and smuggle cancer signals their neighbors A new discovery published in the Nov. 2015 issue of The FASEB Journal shows that cancer cells use previously unknown channels to communicate with one another and with adjacent non-cancerous cells.
Not only does this cast an important light on how cancer metastasizes and recruits cellular material from healthy cells,
especially the mouse model, will be used by academics to isolate healthy cells modified by tumors, and by the pharmaceutical industry in the quest for novel anticancer drugs that block tumor-organ communication,
"said Anne Burtey, Ph d.,study author from the Department of Biomedicine, at the University of Bergen in Bergen, Norway."
with increased abilities to diffuse within tumors and even reach the healthy cells involved in tumor progression."
"To make this discovery, Burtey and colleagues studied the exchange of molecules between cells, by color-coding them with red or blue cellular fluorescent'dyes'or'tags.'
suggesting that this protein is a key regulator of cell-cell communication in cancer. Live cell imaging confirmed that the transfer is contact-dependent.
#New research opens door to understanding human tonsil cancer Researchers at Simon Fraser University and the BC Cancer Agency have developed a groundbreaking method to identify
and separate stem cells that reside in the tonsils. Their research, which sheds new light on the fight against oral cancer, is published today in the journal Stem Cell Reports.
While stem cells in many other body tissues have been studied well, little is known about these stem cells,
Ninety per cent of human tonsil cancers show evidence of HPV (human papillomavirus) infection. But little is known about its role in causing these cancers.
Researchers suspect it is a key player, as HPV is the major risk factor for cervical cancer.
Kang, who is working with BPK professor Miriam Rosin, director of the BC Oral Cancer Prevention Program,
and UBC professor Connie Eaves of the Terry Fox Laboratory, was interested in finding out why the tonsil is particularly susceptible to HPV
and made them incorporate a cancer-causing gene normally transmitted by HPV, the cells grew abnormally in a special tissue culture system,
and created what one might imagine what the beginning stages of human tonsil cancer would look like."
as it is the first stage of human cancer development that researchers need to learn how to detect
Cancer of oropharynx, or the tonsils in particular, is an important health concern with rising incidence worldwide, especially in men.
The researchers, including Dr. Raj Kannan of the BC Cancer Agency's Terry Fox Laboratory,
#A newly discovered tumor suppressor gene affects melanoma survival Of the hundreds of genes that can be mutated in a single case of melanoma,
only a handful may be true"drivers"of cancer. In research that appeared today in Nature Genetics,
a Weizmann Institute of Science team has revealed now one of the drivers of a particularly deadly subset of melanomas-one that is still seeing a rise in new cases.
This gene is identified a newly member of a group of genes called tumor suppressor genes.
It is mutated in some 5. 4%of melanomas. Furthermore its expression was found to be lost in over 30%of human melanomas;
and this loss, according to the finding, was associated with reduced patient survival. This discovery might open new doors to understanding how this cancer grows and spreads,
and it may lead in the future to new directions in treating this disease. Prof. Yardena Samuels and her team in the Institute's Molecular Cell biology Department were specifically searching for tumor suppressor genes in their database,
which consists of more than 500 melanoma genomes and exomes-protein-building sequences-making it the largest melanoma dataset to date.
As their name suggests, tumor suppressor genes normally inhibit cell growth, including that of cancer cells.
However, when mutated, they act like defective brakes on cellular proliferation. Thus studying these genes is crucial in cancer biology."
"The identification of targetable alterations in melanoma is need an urgent. An in depth understanding of the functional effects of mutations in these genes is the first step toward revealing the underlying mechanism of melanoma growth,
"says Dr. Nouar Qutob, a postdoctoral fellow in Samuels'lab who participated in this research. Indeed, the melanoma genome sequences contained mutations in known tumor suppressor genes,
but there was also a new gene that stood out in the team's search, named RASA2.
The researchers'next step was to conduct a series of functional experiments to understand exactly what this gene does.
They cloned both the normal protein and the most recurrent mutated versions to see their effects on melanoma cells.
They found that RASA2 regulates a key protein in the cell, called RAS. RAS has been identified as a major oncogene that contributes to the unchecked growth of cells.
When they restored the production of the protein in melanoma cells that harbored RASA2 mutations,
these cells stopped growing and eventually died. Patients with dysfunctional RAS pathways tend to have a worse prognosis than those with other types of melanoma,
and, until now, scientists have not managed to create drugs that can target this pathway.""As the RAS pathway is highly dysregulated in cancer,
the discovery of an alternative mechanism for its activation is likely to stimulate an avalanche of further research in this field,
to find out what proteins it communicates with in healthy cells and melanoma, as well as in the cells'response to targeted therapy,
"Most targeted cancer therapies nowadays work by inhibiting the products of oncogenes that are overactive in melanoma cells.
However, loss or mutations in tumor suppressor genes like RASA2 also contribute to melanoma development;
#DNA in blood can track cancer development and response in real time Scientists have shown for the first time that tumour DNA shed into the bloodstream can be used to track cancers in real time as they evolve
and respond to treatment, according to a new Cancer Research UK study published in the journal Nature Communications today (Wednesday).
Over three years, researchers at the University of Cambridge took surgical tumour samples (biopsies) and blood samples from a patient with breast cancer that had already spread to other parts of her body.
and timing of genetic changes appearing as the cancer developed and responded to treatment. The results provide the first proof-of-principle that analysing tumour DNA in the blood can accurately monitor cancer within the body.
Study author Professor Carlos Caldas, senior group leader at the Cancer Research UK Cambridge Institute, said:"
"This definitively shows that we can use blood-based DNA tests to track the progress of cancer in real time.
The findings could change the way we monitor patients, and may be especially important for people with cancers that are difficult to reach,
as taking a biopsy can sometimes be quite an invasive procedure.""The patient in the study had had breast cancer that already spread to a number of other organs.
and Nitzan Rozenfeld laboratories at the Cancer Research UK Cambridge Institute-were even able to distinguish between the different secondary cancers
"We were able to use the blood tests to map out the disease as it progressed. We now need to see if this works in more patients and other cancer types,
but this is an exciting first step.""Dr Kat Arney, science information manager at Cancer Research UK, said:"
"Spotting tumour DNA in the bloodstream is a really promising area of research, and has the potential to give doctors valuable clues about a patient's disease without having to take repeated tumour samples."
"For now, surgical biopsies still play an important role in diagnosing and monitoring cancers. But this work gives us a window into the future,
where we'll use less invasive techniques to track the disease in real time
#Scientists paint quantum electronics with beams of light A team of scientists from the University of Chicago
and the Pennsylvania State university have discovered accidentally a new way of using light to draw and erase quantum-mechanical circuits in a unique class of materials called topological insulators.
#New field of application for versatile helper In Alzheimer's disease proteins clump together to long fibrils causing the death of nerve cells.
Scientists, therefore, hope to deploy them as agents in the treatment of neurodegenerative diseases. Using the example of a small heat shock protein,
This also includes the potentially disease-causing proteins that collect in the cells of patients with neurodegenerative disorders--for example
Heat shock proteins are associated also with other nervous system disorders like Parkinson's disease and multiple sclerosis. Although it is still unclear what role these catastrophe aid workers play in the various ailments,
If the precise mechanisms by which these heat shock proteins hook up to their disease-causing counterparts were known,
scientists could deploy this knowledge to develop agents utilizing these mechanisms to fight disease. Two ways out of the chaos A group of researchers led by Bernd Reif
it would improve their ability to attach to the disease-causing fibrils--a first step in the development of new agents against Alzheimer's and other neurodegenerative diseases.
#CWRU researcher lands grant to build stealthy brain tumor treatment A Case Western Reserve University researcher has received a 5-year,
stealth bombs that slip past the brain's defenses to attack an incurable form of cancer.
Efstathios Karathanasis, a biomedical engineer at Case School of engineering, has developed chainlike nanoparticles that can carry drugs across the blood-brain barrier that keeps standard medicines from reaching their target--a highly aggressive brain cancer called
The researchers expect the chemotherapy will destroy the majority of tumor cells and the inhibitor will eliminate cancer cells that are resistant
and can cause brain tumors to reoccur. Their goal is to develop a treatment that eradicates the cancer with one safe dose."
"The grant enables our labs to integrate our technologies, "Karathanasis said.""We need integration to solve this problem."
"Glioblastoma multiforme is the most common and most malignant tumors of glial cells, which provide structure to the brain.
The median survival rate among adults is just under 15 months, according to the American Brain Cancer Association.
when tumors are present, preventing drugs from crossing from the blood stream into the diseased tissue.
"Brain tumor cells are often invasive and spread throughout the normal brain, and drugs--if they get in--do nothing because of resistance that develops."
"To reach inside tumors, Karathanasis'lab developed a short chain of magnetic nanoparticles made of iron oxide
and attach to the tumors'vascular walls. When nanochains congregate inside a tumor, the researchers place a wire coil,
called a solenoid, outside near the tumor. Electricity passed through the solenoid creates a weak radiofrequency field.
The field causes the magnetic tails of the chain to vibrate bursting the liposome spheres,
releasing their drug cargo into the brain tumors. In testing with mouse models of aggressive brain tumors, the technology took out far more cancer cells, inhibited tumor growth better and extended life longer than traditional chemotherapy delivery.
The targeted delivery system also used far less drug than used in traditional chemotherapy, saving healthy tissue from toxic exposure.
and to form tumors. Normal neural cells do not. In testing with mouse models of the cancer, models injected with an inducible nitric acid synthase inhibitor had fewer and smaller tumors compared to control models.
In addition to the grant money, the researchers will have access to the National Cancer Institute's Alliance for Nanotechnology in Cancer,
and will exchange ideas and resources, Karathanasis said. The Karathanasis and Rich labs will work with Mark Griswold, professor of radiology at Case Western Reserve School of medicine,
or writing information on a memory chip is done within a single memory cell, without bleeding over into neighboring cells.
An abnormally high or low white blood count, for instance, might indicate a bone marrow pathology or AIDS.
The rupturing of white blood cells might be the sign of an underlying microbial or viral infection.
Strangely shaped cells often indicate cancer. While this old, simple technique may seem a quaint throwback in the age of high-technology health care tools like genetic sequencing
and disease, appear today in the Proceedings of the National Academy of Sciences.""This is a fundamental advance that is broadly applicable
and thereby maintain health as well as contribute to various diseases.""This newly discovered mechanism encompasses multiple factors,
which we increasingly note is occurring at the interface of health and disease, "Marth explained."
"In retrospect from published literature and from studies in progress, we can now see how sepsis,
diabetes and inflammatory bowel disorders can arise by the targeted acceleration or deceleration of secreted protein aging and turnover."
"The discovery of this mechanism provides a unique window into disease origins and progression,"Marth added."
"It has been known that circulating glycosidase enzyme levels are altered in diseases such as sepsis, diabetes, cancer and various inflammatory conditions.
We are beginning to see previously unknown molecular pathways and connections in the onset and progression of disease
This discovery could provide new clues about genetic diseases and allow researchers to reprogram cells by directly modifying the loops in genomes.
or mechanical stress, can also have undesirable consequences in terms of the material's strength, structure and performance.
and animals (it is responsible for neurodegenerative diseases such as spongiform encephalopathies). According to a new SISSA study, the mechanism underlying this change is a metal, copper,
"nor do we know any treatments to cure prion diseases. Our research has uncovered finally a critical cofactor,
"On that occasion, we hypothesized that the pathological genetic mutations present in the prion protein could affect copper coordination".
(or"bad")form capable of causing degeneration of nervous tissue and diseases, some of which very severe.
Among the diseases are Creutzfeld Jakob disease in humans and"mad cow disease in cattle. Unique in nature
steel braces straighten crooked teeth, steel scalpels remove tumors. Most of the goods we consume are delivered by ships
Steel surgical tools can still carry microorganisms that cause deadly infections. Now researchers at the Harvard John A. Paulson School of engineering and Applied sciences (SEAS) have demonstrated a way to make steel stronger, safer and more durable.
and skin cancers Scientists from the University of Granada (UGR) have patented an effective drug for treating cancer stem cells (CSCS) in breast, colon, and skin cancers.
The researchers have proved the anti-tumor effects of the drug on immunodeficient mice. The new compound and its derivatives enabled the researchers to reduce tumor activity by 50 percent after 41 days of treatment with the drug,
administered twice a week, to mice with induced tumors. They have managed also to successfully describe the mechanisms by which the drug acts on the cancer stem cells (CSCS.
This crucial scientific breakthrough has been made by the UGR research groups"Research and development of Pharmaceutical Drugs, "directed by Professor Joaquín Campos Rosa, and"Advanced Therapies:
Differentiation, Regeneration and Cancer",directedby Professor Juan Antonio Marchal Corrales. The Córdoba-based company Canvax Biotech has participated also in the development of the patent.
A nontoxic drug One of the major advantages of the drug is that it is nontoxic.
Moreover, from a pharmaceutical perspective this anti-tumor drug can be produced successfully in large quantities. The researchers were able to obtain the required amount of the synthesis in just five days.
the scientists had managed already to create an effective drug (called Bozepinib) for treating cancer stem cells,
which maintains the biological activity of its predecessor as an effective anti-tumor drug, but which can also be synthesized
In order to be able to test the new drug on mice and gauge its effectiveness on human tumors,
first of all they had to inject human tumor cells into immunodeficient mice (to ensure they did not reject these cancerous cells).
they discovered that some of the compounds effectively inhibited the growth of the tumor cells and the migration ability of these cells to other healthy tissues,
a huge advantagewhen compared to other cancer treatments such as chemotherapy. Althoughcscs are only found in small quantities in tumors,
from a clinical perspective the ability to target them directly is of fundamental importance, given that they are responsible for originally causing the tumor, relapses and resistance to anticancer treatments.
The next step: Lungs and pancreas Having proved the preclinical effectiveness of the new drug in treating cancer stem cells in breast, colon,
and skin cancers, the scientists will proceed now to study the drug's effect on lung and pancreas cancers, two of the most aggressive types.
They must also complete further ADME-Tox("absorption, distribution, metabolism, excretion and toxicity")studies of the compound's behavior within the organism, a necessary step before carrying out clinical trials.
which cells are transplanted into the injury site, "says research supervisor Dr James St john, from Griffith's Eskitis Institute for Drug Discovery.
"In Australia, more than 12,000 people live with spinal cord paralysis and there is at least one new occurrence every day,
the current outcome for patients is permanent paralysis, with an overall cost to the community of $2 billion a year."
"In light of the overwhelming impact of spinal cord injury, new therapeutic interventions for drug discovery and cell therapy are needed urgently."
"What is needed now is to make the transplantation therapy more effective and suitable for patients with a range of different spinal cord injuries."
and better integrate into the injury site. In turn, this will help the spinal cord to regenerate more effectively."
or high risk atherosclerotic plaques--inflamed fatty deposits in the artery wall and a main contributor to cardiovascular disease (CVD).
and causing a heart attack or stroke. CVD remains the leading cause of morbidity and mortality in developed nations,
Atherosclerosis is a complex disease with many stages, ranging from plaques that can remain clinically silent for decades("stable")to dangerous("vulnerable")plaques.
although few focus on the important clinical endpoint of thrombosis.""Our results showed that the fluorescence ACPP probes were able to distinguish high risk plaques with high sensitivity
#New drug candidate is promising therapeutic option for angiogenic retinal diseases A research team led by scientists at Beth Israel Deaconess Medical center (BIDMC)
and retinopathy of prematurity (ROP) by preventing the overgrowth of blood vessels that are characteristic of these two retinal diseases.
a discovery that offers a promising alternative to current therapies for these retinal diseases, which require monthly injections of large molecules directly into the eyeball."
"Angiogenesis, the abnormal overgrowth of blood vessels, underlies many severe diseases, and when angiogenesis develops in the eye's retina it causes decreased vision
and can even lead to blindness, "said the study's corresponding author Richard L. Sidman, MD, an investigator in the Department of Neurology at BIDMC and Bullard Professor of Neuropathology (Neuroscience), Emeritus, at Harvard Medical school.
whose studies have focused on disease mechanisms in mouse neuro-genetic disorders, including disorders of the retina,
who develop a similar retinal disease as a side effect of high-level oxygen treatments used until their lungs develop sufficiently to handle the much lower oxygen levels in room air.
and, in rare cases, can cause bleeding or infection in the eye,"said Sidman. Furthermore, he added,
not all patients respond to these agents and, for many patients, responsiveness decreases after about six months."
"In addition to future clinical trials on AMD and ROP, we think that diabetic retinopathy and certain forms of cancer may also prove to be responsive to Vasotide,
"said Sidman.""This is a very exciting development in that it has the potential to allow the self-administration of a sight-saving drug to patients with AMD,
"said Harold F. Dvorak, MD, Mallinckrodt Distinguished Professor of Pathology at HMS and BIDMC, whose laboratory first identified the VEGF signaling protein nearly 30 years ago o
This treatment is particularly effective in children with autoimmune lymphoproliferative syndrome (ALPS), a chronic genetic disorder characterized by the buildup of white blood cells in the organs.
Patients with ALPS and other autoimmune disorders often have immune systems that destroy their body's own healthy blood cells.
The resulting decrease in blood cells causes symptoms such as anemia, uncontrolled bleeding, and infection. Few effective and well-tolerated therapies exist to manage these chronic autoimmune issues.
as they are associated often with long-term health effects, such as osteoporosis and higher risk of infection."
"To improve disease management for patients with ALPS and similar autoimmune disorders, a research team led by Teachey and his colleague Karen Bride, MD,
#New genetic discovery advances understanding of prostate cancer A new and important genetic discovery, which sheds light on how prostate cancers develop
and spread, has been made by an international research team led by scientists at The University of Nottingham.
Prostate cancer is one of the most common cancers affecting men. In the UK about one in eight men will develop it at some point in their lives, with older men and those with a family history of prostate cancer most at risk.
It is not yet possible to accurately distinguish between'indolent'prostate cancers, which need little, if any treatment,
and'aggressive'cancers, which require intensive interventions. Now in new research published in Oncotarget, a multi-disciplinary team at Nottingham, Weill Cornell Medical school,
Lund University in Sweden and Copenhagen University in Denmark, have identified a significant gene called mir137 that is switched off in prostate cancer cells.
"With many men continuing to die from metastatic prostate cancer, there is an urgent need to develop new ways to enable the early identification of aggressive cancers
when such tumours remain localised within the prostate gland when surgery is most effective. We also need to make sure that men with indolent disease do not receive unnecessary treatment
which can lead to urinary continence and sexual dysfunction.""The researchers studied the role of androgens in prostate cancer.
Androgens are important signaling molecules, which play an essential role in men's health by driving the development, repair and regeneration of the prostate and other tissues.
However defective and amplified androgen signaling can trigger prostate cancer and its spread. For this reason, many available prostate cancer treatments are aimed at blocking androgen signaling.
However, resistance to such therapies is a major clinical challenge. The gene identified by the team,
In prostate cancer where mir137 is switched off, the effect of androgen signaling is increased. Therefore the loss of mir137 leads to enhanced androgen signaling which contributes to prostate cancer initiation and progression.
The study has identified also many new potential targets for the next generation of drugs to treat prostate cancer.
New research is now underway in the Mongan's laboratory at Nottingham to test the effect of various pharmacological treatments in preclinical prostate cancer studies
#Study finds how Alzheimer's-associated protein tangles spread through the brain Massachusetts General Hospital (MGH) investigators have discovered a mechanism behind the spread of neurofibrillary tangles-one of the two hallmarks of Alzheimer's disease-through the brains
of affected individuals. In a report that has been released online in the journal Nature Communications, the research team describes finding that a particular version of the tau protein,
while extremely rare even in the brains of patients with Alzheimer's disease, is able to spread from one neuron to another
"It has been postulated that tangles-the abnormal accumulation of tau protein that fills neurons in Alzheimer's disease-can travel from neuron to neuron as the disease progresses,
spreading dysfunction through the brain as the disease progresses. But how that happens has been uncertain,
"says Bradley Hyman, MD, Phd, director of the MGH Alzheimer's disease Research center and senior author of the report."
indicating that once a certain amount of the pathologic version of the protein has been taken up,
and uptake of this form of tau is an important step in the spread of disease from one brain region to another,
targeting the mechanisms of the spreading might hold promise to stabilize disease
#Manipulating cell signaling for better muscle function in muscular dystrophy Every heart beat and step in our daily lives is dependent on the integrity of muscles
and the proteins that keep them strong and free of injury as they contract and relax.
Researchers at the University of Michigan Health System have identified a new way of triggering the instructions normally given by the muscle protein dystrophin,
Their study published online ahead of print in PNAS Early Edition suggests a new therapeutic strategy for patients with Duchene muscular dystrophy
and the impaired nnos function that is seen in muscular dystrophy, "says Michele, senior study author and professor of molecular & integrative physiology and internal medicine at the University of Michigan."
the nnos activity that is reduced in muscular dystrophy was restored. The drug worked by bypassing the defective steps in the protein complex pathway,
Still the study is"an important first step to show that manipulating AMPK-nnos signaling at least has the potential to help muscle function in muscular dystrophy"
says Michele whose lab at the University of Michigan Cardiovascular Research center focuses on inherited forms of skeletal and cardiac diseases.
Their work was supported by funding from the Muscular dystrophy Association and the National institutes of health, along with funding from the U-M Cardiovascular Translational Research and Entrepreneurship training program.
Dilated cardiomyopathy is a leading cause of death for those with DMD. Other researchers have started investigating the possibility that phosphodiesterase inhibitors,
Drugs tested by the U-M appear to correct the signaling pathway that is disrupted in muscular dystrophy at an earlier step than the phosphodiesterase inhibitors s
genetics and disease diagnosis. But carrying out such analyses requires expensive lab equipment, making its application out of reach for many people who live in resource-limited places.
After only a 10-minute run, the device could detect the Hepatitis b virus in blood serum at a level low enough to flag an early-stage acute infection,
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