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    hiv treatment gentaur antibodiesUntreated HIV infection destroys a person's immune system by killing infection-fighting cells, but precisely when and how HIV wreaks this destruction has been a mystery until now. New research by scientists at the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health, reveals how HIV triggers a signal telling an infected immune cell to die. This finding has implications for preserving the immune systems of HIV-infected individuals.

    HIV replicates inside infection-fighting human immune cells called CD4+ T cells through complex processes that include inserting its genes into cellular DNA. The scientists discovered that during this integration step, a cellular enzyme called DNA-dependent protein kinase (DNA-PK) becomes activated. DNA-PK normally coordinates the repair of simultaneous breaks in both strands of molecules that comprise DNA. As HIV integrates its genes into cellular DNA, single-stranded breaks occur where viral and cellular DNA meet. Nevertheless, the scientists discovered, the DNA breaks during HIV integration surprisingly activate DNA-PK, which then performs an unusually destructive role: eliciting a signal that causes the CD4+ T cell to die. The cells that succumb to this death signal are the very ones mobilized to fight the infection.

    According to the scientists, these new findings suggest that treating HIV-infected individuals with drugs that block early steps of viral replication -- up to and including activation of DNA-PK and integration -- not only can prevent viral replication, but also may improve CD4+ T cell survival and immune function. The findings also may shed light on how reservoirs of resting HIV-infected cells develop and may aid efforts to eliminate these sites of persistent infection.

    Monday, 29 July 2013 13:54

    Mole or cancer?

    melanoma-cf-1-gene-knock-in-technology-ipsc-generation-cell-line-gene-modification-cel-line-model-diseaseMost adults have between 10 and 40 moles on their bodies, and the distinction between innocent dark speck of a cancer is not easy.
    Dr. Mary Lupo, consultant dermatologist from New Orleans advises the skin of the whole body can be accessed once a month and it's not alone. This could help a close, preferably once and later as instructed to do consult a dermatologist, who can focus on certain features of the skin individually.

    On moles should be monitored for some strictly defined factors: color, position, size and integrity.

    If there is something offensive about unemployment of a mole on her should be given special attention. Pinkish spot from which or about which there is a scaly skin, not available sunburn and is usually located on the face, hands or shoulders is often the first suspect - actinic keratosis. They quickly pass. In over 20% of cases, however, these "precancerous" formations lead to squamous cell carcinoma. Patients and even dermatologists might confuse these signs of eczema, but it does not go alone with such speed.

    Speck that looks fresh pink and shiny, located on the head, neck or ears can be basal cell carcinoma. This most common type of skin cancer rarely metastasizes, but its formation are especially dangerous. Statistically, if it is an ear or lip lies strongly increased risk of spread to the lymph nodes and from there - to the lungs.

    Reddish, scaly and slightly elevated above the rest leather stain hiding potential of squamous cell carcinoma. You may have lesions - small wounds that have a high potential for metastasis and often can be fatal.
    Spots that are asymmetric with uneven shapes and colors, irrespective of where the body, most often a sign of melanoma - the most fatal form of skin cancer. Its formations are usually close to the size of an eraser on a pencil. Their color can be overflowing or heterogeneous and include: dark blue or dark red, deep brown and

    immune cell gentaur antibodiesMelbourne researchers have discovered that the death of immune system cells is an important safeguard against the development of diseases such as type 1 diabetes, rheumatoid arthritis and lupus, which occur when the immune system attacks the body's own tissues.

    The finding suggests that these so-called autoimmune diseases could be treated with existing medications that force long-lived immune system cells to die.

    In the development of the immune system, some cells are produced that have the potential to attack the body's own tissues, causing autoimmune disease. The death of these 'self-reactive' immune cells through a process called apoptosis is an important safeguard against autoimmune disease.

    But Dr Kylie Mason, Dr Lorraine O'Reilly, Dr Daniel Gray, Professor Andreas Strasser and Professor David Huang from the Walter and Eliza Hall Institute, and Professor Paul Waring from the University of Melbourne have discovered that when immune cells lack two related proteins, called Bax and Bak, the cells can attack many healthy tissues, causing severe autoimmune disease. The research is published online January 22 in the journal Proceedings of the National Academy of Sciences.

    Bax and Bak are members of the 'Bcl-2 protein family', a large group of proteins that control cell death. Dr O'Reilly said it was thought that Bax and Bak acted like an irreversible switch in cells, determining when cells die by apoptosis. In healthy cells, Bax and Bak are in an 'inactive' form, but when cells are under stress or receive external signals instructing them to die, Bax and Bak switch into an 'active' form that starts the destruction of the cell by apoptosis. Without Bax and Bak, cells are highly protected against apoptosis.

    Dr O'Reilly said that some immune cells that lacked the proteins Bax and Bak were able to attack healthy tissues in many organs of the body. "Normally, these 'self-reactive' immune cells are deleted during development," she said. "In the absence of Bax and Bak, enough self-reactive cells survive development to persist in the body and cause autoimmune disease in organs such as the kidneys (glomerulonephritis), similar to what is seen in the most severe form of lupus.

    "Our findings confirm that defective apoptosis of immune cells can cause autoimmune disease, and that Bax and Bak are important determinants of immune cell death. We were also interested to see that, in our model, loss of Bak on its own was sufficient to cause autoimmune disease, albeit to a lesser extent than losing both Bak and Bax. This supports a recent discovery that humans with mutations in the BAK gene are predisposed to certain autoimmune diseases."

    The research provides hope for people with autoimmune diseases as Bax and Bak activity can be triggered by a new class of potential anti-cancer agents, called BH3-mimetics, which are currently in clinical trials for certain types of leukemia in Melbourne, Dr O'Reilly said. "Our findings suggest that BH3-mimetics might be an exciting new option for treatment for autoimmune conditions, by activating Bax and Bak and making the self-reactive immune cells which are causing the autoimmune disease to die," she said.

    Due to hormonal changes occurring in women's bodies after '40, women should pay particular attention to vitamin D. Female body may procure vitamins in three ways: through food, naturally rich in vitamins and with added ones by exposing the skin to sunlight and through dietary supplements.

    Although sunlight and natural foods are the best source for each age, women over 40 sometimes need to take supplements to prevent vitamin deficiency. After that age, the recommended daily dose of vitamins for the fairer sex is 15 micrograms.
    The main foods that are rich in vitamin D include: mushrooms, fatty saltwater fish, eggs, liver and alfalfa. If it is not possible to obtain the vitamins in adequate amounts with food, it is necessary to take nutritional supplements.

    25-hydroxyvitamin D supports the growth, development and maintenance of bone, helps the regulation of blood pressure and activity of the immune system by affecting cells such as macrophages and T cells. It plays an important role in cellular differentiation. Women who do not get enough vitamin D under highly increased risk of developing cancer, hypertension, osteoporosis, and autoimmune diseases such as rheumatoid arthritis and insulin-dependent diabetes.
    The World Health Organisation recommends taking 15 micrograms of complex substances every day. Except for women over 40, this recommendation applies to pregnant or lactating mothers. In pharmacies, without prescription sell many supplements and vitamins that support the required balance, but if taken without the express prescription by a doctor can cause a number of side effects: diarrhea, vomiting, weight loss, bone and joint pain and fatigue. They can intervene in the action of drugs based on corticosteroids.

    Women suffering from kidney or heart disease or high levels of calcium and phosphorus in the blood should not take supplements with vitamin D.
    It is possible overdose of vitamins. The maximum dose that is tolerated by the body is about 150 micrograms per day. If this dose is exceeded, excess compound assumed it was too much to be removed from the body and acts as a toxin. Diseases of hypervitaminosis D, causing cardiac arrhythmias develop kidney stones, severe weight loss, kidney damage, and the walls of blood vessels, muscle weakness, and bladder problems.

    Deficiency of vitamin D e much more widespread and common than overdosing because usually noticed only when they develop any of the conditions surrounding it. The reasons for the deficit are endless, but among the main worldwide are: women who lived much of north and are subjected to short days and long nights or women who cover their skin for religious reasons - and in both cases it is strongly suppressed at natural sources of vitamin D - sun. The second is obesity. Ladies overweight more likely to develop inflammatory condition of the gastrointestinal tract that often go unnoticed, but impair the absorption of vitamin coming with food.
    You should always seek medical advice before accepting any pharmaceutical product, even vitamins.

    Methadone reduces the risk of HIV transmission in people who inject drugs (PWID), as reported by an international team of researchers in a paper published October 5 in the online edition of theBritish Medical Journal. This team included Dr. Julie Bruneau from the CHUM Research Centre (CRCHUM) and the Department of Family Medicine at the University of Montreal.

    "There is good evidence to suggest that opiate substitution therapies (OST) reduce drug-related mortality, morbidity and some of the injection risk behaviors among PWID. However, to date there has been no quantitative estimate of the effect of OST in relation to HIV transmission. This new study provides solid evidence demonstrating the link between these treatments and a reduced risk of HIV transmission," notes Dr. Bruneau, one of the six investigators who worked with Dr. Matthew Hickman, the study's principal investigator and Professor in Public Health and Epidemiology at the University of Bristol (UK).

    "These results are important given that increases in HIV incidence have been reported among PWID in a number of countries in recent years, where opiate substitution therapies are illegal or severely restricted," adds Dr. Bruneau. 

    Injection drug use is a major risk factor for the transmission of HIV and AIDS. It is estimated that around 5-10% of HIV infections worldwide are due to injection drug use. Methadone and buprenorphine are the main forms of drug prescribed for addicts and are frequently prescribed as opiate substitution therapies.

    The results of this study are the fruit of an international collaborative effort. Authors from the US, Canada, Italy and Australia carried out a review and pooled analysis (known as a meta-analysis) of several published and unpublished studies from multiple countries (including the USA, Canada, the UK, the Netherlands, Austria, Italy, Thailand, Puerto Rico and China) to determine the association between OST and HIV transmission among PWID. The nine selected studies looked predominantly at males between 26 and 39 years old and totalled 819 incidents of HIV infection with 23,608 person-years of follow-up.

    After analysing these studies, authors found that OST was associated with a 54% reduction in risk of HIV infection among PWID. There were differences between the studies, including different background rates of HIV infection, making it impossible to calculate an "absolute risk reduction" for HIV infection that would translate to all settings. And not all studies reported adjustments to the intervention to take account of other factors that might influence the association between OST and HIV infection. But the impact of OST on HIV was strong and consistent in further analyses in the paper. There was weak evidence to suggest that longer duration of OST exposure may be associated with greater benefit.

    For Dr. Bruneau, the results of this study favour the promotion of opiate substitution therapies: "These therapies can reduce HIV transmission among PWID not only in countries in which there is a high incidence of this disease, but also in Quebec where there has been an increase in the use of illicit opiates intravenously, particularly among youths, and where access to OST is problematic."

    Wednesday, 24 July 2013 09:41

    New front in the war against infection

    proffemaleAlthough not completely destroy bacterial and viral infections, penicillin has been a revolution in medicine and its introduction has saved hundreds of millions of lives in the last century. It was unique for its broad spectrum of activity. But since its introduction in medical practice so far appeared many new, exotic and constantly evolving strains of viruses and bacteria that are terrible for health capability - develop resistance to even our most powerful antibiotics.

    Scientists at the lab "Lincoln" at MIT are about to end this constant race between human antibiotics and antibiotic resistance of microorganisms.
    They created a drug that has proven effective against almost all strains of 15 of the most common viruses in the world. Rhinoviruses that cause the common cold, H1N1 flu, stomach viruses, polio virus, dengue fever and other hemorrhagic viruses, causing internal bleeding.

    At present there are few drugs which are effective against specific viruses, such as HIV protease inhibitors controlling agent responsible for AIDS. Unfortunately, they are expensive and often - susceptible to viral resistance. Therefore, the researchers introduced a new approach to the problem - light, which searches and finds the infected cells, not with the virus, and with any type of viral agents. Once localized, these cells are destroyed to prevent the spread of infection.

    When a virus particle infects a cell, it "distracts" cellular structures and makes them subject to one goal: to create more copies of the virus. They leave the cell, often destroying her in the process and invade new cells for the same purpose. During the process of replication, viruses establish long strands of the double-stranded RNA which is not present in human or animal organisms. The human body has a protective mechanism that is triggered by the detection of similar chains, but many viruses are able to evade detection and cause delayed immune response that usually starts too late.

    To prevent this problem, Todd Rider, head of the research group introduced a new strategy against the attackers. According to it, a much more efficient than the current inducing an enhanced immune response would be, if coupled with a protein binding to the foreign RNA of another protein that induces apoptosis - programmed cell death. Similar compounds exist in nature and the team was able to combine them. Because of their natural origin, they are capable of little aid to pass through the cell membranes of all human tissues and cells. When the drug gets into the infected cell, he programmed for self-destruction, but through uninfected cells, this remains intact.

    The drug has been proven non-toxic, and its few side effects do not cause serious health threats. It has already passed laboratory and experimental stage and soon became its clinical trials. If they also succeed, scientists are convinced: up to 3 years the drug could be on the market.
    They are proud of their successes achieved so far because they believe they have found a "penicillin of the 21st century."


    Downs-syndrom-Gentaur-antibodies-chromosome-therapyScientists have corrected the genetic fault that causes Down's syndrome– albeit in isolated cells – raising the prospect of a radical therapy for the disorder.

    In an elegant series of experiments, US researchers took cells from people with DS and silenced the extra chromosome that causes the condition. A treatment based on the work remains a distant hope, but scientists in the field said the feat was the first major step towards a "chromosome therapy" for Down's syndrome.

    "This is a real technical breakthrough. It opens up whole new avenues of research," said Elizabeth Fisher, professor of neurogenetics at UCL, who was not involved in the study. "This is really the first sniff we've had of anything to do with gene therapy for Down's syndrome."

    Around 750 babies are born with DS in Britain each year while globally between one in a 1000 and one in 1100 births are DS babies. Most experience learning difficulties.

    Despite advances in medical care that allow most to live well into middle age, those who have the disorder are at risk of heart defects, bowel and blood disorders, and thyroid problems.

    Though a full treatment is still many years off, the work will drive the search for therapies that improve common symptoms of DS, from immune and gastrointestinal problems, to childhood leukaemia and early-onset dementia.

    "This will accelerate our understanding of the cellular defects in Down's syndrome and whether they can be treated with certain drugs," said Jeanne Lawrence, who led the team at the University of Massachusetts.

    "The long-range possibility – and it's an uncertain possibility – is a chromosome therapy for Down's syndrome. But that is 10 years or more away. I don't want to get people's hopes up."

    In a healthy person, almost every cell in the body carries 23 pairs of chromosomes, which hold nearly all of the genes needed for human life. But glitches in the early embryo can sometimes leave babies with too many chromosomes. Down's syndrome arises when cells have an extra copy of chromosome 21.

    Lawrence's team used "genome editing", a procedure that allows DNA to be cut and pasted, to drop a gene called XIST into the extra chromosome in cells taken from people with Down's syndrome.

    Once in place, the gene caused a buildup of a version of a molecule called RNA, which coated the extra chromosome and ultimately shut it down.

    Previous studies found that the XIST gene is crucial for normal human development. Sex is determined by the combination of X and Y chromosomes a person inherits: men are XY, and women are XX. TheXIST gene sits on the X chromosome, but is only active in women. When it switches on, it silences the second X chromosome.

    Lawrence's work shows that the gene can shut down other chromosomes too, a finding that paves the way for treating a range of other "trisomy" disorders, such as Edward syndrome and Patau syndrome, caused by extra copies of chromosomes 18 and 13 respectively.

    Writing in the journal Nature, the team describes how cells corrected for an extra chromosome 21 grew better, and developed more swiftly into early-stage brain cells. The work, the researchers write, "surmounts the major first step towards potential development of chromosome therapy".

    The work is already helping scientists to tease apart how an extra chromosome 21 causes a raft of problems that strike people with Down's syndrome at various ages. "By the time people with Down's syndrome are in their 60s, about 60% will succumb to dementia. One question is, if we could turn off the extra chromosome in adults, would that stop or ameliorate their dementia?" said Fisher. Another approach would cut the risk of leukaemia by silencing the extra chromosome in bone marrow cells.

    The US team has already begun work that aims to prevent Down's syndrome in mice, by silencing the extra chromosome 21 in early-stage embryos. "That would correct the whole mouse, but it's not really practical in humans," said Lawrence.

    A chromosome therapy for humans would be fraught with practical and ethical difficulties. To prevent Down's syndrome, the genome editing would have to be performed on an embryo or foetus in the womb, and correct most, if not all, of the future child's cells. That is far beyond what is possible, or allowed, today.


    Tuesday, 23 July 2013 11:15

    Video Game fight the cancer

    Cell-Slider-cell-culture-pcr-knockin-mouse-targatt-knockin-rat-pcr-premix-knockout-mouse-mice-virusCenter for Cancer in Britain hired a game studio to produce for them a computer game in which players will take on the role of doctors. It allows the audience to analyze in real time the actual and current scientific data and named Cell Slider.
    From the center said that for the first three months' mobile researchers "analyzed data for scientific teams would take over 3 years.

    The development of technology allowed the scientific world to identify many new causes of cancer - carcinogens and mutations. But the colossal amounts of data that are piling up faster than they can be analyzed, often significantly delayed the work of scientists. Problem with the data is that most computers have to be specifically programmed for each study, which creates a likelihood of mistakes and too slow for their needs. Because data can be analyzed by eye, they decided to turn it into a game.

    According to the center's director - Dr. Joanna Reynolds, the accuracy with which the human brain is able to analyze the information in no way inferior to the analytical power of the computer, but while introducing faster software, a brain is more effective than a single processor .
    Since it became available for free access on the Internet, Cell Slider scored over 350 000 players from around the world who have committed over 1,600,000 accurate analysis of the information forwarded in the form of game information.

    And the principle of action is inspired by the program SETI @ home: a multinational enterprise to search for extraterrestrial life, receiving huge amounts of data from satellites and satellites of the planet and the Internet and sends them into small pieces and parcels of volunteers. These volunteers run the program on your computer, it automatically analyzes the data and a few minutes sent them back to ready the backup type.

    kinase antibodies gentaurThe process researchers use to generate induced pluripotent stem cells (iPSCs) -- a special type of stem cell that can be made in the lab from any type of adult cell -- is time consuming and inefficient. To speed things up, researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) turned to kinase inhibitors. These chemical compounds block the activity of kinases, enzymes responsible for many aspects of cellular communication, survival, and growth.

    As they outline in a paper published September 25 in Nature Communications, the team found several kinase inhibitors that, when added to starter cells, help generate many more iPSCs than the standard method. This new capability will likely speed up research in many fields, better enabling scientists around the world to study human disease and develop new treatments.

    "Generating iPSCs depends on the regulation of communication networks within cells," explained Tariq Rana, Ph.D., program director in Sanford-Burnham's Sanford Children's Health Research Center and senior author of the study. "So, when you start manipulating which genes are turned on or off in cells to create pluripotent stem cells, you are probably activating a large number of kinases. Since many of these active kinases are likely inhibiting the conversion to iPSCs, it made sense to us that adding inhibitors might lower the barrier."

    According to Tony Hunter, Ph.D., professor in the Molecular and Cell Biology Laboratory at the Salk Institute for Biological Studies and director of the Salk Institute Cancer Center, "The identification of small molecules that improve the efficiency of generating iPSCs is an important step forward in being able to use these cells therapeutically. Tariq Rana's exciting new work has uncovered a class of protein kinase inhibitors that override the normal barriers to efficient iPSC formation, and these inhibitors should prove useful in generating iPSCs from new sources for experimental and ultimately therapeutic purposes." Hunter, a kinase expert, was not involved in this study.

    The promise of iPSCs

    At the moment, the only treatment option available to many heart failure patients is a heart transplant. Looking for a better alternative, many researchers are coaxing stem cells into new heart muscle. In Alzheimer's disease, researchers are also interested in stem cells, using them to reproduce a person's own malfunctioning brain cells in a dish, where they can be used to test therapeutic drugs. But where do these stem cells come from? Since the advent of iPSC technology, the answer in many cases is the lab. Like their embryonic cousins, iPSCs can be used to generate just about any cell type -- heart, brain, or muscle, to name a few -- that can be used to test new therapies or potentially to replace diseased or damaged tissue.

    It sounds simple enough: you start with any type of differentiated cell, such as skin cells, add four molecules that reprogram the cells' genomes, and then try to catch those that successfully revert to unspecialized iPSCs. But the process takes a long time and isn't very efficient -- you can start with thousands of skin cells and end up with just a few iPSCs.

    Inhibiting kinases to make more iPSCs

    Zhonghan Li, a graduate student in Rana's laboratory, took on the task of finding kinase inhibitors that might speed up the iPSC-generating process. Scientists in the Conrad Prebys Center for Chemical Genomics, Sanford-Burnham's drug discovery facility, provided Li with a collection of more than 240 chemical compounds that inhibit kinases. Li painstakingly added them one-by-one to his cells and waited to see what happened. Several kinase inhibitors produced many more iPSCs than the untreated cells -- in some cases too many iPSCs for the tiny dish housing them. The most potent inhibitors targeted three kinases in particular: AurkA, P38, and IP3K.

    Working with the staff in Sanford-Burnham's genomics, bioinformatics, animal modeling, and histology core facilities -- valuable resources and expertise available to all Sanford-Burnham scientists and the scientific community at large -- Rana and Li further confirmed the specificity of their findings and even nailed down the mechanism behind one inhibitor's beneficial actions.

    "We found that manipulating the activity of these kinases can substantially increase cellular reprogramming efficiency," Rana said. "But what's more, we've also provided new insights into the molecular mechanism of reprogramming and revealed new functions for these kinases. We hope these findings will encourage further efforts to screen for small molecules that might prove useful in iPSC-based therapies."

    genome-breast-cancer-gentaur-antibodiesTwo recent studies by CRG researchers delve into the role of chromatin modifying enzymes and transcription factors in tumour cells.

    In one, published on September 9 in Genes & Development, it was found that the PARP1 enzyme activated by kinase CDK2 is necessary to induce the genes responsible for the proliferation of breast cancer cells in response to progesterone. In addition, extensive work has been undertaken to identify those genes activated by the administration of progesterone in breast cancer, the sequences that can be recognised and how these genes are induced. This work will be published on November 21 in the journal Molecular Cell.

    Cancer is a complex set of diseases and only thanks to advances in genomic techniques have researchers begun to understand, at a cellular and molecular level, the mechanisms which are disrupted in cancer cells, a prerequisite for developing effective strategies to treat these diseases.

    One clear example of this is breast cancer. It has long been known that hormones such as estrogen and progesterone encourage the proliferation of cancer cells. Because of this, one of the most common treatments is the administration of hormone receptor blockers. The block, however, affects all the cells of the body not only the cancer cells, and causes a number of side effects in patients. Additionally, most cancers develop resistance after a time and continue to grow despite anti-hormone therapy. To treat these patients it is necessary to understand the mechanisms that trigger the proliferation, which will allow their direct inhibition.

    The scientists from the Cromatin and Gene Expression lab at the CRG, led by Miguel Beato, are dedicated to understanding how hormones activate cell division in breast cancer, focusing on regulating the expression of the genes that control the cell cycle.

    Hormone receptors are transcription factors that bind to DNA sequences in the vicinity of the genes they regulate. But the DNA of the genes is packed into a dense structure known as "chromatin," which is considered a barrier preventing the access of transcription factors to genes. Therefore the chromatin must be decompacted for the transcription factors to activate the target genes expressed in RNA and subsequently translate them into proteins that stimulate cell proliferation. This is where the progesterone, via its receptor, activates various enzymes initiating chromatin opening.

    In the study published on September 1 in the journal Genes & Development, the researchers looked at the role of an enzyme, PARP-1, which is primarily responsible for the repair of cuts in DNA. "It was not known how PARP-1 is activated and we found that it happens via the activation of another enzyme, CDK2, which phosphorylates and activates PARP-1, which in turn modifies the histone H1 and the chromatin displacement. And if PARP1 does not do this, many of the progesterone's target genes are not regulated," explains Roni Wright, first author of the study. Wright is a postdoctoral researcher in Beato's lab. She believes that much remains to be discovered in this area of research. "This experiment was conducted on cell lines, but now we have to do it on real, patient cells to see if their behaviour is the same," adds the researcher.

    How do we know how the proliferation of cancer cells is controlled?

    Gene regulation (how genes activate and deactivate) is the key to the overall understanding of how our genome works and when this function is altered. "It is important to discover the mechanism by which genes are activated around chromatin," explains Miguel Beato, head of the Chromatin and Gene Expression group. The chromatin packs the DNA at several levels, the first being the "nucleosomes," which help stabilise the DNA chain. "It was thought that the chromatin structure was not relevant to explaining how genes turn on and off, but we have discovered that it is crucial," adds Beato.

    The second study, published online on November 21, 2012 in the journal Molecular Cell, addresses this issue. Firstly, all the genes that progesterone activates or represses in breast cancer cells were identified. Then the researchers identified which DNA sequences recognise the progesterone receptor in the genome. They found that these represented only a small proportion of the possibilities, making them think that interaction with DNA was not sufficient. It was necessary for the sequences which bind to the receptor to be incorporated into nucleosomes, which also provide interaction sites. "It seems that chromatin has a lot to do with determining which genes are activated and which are not," says Cecilia Ballaré, first author of this second paper.

    The researchers believe that the only way to create increasingly specific and effective cancer treatments is by studying the role of all the elements that regulate gene expression and cell proliferation in response to hormones. "Knowing the exact way progesterone affects the proliferation of cancer cells may help develop more specific treatments that fight only cancer cells and thus produces fewer side effects," adds Ballaré.