alternative versions of the receptor that seem to appear in prostate cancer cells as the disease develops We don t really understand yet how these arise or exactly how they act explains Imperial College London s Professor Charlotte Bevan whose lab funded largely by Prostate Cancer UK studies the androgen receptor But there s quite a lot of evidence from laboratory studies that their presence or absence in prostate cancer cells is linked to disease resistance The US team led by Dr Emmanuel Antonarakis at Johns Hopkins University Hospital in Baltimore set out to discover whether one of these variants androgen receptor splice variant 7 or AR V7 could be detected in the blood of men who were about to start treatment with either abiraterone or enzalutamide AR V7 had previously been implicated in drug resistance in lab studies So we hypothesized that the detection of AR V7 in men with advanced prostate cancer would be associated with resistance to abiraterone or enzalutamide Antonarakis s team wrote in the New England Journal They found that it did indeed predict drug resistance none of the men who had AR V7 in tumour cells extracted from blood samples showed any sensitivity to either drug A graphic representing the androgen receptor molecule This is a really interesting finding Bevan told us To those of us in the field this isn t all that surprising it s what a lot of laboratory results have predicted But it s great to see the idea validated in patients rather than cells in the lab The discovery also yields clues as to the how the resistance can be overcome AR V7 is missing the portion of the normal androgen receptor that receives instructions to tell the prostate cancer cells to grow and it s these instructions that both new drugs are designed to shut off Because this receiver is missing AR V7 is permanently switched on and able to transmit signals from a second region of the molecule known as the N terminus And this allows it to fuel the growth of prostate cancer cells This implies that drugs that target the androgen receptor s N terminus could offer an extra option for men whose disease has developed resistance to our current drugs says Bevan Such drugs are already being worked on she told us Testing times But the immediate implication of the research is in laying the groundwork for a test to tell who is likely to benefit from these drugs something that has economic as well as health consequences These are very expensive drugs says Cardiff University s Professor Malcolm Mason one of the UK s leading prostate cancer doctors Anything that could show how best to use them could have a

    Original URL path: http://scienceblog.cancerresearchuk.org/2014/09/05/prostate-cancer-researchers-begin-to-unpick-drug-resistance/ (2016-02-11)
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  • Today’s headlines about tamoxifen - Cancer Research UK - Science blog
    aches and pains are like nothing on earth I will be 50 this year and before BC breast cancer had planned to reward myself with an overseas holiday this wont happen because I could not manage it I manage to go to work full time but weekends are spend doing absolutely nothing as I have no energy I Have not had one pain free day since taking this drug I regularly have to take strong pain medication just to be able to stand the pain to sleep for the few hours I do at night The hot flushes are crap The tingling in my fingers and toes But the joint pain I cannot describe it I sometimes think people think I am over exaggerating when I say I am not going to take this drug any more My quality of life is non existent What is the point in beating cancer if you have a miserable existence I take fish oil glucosamine have massages do aqua aerobics eat healthy drink lots of water rarely drink alcohol as tamoxifen has turned me off of many wines I used to love as well as many foods I used to love My next oncologist follow up is in March Will discuss with him what is next They are thinking about giving me a course of steroids to see if that helps but yay more weight gain and apparently send you a little bit loopy Not sure what if I can continue to keep taking this rotten drug And why is more research not being done in finding something else that is more tolerable Christina Johnston February 14 2014 I have been on tamoxifen for 3 months I m trying to cope but it s very hard I have hot flushes which are worse at night and because of this I get very little sleep My body aches all the time and I am unable to do things that I did before without a thought I m exhausted most of the time I get nausea everyday and some days I vomit I cannot enjoy anything anymore as I am limited to what I can do I will keep going with the tablets as I am too scared to come of them Here s hoping the pain eases as time goes on Julie November 23 2013 I have read this article and comments in an attempt to convince myself to stay on tamoxifen Surgery was fine chemo dreadful side effects and radiotherapy a breeze I have been on tamoxifen for 13 months I can cope with the hot flushes that occur every day For me the feeling like I have been beaten up almost every day walking around some days like an old woman I am a young 48 year old who prior to cancer was a regular runner and pretty fit for my age and struggling to get up from a chair cannot help but have a massive impact on the day to day quality of life By taking tamoxifen now maybe it will increase my life by 10 years but would 10 less years but living normally be worthwhile However I don t want cancer to return so I continue and some days are better than others I can understand The people who criticise women who come off this drug but they aren t the ones living with the severe side effects that some people live with I will continue as long as I can and tomorrow hopefully will be better than today Anyone who has been through the fantastic but difficult treatment that cancer expertise gives has already proven themselves as amazing Tamoxifen is undoubtedly massively impactive day to day for some Anyone who knows anyone taking it please give support and reassurance I know it s helping extend my life and I want to see my children grow up Dig in there ladies I for one will do my best to Dorothy Newbery November 10 2013 Nobody has mentioned terrible loss of hair which really worries me Kate Mallon October 25 2013 I have given up Tamoxifen after 2 months My cancer was grade 1 lymph nodes were clear and I had a mastectomy and reconstruction at the same time I had already had a mastectomy and recon in my right breast 10 years previous The side affects of this drug were horrendous I am post menopausal Constant hot flushes with the perspiration soaking my clothes Pain in my lower back Tingling fingers Joint ache Nausea Constant headaches Itchiness discharge private parts Blurred vision Insomnia Pain above my eye Bloatedness Weight gain 14lbs Pain in feet sometimes difficulty in walking Shivers Depression Breathlessness Throbbing and heat at reconstruction I approached my GP about the symptoms and was told they may settle down the breast care nurses all said give it 6 months This is a vicious drug which costs around 130 for a 5 year treatment My quality of life was virtually non existent so I have decided to take my chances at 63 five years of these side affects is too much Nan Wallace October 11 2013 I would like to know what if any research is taking place to find a kinder treatment for women like myself who have extreme reactions to the oestrogen removing drugs currently available I tried so hard to comply but was unable to endure the awful side effects Richardson Carter October 5 2013 Standard of Care sucks Few are cured some for 5 years but all are tormented some times to the point of no return Who came up with the idea of chemo radiotherepy Nan Wallace September 15 2013 I started taking Tamoxifen 07 06 11 after one week I had a range of symptoms Severe pain in head above right eye I very rarely have a headache Very itchy armpits below breasts and behind knees Itching and heat in private parts which developed into nappy rash Joint aches particularly knees small bones

    Original URL path: http://scienceblog.cancerresearchuk.org/2013/09/04/todays-headlines-about-tamoxifen/ (2016-02-11)
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  • Tamoxifen – incremental progress, massive impact - Cancer Research UK - Science blog
    Atlantic to ing and fro ing and the declaration of a war on cancer by President Nixon there was a renewed interest in developing an oestrogen blocker to treat breast cancer ICI46 474 was developed into tamoxifen and doctors started giving it to patients in the early 70s And the drug was licensed for the treatment of advanced breast cancer in the UK in 1972 Tamoxifen for breast cancer treatment However tamoxifen is a complicated beast Its effects and side effects seem to depend on the exact dose and duration of therapy There were also genuine fears about women becoming resistant to tamoxifen if they were given it for too long So clinicians were unsure how best to use it and many clinical trials were carried out during the 70s and 80s both in the US and Europe including several funded by Cancer Research UK to answer these questions The answers started to become clear in the 1980s when the Early Breast Cancer Trialists Collaborative Group funded by Cancer Research UK published a series of papers analysing all the data from these trials They showed that tamoxifen was effective at preventing breast cancer from returning when given for a few years after chemotherapy The group have since published a series of updates of their work and their papers have been hugely influential in improving tamoxifen treatment for women worldwide For example in 1998 they found that tamoxifen was also effective for treating premenopausal women potentially saving many more lives Tamoxifen for cancer prevention Another striking finding by Cancer Research UK s Professor Jack Cuzick was that tamoxifen stopped new cancers developing in the opposite breast in women who had been treated for breast cancer This suggested that tamoxifen or drugs based on it might actually be able to prevent breast cancer Cancer Research UK has supported two large trials IBIS I and IBIS II to answer this question you can see a video about IBIS II here Slow steady progress These have all been incremental steps over a long time but they add up The tamoxifen story is yet another example of how scientific research can seem like it proceeds with the pace of a snail but with the momentum of a glacier Today saw another small but incredibly important chapter in the tamoxifen story the discovery again involving Cancer Research UK scientists in London and Cambridge of how tamoxifen stops cells dividing and how cells eventually develop resistance to the drug The ins and outs of this complex mechanism involve a molecular switch inside cells which is made up of two proteins Pax2 and ErbB2 Dr Jason Carroll the lead author on the paper which was published in Nature explains We knew that women developed resistance to tamoxifen but previously our understanding of why this occurred could be compared with trying to fix a broken car without knowing how the engine worked Now we understand how all the engine parts operate and we can try to think about ways

    Original URL path: http://scienceblog.cancerresearchuk.org/2008/11/12/tamoxifen-incremental-progress-massive-impact/ (2016-02-11)
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  • New breast cancer ‘blood test’ is still work in progress - Cancer Research UK - Science blog
    lives Nevertheless both these types of test look for changes in our DNA sequence the code that contains information about how to make proteins But over the last few decades it s become apparent that on top of our DNA lies a whole extra layer of information so called epigenetic information And it s this that Dr Flanagan s team in particular PhD student Kevin Brennan has been studying DNA molecules are like a twisted ladder Beyond our DNA DNA molecules are long twisted ladder like molecules that live in the nucleus of each of our cells Before a gene in our DNA can be activated i e the information on the rungs of the ladder are read one or more proteins first needs to stick to the outside of the DNA ladder to physically untwist it Cells carefully control which genes are active i e which bits of the ladder are untwisted at any given point in time by adding tiny chemical tags to the DNA known as epigenetic markers Some tags called methyl groups attract clusters of proteins that keep the DNA ladder tightly closed meaning that genes can t be switched on The process of adding these methyl groups is known as methylation Scientists studying DNA methylation have discovered that it tends to occur in clumps along the length our DNA and that these patterns are copied from cell to cell as they divide Researchers have also found evidence that exposure to various things over the course of our lives can influence our epigenetic patterns things like tobacco smoke radiation alcohol and diet And they ve also discovered that these patterns go completely catastrophically awry in cancer This allows cancer cells to turn on genes that should be off and vice versa and grow and divide out of control Putting all this together raises an interesting question Can looking at these epigenetic patterns before cancer develops and at differences in these patterns between individuals yield any clues about a person s chances of subsequently developing the disease Epigenetics and cancer risk Several studies in recent years have suggested that the answer could be yes For example in 2008 blood samples from bladder cancer patients in a Spanish study were found to have different methylation patterns from people without the disease And last year a US study also of bladder cancer found a similar thing One important point about all these studies is that they looked at DNA from white blood cells the cells of our immune systems But although the immune system is heavily involved in cancer as we ve blogged about before this wasn t why researchers looked here It was because they had no choice the red cells in our blood don t contain any DNA In Dr Flanagan s words they re all we can get our hands on for this type of research In 2009 Dr Flanagan s team published results of a study of methylation patterns in the DNA from breast cancer

    Original URL path: http://scienceblog.cancerresearchuk.org/2012/05/03/new-breast-cancer-blood-test-is-still-work-in-progress/ (2016-02-11)
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  • NCRI Cancer Conference 2009: Aurora, BRCA and unstable chromosomes - Cancer Research UK - Science blog
    Cancer news Science blog NCRI Cancer Conference 2009 Aurora BRCA and unstable chromosomes NCRI Cancer Conference 2009 Aurora BRCA and unstable chromosomes Category Science blog October 9 2009 Helen George Professor Ashok Venkitaraman reported his research on unstable chromosomes With just 24 hours notice Professor Ashok Venkitaraman stepped in at the NCRI conference to deliver an enlightening talk on how chromosomes become unstable in cancer after the planned speaker had to cancel at the last moment Professor Venkitaraman s specialist field is chromosome instability the way the cell s genetic information becomes more and more garbled in the development and progression of cancer His goals are to understand exactly how chromosomal instability can drive the development of cancer and to translate this knowledge into advances in cancer diagnosis and treatment Insights from BRCA2 Professor Venkitaraman has focused a large part of his research on the BRCA2 gene People who carry inherited faults in this gene have a high chance of developing breast and ovarian cancer at some point in their lives Studying exactly why this happens has lead to insights that are applicable to a wide range of cancers As Professor Venkitaraman puts it We can learn a lot about the genetic drivers of cancer by studying genes that we know are involved in familial cancers The protein produced from the BRCA2 gene teams up with our cells molecular repair kits to patch up breaks in our DNA that occur during everyday life But without a working copy of BRCA2 our cells can t repair this damage properly And that s not all more recently Professor Venkitaraman has found that BRCA2 is needed for a cell to divide into two daughter cells As he explained most cells that lose BRCA2 activity will usually die But occasionally these damaged cells are able to continue to survive in certain tissues like the breast and ovaries as they grow and divide their genetic material becomes more and more damaged and over time this can lead to cancer The Aurora story The second part of his talk focused on the fascinating story of Aurora A a protein that is present in unusually high levels in about a third to a half of common cancers Under normal circumstances Aurora A is an integral part of a system of checkpoints that ensures that cells only divide at exactly the right time But Professor Venkitaraman believes that if the levels of Aurora A get too high this can over ride one of these checkpoints and force cells to divide when they re not ready to This can lead to chromosomal instability and may contribute to the onset of cancer Interestingly many drugs including taxanes like paclitaxel target cancer cells at this particular checkpoint and there s now evidence that high levels of Aurora A can cause resistance to these drugs This latest discovery is now being used to try to improve cancer treatments with the launch of a new trial to find out whether blocking Aurora A

    Original URL path: http://scienceblog.cancerresearchuk.org/2009/10/09/unstable-chromosomes/ (2016-02-11)
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  • Research on hairy-cell leukaemia shows the promise of new DNA-scanning technologies - Cancer Research UK - Science blog
    have characteristic hair like spikes on their surfaces when viewed down a microscope you can just about make these out in the photo at the top of this post In spite of remarkable progress in the diagnosis and treatment of HCL in the past 50 years scientists had failed to pinpoint any common shared genetic changes that cause the disease Such work had included so called genome wide association or SNP studies in which scientists scan DNA taken from thousands of people looking for common genetic variations or markers associated with cancer Like pins on a map these markers highlight certain locations in the genome pointing researchers towards nearby genes that might be involved in disease But for HCL these clues were few and far between In their bid to finally pinpoint common genetic changes the Italian team decided to delve deeper into the genetic code using powerful next generation DNA sequencing technologies Rather than scanning only for markers next generation sequencing is capable of reading every single letter of the genetic code So rather than sticking pins in a map next generation sequencing reveals the whole landscape at once It s only in recent years that such work has become possible as advances in technology make it cheaper and faster to read DNA than ever before To put it in perspective the Human Genome Project took about 13 years and cost many millions of pounds to sequence the human genome Now a whole genome can be sequenced in a matter of weeks for a few thousand pounds And the price is dropping all the time The beginning a sick patient The work started in March 2009 when a 47 year old man turned up at his doctor s with symptoms of fever and pneumonia Subsequent tests showed that he had a low number of white blood cells in his blood and an enlarged spleen both common symptoms of HCL Further tests proved that he had HCL and he was given a chemotherapy drug called pentostatin Following 5 months of treatment his cancer cells stopped growing his symptoms went away and cancer cells no longer showed up in his bloodstream Along the way the researchers took samples of both the man s healthy cells and his leukaemia cells They then used next generation sequencing machines to read the entire DNA code of these cells Their aim was to compare and contrast the DNA from healthy and cancer cells to spot the genetic changes that were driving the disease An intriguing result The sequencing revealed five faults that were present in the man s cancer cells but not in his healthy ones And one fault in particular caught the eye of the researchers It was in a gene called BRAF This was intriguing because the scientists already knew that this fault called V600E was involved in other cancers such as malignant melanoma and some thyroid cancers The researchers wanted to know more was this just a coincidence or could BRAF be

    Original URL path: http://scienceblog.cancerresearchuk.org/2011/06/11/research-on-hairy-cell-leukaemia-shows-the-promise-of-new-dna-scanning-technologies/ (2016-02-11)
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  • Bowel cancer cells forget which way is ‘up’ - Cancer Research UK - Science blog
    do know that faults in APC are thought to be a critical step in the development of bowel cancer Cancer Research UK scientists along with colleagues in the Netherlands recently discovered that APC plays an important role in controlling bowel stem cells When it s lost in these cells they rapidly grow out of control and form tumours But how does APC normally act to keep stem cells well behaved Looking in 3 D Until recently it s only been possible to look at cells growing in flat layers in plastic dishes in the lab i e two dimensional microscopy But advances in technology mean that scientists can now study cells buried within deep layers of living tissue To understand more about APCs involvement in stem cells the researchers used cutting edge three dimensional microscopes to study bowel tissue taken from humans and mice either carrying faulty cancer causing APC or a working version of the gene And they noticed something intriguing Dividing in one direction All cells divide by erecting molecular scaffolding around their nucleus in a structure called the spindle This provides a frame upon which to divide newly copied DNA between the two new cells there s more about cell division and the spindle on our website including an explanatory animation here When they looked at the 3D structure of the growing bowel cells the researchers discovered that in all the healthy stem cells the spindle was always lined up at right angles to the wall of the gut This meant that new cells lined up from the outside towards the centre of the gut The outermost cell nearest the gut wall remained as a stem cell while the innermost cell became a bowel lining cell This alignment means that new lining cells are always created facing in the right direction towards the centre of the gut tube They get pushed forward by more new cells being made by the stem cell behind them and eventually are shed into the bowel But Dr Nathke and her team noticed something very different about the stem cells lacking APC Their spindles didn t line up neatly with each other instead the cells divided in all directions making a disorganised mess of cells with pre cancerous characteristics Here s a simple diagram showing what they saw click the image to enlarge it But this wasn t the only strange thing they noticed Dividing up DNA When cells divide they copy all their DNA and distribute it between the two new cells In many cases each cell gets a mixture of old and new DNA But this isn t always the case in stem cells some scientists have proposed an immortal strand hypothesis in which the template i e old DNA stays in the stem cell while the new copy gets passed onto the other daughter cell To find out whether this was happening in the bowel the researchers used a chemical to label the DNA in bowel stem cells Looking

    Original URL path: http://scienceblog.cancerresearchuk.org/2010/07/27/bowel-cancer-cells-forget-which-way-is-%e2%80%98up%e2%80%99/ (2016-02-11)
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