 Your new post is loading...
More than 80 genetic markers that can increase the risk of developing breast, prostate or ovarian cancer have been found in the largest study of its kind.
The way cancer cells can make a completely chaotic mess of their genetic code in order to thrive has been explained by UK researchers.
Science World Report Main culprit behind breast cancers discovered Daily News & Analysis The findings came from a team of researchers led by Reuben Harris, Ph.D., associate professor of biochemistry, molecular biology and biophysics and also a...
Charles Lineweaver ( Australian National University) and Paul Davies(Beyond Center for Fundamental Concepts in Science at Arizona State University.) have proposed a theory of cancer based on its ancient evolutionary roots. We think that as cancer progresses in the body it reverses, in a speeded-up manner, the arrow of evolutionary time. Increasing deregulation prompts cancer cells to revert to ever earlier genetic pathways that recapitulate successively earlier ancestral life styles. We predict that the various hallmarks of cancer progression will systematically correlate with the activation of progressively older ancestral genes. The most advanced and malignant cancers recreate aspects of life on Earth before a billion years ago. Click on image or title to learn more.
Scientists believe we have a better chance of tackling the disease by knowing what tumour cells are saying to one another and then cutting off communications. One of the authors, physicist Eshel Ben-Jacob of Tel Aviv University in Israel, has argued for some time that many single-celled organisms, whether they are tumour cells or gut bacteria, show a rudimentary form of social intelligence – an ability to act collectively in ways that adapt to the prevailing conditions, learn from experience and solve problems, all with the “aim” of improving their chances of survival. He even believes there is evidence that they can modify their own genomes in beneficial ways. Many bacteria can engage in similar feats of communication and coordination, which can produce complex colony shapes such as vortex-like circulating blobs or exotic branching patterns. These displays of “social intelligence” help the colonies survive adversity, sometimes to our cost. Biofilms, for example – robust, slimy surface coatings that harbour bacteria and can spread infection in hospitals – are manufactured through the co-operation of several different species. Click on the image or title to learn more.
Uterine cancer is the fourth most common cancer among women, and the most common gynecological cancer. Researchers at the University of Iowa are using high-performance computing (HPC) to investigate how a tumor develops in normal uterine epithelium. The majority of cancer research presumes that every cell in a tumor is driven by the same genetic alterations and follows same pathway to malignancy. Dr. Donghai Dai, associate professor of obstetrics and gynecology in the Carver College of Medicine, doesn’t think that’s the case. He believes the billions of cells that make up a tumor may each have their unique mutations that cause them to deviate from normal cell behavior. So, Dai and his team are taking a single-cell approach to studying the development of tumors. With complex mathematical models and the Helium computing cluster, administered by Information Technology Services, they can run simulations on millions of representative uterine cells each day. The researchers determine the fate of the cells through incorporation of the combined effect of numerous random mutations and varying hormonal stimulations. Click on the image or title to learn more.
Black cottonwood trees (Populus trichocarpa) can clone themselves to produce offspring that are connected to their parents by the same root system. Now, after the first genome-wide analysis of a tree, it turns out that the connected clones have many genetic differences, even between tissues from the top and bottom of a single tree. The variation within a tree is as great as the variation across unrelated trees. Such somatic mutations — those that occur in cells other than sperm or eggs — are familiar to horticulturalists, who have long bred new plant varieties by grafting mutant branches onto ‘normal’ stocks. But until now, no one has catalogued the total number of somatic mutations in an individual plant. The findings have parallels to cancer studies, which have recently shown that separate parts of the same tumor can evolve independently and build up distinct genetic mutations, meaning that single biopsies give only a narrow view of the tumor’s diversity.
Via Dr. Stefan Gruenwald, Complexity Digest
Cells are naturally receptive to external influence, and this gives an opportunity to manipulate a cell to achieve a desired function or outcome. To do this a deeper understanding of when and where to apply external influences is required. The application of network controllability theory may be the key to systematic reasoning about which nodes to target to achieve global impact toward a desired outcome, and when to target them in a perturbed system, such as cancer. Interesting paper discussing possibilies of applying systems theory of networks to biology. Worth a read. Click on image or title to learn more.
Researchers have revealed how white blood cells move to infection or inflammation in the body; findings which could help lead to developing drug therapies for immune system disorders. Click on the image or title to learn more.
University of Texas Medical Branch at Galveston researchers have found a surprising connection between a key DNA-repair process and a cellular signaling network linked to aging, heart disease, cancer and other chronic conditions. The discovery promises to open up an important new area of research — one that could ultimately yield novel treatments for a wide variety of diseases. Learn more...
Via Dr Richard Badge
Biotech market update from Richard Hemming.
|
Scientists report the first successful blocking of tumor development in a genetic mouse model of an incurable human cancer.
Via E. Paul Zehr
While prostate cancer is the most common cancer in elderly Western men it also, but more rarely, strikes patients aged between 35 and 50.
The full lecture title is "Cancers - Their Genomes, Microenvironments, and Susceptibility to Bacteria-based Therapies" by Bert Vogelstein. The Johns Hopkins Center for Biotechnology Education and the Department of Biology in the Krieger School of Arts and Sciences hosted the American Society for Microbiology's Conference for Undergraduate Educators (ASMCUE) on the Homewood campus. Bert Vogelstein gave the closing plenary lecture, "Cancers - Their Genomes, Microenvironments, and Susceptibility to Bacteria-based Therapies". He teaches at John Hopkins University.
ASMCUE, now in its 18th year, is a professional development conference for approximately 300 educators. Each year, its steering committee organizes a program that offers access to premier scientists in diverse specialties and to educators leading biology education reform efforts. For more information on the conference, go to http://www.asmcue.org/page02d.shtml
Via Dr. Stefan Gruenwald
Over the years, researchers in the laboratory of ETH-professor Ari Helenius have elucidated the tricks and tactics viruses use to enter human cells and exploit them for their own multiplication and spread. Jason Mercer, in a collaboration with Berend Snijder and colleagues from the Universtiy of Zürich have just released a publication which puts forward new insights into how viruses enter human cells. "For the first time we were able to demonstrate a mechanism by which a virus uses the cellular waste-disposal system to facilitate release of the viral DNA, which is subsequently multiplied, and used for the formation of new virus particles" he says. In addition, the researchers were able to block the release of viral DNA – using a drug which is already approved for human use. Complete protein inventory During infection, viruses communicate with the host cell and they "abuse" a specific set of host proteins to assist them during their life-cycle. In collaboration with the group of University Professor Lukas Pelkmans, Jason Mercer set out to identify the cellular proteins which the vaccinia virus requires. The idea being that this knowledge may be helpful when developing new strategies to stop infection Click on the image, or the title or read more at: http://phys.org/news/2012-10-virus-exploitscellular-disposal.html#jCp
The emergence of disease-causing bacteria which are resistant to known antibiotics is one of the most important current global health challenges. Drug-resistant "superbugs" kill thousands of people every year. This is a growing problem, because new antibiotics are not being discovered fast enough to keep up with the rate of evolution of resistance. Using a simple theoretical model of a bacterial population which expands to colonize a new territory, Philip Greulich, Bartlomiej Waclaw and Rosalind Allen of the Universiy of Edinburgh show that a non-uniform concentration of antibiotic can greatly speed up the evolution of resistance, compared to the case where the drug is evenly distributed. Non-uniform drug distributions are expected to be very common: for example, drugs in our body accumulate to different levels in different organs. Importantly, the speedup in evolution of resistance that is predicted by the model depends on the sequence of genetic mutations by which the bacteria become drug resistant. It only happens if all the mutations along the pathway increase the drug resistance. Unfortunately, this seems to be the case for many commonly-used antibiotics. This research shows that simple, statistical physics models can provide important insights into biological problems. The theory developed by the Edinburgh researchers may also be relevant to the evolution of cancer cells resistant to chemotherapeutic drugs, suggesting that the highly non-uniform microenvironments found inside tumours may present a major obstacle to the successful treatment of the tumour before drug resistance emerges.
Up until now, scientists could only calculate the mass of large groups of molecules, by ionizing them (giving them an electric charge) and then seeing how strongly they interacted with an electromagnetic field, a technique known as mass spectrometry. They had no way, however, of measuring the mass of a single molecule. This has now changed with Caltech scientists have created an ultra-sensitive device that can weigh an individual molecule for the first time. By weighing each molecule, they were able to determine exactly which kind of IgM it was, hinting at potential future medical applications. The initial demonstration weighed a immunoglobulin M, or IgM molecule hinting at future medical applications. A kind of cancer known as Waldenström macroglobulinemia, for instance, is reflected by a particular ratio of IgM molecules in a patient’s blood, so future instruments building on this principle could monitor blood to detect antibody imbalances indicative of cancer. Click on the image or title to learn more.
BBC article summarising report in Nature Medicine: Chemotherapy can undermine itself by causing a rogue response in healthy cells, which could explain why people become resistant, a study suggests. Click on image or title to learn more..
Tumeric is long held in to have healing effects in ayurvedic medicine. Curcumin, a bioactive ingredient in the fragrant orange spice tumeric, is thought to be effective in suppressing tumor growth and promoting chemoprevention of certain cancers. In this review article Bassel El-Rayes et al. summarise the recent studies which describe preventive and therapeutic effects of curcumin and its analogues. In particular they concentrate on the breast cancer model, as curcumin has shown responses in reversing the human breast cancer cell resistance against paclitaxel and may be responsible for the lower incidence of breast cancer in Asian countries. Click on image or title to learn more.
Article based on a talk given by Mark Boguski of Harvard Medical School at a recent healthcare conference in Boston. Article is by Jim Golden a practising LIfe Science data scientist and worth reading.
(via Medical Xpress) Recent clinical studies have indicated that long-term usage of non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin can significantly reduce the risk of various cancers — some up to 30 per cent. Previous studies have shown that cancer cells are less likely to divide if the white blood cells can be prevented from contacting the precursor cancer cells, suggesting that white blood cells – the immune cells – have the ability to promote disease by providing some kind of growth signal. A new study published in Current Biology from teams at Bristol and Sheffield Universities in the UK , show that at least in part, taking drugs like aspirin, which are generally taken for cardiovascular problems, prevent the development of cancer by starving the cancer cells of this source of white blood cell early-growth support. Learn more...
Cancer is not a single disease. It’s hundreds of diseases. Each tumor can be many diseases that are constantly evolving, both in response to the environment in which the cancer cells grow and to treatments that are thrown at them.Understanding the complexity and interaction networks that govern why cells go into a cancering state is critical to understanding the diseases. This older article by David Gorski helps explain just why finding cures for cancer have been so elusive... Read more...
|
Protein activity is strictly regulated. Incorrect or poor protein regulation can lead to uncontrolled growth and thus cancer or chronic inflammation. Members of the Institute of Veterinary Biochemistry and Molecular Biology from the University of Zurich have identified enzymes that can regulate the activity of medically important proteins. Their discovery enables these proteins to be manipulated very selectively, opening up new treatment methods for inflammations and cancer. The work was published online on March 10, 2013 in Nature Structural & Molecular Biology. A related article was also published online at the same time in the same journal. For a healthy organism, it is crucial for proteins to be active or inactive at the right time. The corresponding regulation is often based on a chemical modification of the protein structure: Enzymes attach small molecules to particular sites on a protein or remove them, thereby activating or deactivating the protein. Identification of the enzymes and related mechanisms opens up the possiblity for new related treatments in related processes. Click on the iage or title to learn more.