#New approach holds promise for earlier, easier detection of colorectal cancer Caltech chemists develop a technique that could one day lead to early detection of tumors Chemists at Caltech
have developed a new sensitive technique capable of detecting colorectal cancer in tissue samples a method that could one day be used in clinical settings for the early diagnosis of colorectal cancer.
Colorectal cancer is the third most prevalent cancer worldwide and is estimated to cause about 700,000 deaths every year.
Metastasis due to late detection is one of the major causes of mortality from this disease; therefore, a sensitive and early indicator could be a critical tool for physicians and patients.
but that has also recently been identified as an early indicator of cancer, especially the development of tumors,
if the process goes awry. When all is working well, DNMT1 maintains the normal methylation pattern set in the embryonic stages,
like suppress the growth of tumors or express proteins that repair damaged DNA, and that, in turn, can lead to cancer.
Building on previous work in Barton group, Furst and Barton devised an electrochemical platform to measure the activity of DNMT1 in crude tissue samples those that contain all of the material from a tissue
each composed of a colorectal tumor sample and an adjacent healthy tissue from the same patient.
and the presence of cancer the correlation was with activity. he assay provides a reliable and sensitive measure of hypermethylation,
so this technique could provide a useful route to early detection of cancer when hypermethylation is involved.
portable tests that could be used in the home to catch colorectal cancer in its earliest, most treatable stages.
NA Electrochemistry shows DNMT1 Methyltransferase Hyperactivity in Colorectal Tumors, was supported by the National institutes of health a
#Risk of bowel cancer reduced by taking aspirin for Lynch syndrome patients An international study led by The University of Melbourne has confirmed that long-term regular taking of aspirin
or ibuprofen reduces the risk of bowel cancer by more than half for people with the genetic mutation causing Lynch syndrome.
At least 1 in 1000 people in the population have the genetic mutation that causes Lynch syndrome.
These people have a much higher rate of bowel cancer than the general population and about half would develop the disease without regular screening.
In a paper published in the Journal of the National Cancer Institute University of Melbourne researchers and international collaborators, led by Dr Driss Ait Ouakrim
and Dr Aung Ko Win from the School of Population and Global Health confirmed that those with Lynch syndrome who took aspirin regularly were less likely to develop bowel cancer than Lynch syndrome patients who did not take aspirin.
The research team also uncovered a new finding that Lynch syndrome patients who took ibuprofen regularly,
another nonsteroidal anti-inflammatory drug, were about 60%less likely to develop bowel cancer compared with those who did not take ibuprofen.
This protection was seen in both men and women. he main risk reduction method for these people is to have regular colonoscopy screening.
Almost nothing is known about if and how lifestyle factors and medications can modify their risk of bowel cancer,
Dr Win said. ur data is the first to confirm the finding of a previous international randomised clinical trial that found a protective effect of aspirin on bowel cancer for these high-risk people.
Also, we were able to show the similar protective effect of ibuprofen such as Nurofen on bowel cancer for people with Lynch syndrome,
Dr Win said
#Breakthrough in graphene production could trigger revolution in artificial skin development A pioneering new technique to produce high-quality,
Human calcineurin is already a proven target for drugs treating other illnesses including adult rheumatoid arthritis and lupus,
and the new findings suggest that parasite calcineurin should be a focus for the development of new antimalarial drugs. ur study has great biological and medical significance, particularly in light of the huge disease burden of malaria,
John Laporte Given Professor of Immunology and Infectious diseases. s drug resistance is a major problem for malaria control and eradication,
show the importance of calcineurin through different stages of the malaria life-cycle, implicating the protein as a potential target for blocking malaria transmission.
In addition to opening the door to potential new malaria treatments, these studies suggest that calcineurin could be targeted to treat other parasitic diseases.
Researchers at Boston College working in collaboration with the Harvard Chan group showed that calcineurin is also important for cellular attachment by a related parasite that causes toxoplasmosis. ur study shows that the ability of malaria parasites to engage red blood cells is driven by an ancient mechanism
for cellular attachment said lead author Aditya Paul, a postdoctoral researcher at the Harvard Chan School. n addition to a possible drug target,
calcineurin underlies a very basic aspect of parasite biology. p
#What your clothes may say about you Moving closer to the possibility of aterials that computeand wearing your computer on your sleeve,
or to treat disease. Genes that regulate cell division, for example, are often overactive in cancer; gene editing could silence these genes to stop a cancer.
Clinicians worry that transplanting stem cells to heal diabetes or Parkinson disease raises the risk of endless cell divisions and cancer.
Removing genes that promote cell division could forestall that danger. Long before those uses reach the clinic,
however, gene editing will be used to probe the role of genes, Zhang says. e engineer one cell,
and then we expand a large number of cells, and all the offspring have engineered the same ability to delete on demand.
#Pioneering gene therapy takes aim at inherited blindness Canada first human gene therapy trial for eyeshe replacement of a faulty gene with a healthy ones now underway at the Royal Alexandra Hospital to preserve
and potentially restore vision for people with a genetic disorder that leaves them blind by middle age. t a great privilege to be able to do something very positive for people with choroideremia,
and clinical research team leader. eople have hoped for this for a long time. horoideremia is a form of inherited blindness that affects one in 50,
The disease is caused by a faulty gene that results in the degeneration of the light-sensing retinal cells at the back of the eye.
a private British biopharmaceutical company focused on the development of therapies for retinal dystrophies. e are leading the way in the development of an effective gene therapy treatment for choroideremia,
Alberta Innovates (Alberta Innovation and Advanced education), The Foundation Fighting Blindness, Choroideremia Research Foundation Canada, and private donors.
It may also have relevance for other, far more common causes of blindness, such as retinitis pigmentosa and age-related macular degeneration. f we can maintain the vision our patients have,
we would look at that as a success, says Chan. f there is improvement, that even better. acdonald says he bsolutely impressedby the eye ability to heal itself
said Erica Ollmann Saphire, senior author of the new study, professor at TSRI and director of the Viral Hemorrhagic fever Immunotherapeutic Consortium.
Currently, there are no vaccines or treatments specifically for Marburg infections. The findings were published online ahead of print today in the journal Plos Pathogens.
New Tools to Fight Marburg Virusthe new study builds on previous work in Saphire lab revealing a molecular structure that Marburg virus uses to attach to
shows that mixtures or ocktailsof antibodies can block Ebola virus from infecting new cells and alert the immune system to the presence of the infection.
which collaborated with TSRI for molecular analysis. Some of the new antibodies target a new site on Marburg virus not seen before winglike feature attached to the base of the virus. Antibodies against this newly discovered site protected 90 to 100%of infected animal models from lethal infection.
#Elastic Gel to Heal Wounds A team of bioengineers at Brigham and Women Hospital (BWH), led by Ali Khademhosseini, Phd,
and on the results of using the material in preclinical models of wound healing. e are interested very in engineering strong,
sticking to the tissue at the site of injury and creating a barrier over a wound.
The researchers found that it was possible to combine the gel with silica nanoparticles microscopic particles previously found to stop bleeding to develop an even more powerful barrier to promote wound healing. his could allow us to immediately stop bleeding with one treatment
#Researchers show that telomeres are linked to the origins of idiopathic pulmonary fibrosis Samples from mouse lungs show collagen fibers that generate pulmonary fibrosis.
These results suggest that idiopathic pulmonary fibrosis may be treated by therapies based on the activation of the enzyme telomerase.
Idiopathic pulmonary fibrosis (IPF) causes a gradual loss of respiratory capacity and can be lethal within a few years.
A team of researchers from the Spanish National Cancer Research Centre (CNIO) have discovered now that telomeres
are at the origin of pulmonary fibrosis. This is the first time that telomere damage has been identified as a cause of the disease.
This finding opens up new avenues for the development of therapies to treat a disease for
which there is currently no treatment. This work, carried out by Juan M. Povedano and Paula Martínez from the Telomeres and Telomerase Group at CNIO led by Maria A. Blasco,
Idiopathic pulmonary fibrosis is a respiratory disease? affecting about 8, 000 people in Spain? in which scars are formed in lung tissue that make it rigid, leading to breathing difficulties.
For example, the telomeres of many patients suffering from idiopathic pulmonary fibrosis are shorter than normal.
Furthermore, pulmonary fibrosis is one of the most frequent illnesses among people with mutations in genes involved in telomere maintenance.
These data suggest that there is an association between telomere defects and the disease but demonstration of causation was pending.
most of the animals developed progressive pulmonary fibrosis. The researchers, after finding that the lack of telomeres is lethal for type II alveolar cells,
that telomere damage may cause pulmonary fibrosis. In the words of Martínez: e have seen that acute telomere damage is sufficient to trigger pulmonary fibrosis, even in the absence of environmental damage.
A MODEL THAT REPRODUCES THE DISEASE IN HUMANS Although the mouse lacking telomeres in pulmonary epithelial cells proves the importance of telomeres in the origin of fibrosis,
it does not however reproduce the disease in most human patients. In humans, environmental hazards play an important role in the disease.
Furthermore, short telomeres are also a feature of the disease. Very short telomeres are a permanent damage to cells
and they stop dividing. When this happens, pulmonary tissue will cease to regenerate and instead, a rotectiveprogramme against damage will be triggered that causes scar formation
which leads to fibrosis. The researchers therefore developed an animal model that combines premature shortening of the telomeres due to telomerase deficiency, with low doses of environmental damage.
To induce damage they chose bleomycin, a drug that affects the genetic material of cells and inhibits cell division
when administered in high doses, but not enough to cause pulmonary fibrosis in normal mice at the low doses administered by the authors.
They saw that there is a synergy between the damage caused by bleomycin at low doses
The shortening of the telomeres is not in itself sufficient to generate fibrosis nor, in general, is bleomycin at low doses;
and this triggers pulmonary fibrosis, says Povedano. The new animal models are essential for testing new herapeutic strategies based on the activation of telomerase the enzyme that repairs telomeres,
fits in well with the fact that idiopathic pulmonary fibrosis only occurs in people over 50 years of age;
such as the shortening of telomeres, has enabled us to generate animal models that faithfully reproduce diseases such as idiopathic pulmonary fibrosis,
and to prevent diseases in the future. The DNA molecule is chemically unstable giving rise to DNA lesions of different nature.
That is why DNA damage detection, signaling and repair, collectively known as the DNA damage response, are needed.
which opens up new perspectives for the treatment and prevention of neurodegenerative diseases. The article describing their discovery is published in AAASFIRST open access online-only journal Science Advances. n higher organisms DNA is bound with proteins in complexes called the nucleosome.
and to the development of various diseases, including neurodegenerative, e g. Alzheimer disease. A group of researchers, lead by Vasily M. Studitsky, studied the mechanism of detection of single stranded-dna DNA breaks at
which the connection is lost between nucleotides on one strand in the places where the DNA is associated with histones.
although normally DNA wounds around the histone poolvery tightly says Vasily M. Studitsky, he loops form
when it meets a nucleosome. n terms of applied science discovery of a new mechanism of reparation promises new prospective methods of prevention and treatment of diseases.
which in turn will reduce the risk of disease. If these contacts are destabilized, then by using special methods of drug delivery you can program the death of the affected cells Vasily Studitsky concluded,
Ebola virus and rabies virus, two of the most lethal pathogens known to humans, belong to an order of RNA VIRUSES that share a common strategy for copying their genomes inside their hosts.
Other relatives include Marburg virus, measles, mumps, respiratory syncytial virus and vesicular stomatitis virus (VSV. Scientists study VSV,
which causes acute disease in livestock but typically does not lead to illness in people,
as a model for viruses that are harmful to humans. Now a team from Harvard Medical school, using electron cryomicroscopy (imaging frozen specimens to reduce damage from electron radiation),
and herpes and hepatitis C viruses. But for the class of viruses known as nonsegmented negative-strand RNA VIRUSES,
the rabies protein will look the same, the other L proteins will look the same,
#Tablet technology to help children with autism Monash University researchers have developed the world first tablet technology designed to assist children with developmental disabilities such as autism and Down syndrome.
It is estimated that around three per cent of Australian children have a developmental disability which reduces their ability to concentrate
did not accurately capture the range of cognitive and behavioural problems associated with these disabilities.
The study conducted a randomised trial of 77 children with developmental disabilities. The intervention group with the tablet technology showed improved:
so ascertaining the true impact that these interventions may have on childhood cognition is impossible. he majority of autism apps focus on social skills training which, while important,
I believe that crowd-sourced computing will enable more important scientific advances in cancer treatment and clean energy, for example in the future,
#Protein Suggests a New Strategy to Thwart Infection The newfound ability of a protein of the intestines
and the cells of bacterial invaders could underpin new strategies to fight infections. Writing this week (July 6, 2015) in the journal Nature Structural & Molecular biology,
and those of the disease-causing microbes that invade our bodies. his has the potential to change the game in terms of how we combat microbes,
but its ability to selectively identify many different kinds of pathogens and distinguish those cells from human cells was unknown. he protein is upregulated with infection,
explains Kiessling, nd while no one has shown yet that it is an antimicrobial protein, there are multiple lines of evidence that suggest it is.
the places most likely to be entry points for microbial pathogens. Intelectin performs its surveillance role through its ability to selectively recognize the carbohydrate molecules that reside on the surface of cells.
which are needed urgently as many pathogens have become resistant to the antibiotics now most commonly used to treat infection e
#Noninvasive test predicts death risk from heart disease A noninvasive scan that determines the extent of plaque buildup in the heart accurately predicts the likelihood of heart attack or death over a 15-year period,
if a patient is shown to be at risk for heart disease but not yet showing symptoms. ll high-risk individuals irrespective of their symptom status should be considered for this study.
and more aggressively and hopefully prevent patients from ever having a heart attack. Heart disease is the No. 1 cause of death in the United states, killing 40 percent more people than all types of cancer combined.
But while there are routine screens for many types of cancer, there isn a universally adopted test used to check for heart attack risk in people who are not exhibiting symptoms associated with heart disease.
The researchers say their findings demonstrate that the coronary artery calcification test, a 5-minute procedure that examines the total amount of calcified plaque buildup in the heart arteries,
should fill that void. his test predicts the risk of heart attacks better than any other diagnostic heart test that we have, especially in asymptomatic patients,
Min said. t embodies the goal of precision medicine, namely, to precisely identify and exclude the patients who have
or do not have disease that places them at heightened risk of heart attacks. While previous studies have connected coronary artery calcification test results and long-term patient prognosis
including history of diabetes, elevated cholesterol levels, documented high blood pressure or family history of coronary heart disease.
investigators calculated the risk that participants would die for any reason, not just because of a heart attack,
n all asymptomatic patients, someone with a score of 0 has a minimal risk that they will die from any disease in the next 15 years,
where they create clothing that kills bacteria, conducts electricity, wards off malaria, captures harmful gas and weaves transistors into shirts and dresses. otton is one of the most fascinating and misunderstood materials,
which could help in warding colds, flu and other diseases. Two of Hinestroza students created a hooded bodysuit embedded with insecticides using metal organic framework molecules,
Malaria kills more than 600,000 people annually in Africa. While insecticide-treated nets are common in African homes
or viral infection in less time than it would take conventional tests and it would cost less as well.
and combat highly infectious diseases, including Hepatitis C, SARS or MERS, could also benefit from the user friendly chip
and its rapid results. is award is truly helping our lab become translational, said UCSB mechanical engineering professor Sumita Pennathur. t a big step forward in terms of bringing out nanofluidic technology to real biomedical applications of disease diagnosis
. I so excited for him!
#Researchers identify cause of heart damage in sepsis patients Researchers at the University of Liverpool Institute of Infection
and Global Health (IGH) have discovered a common cause of heart damage in patients with sepsis.
Sepsis is the most common cause of death in hospitalised critically ill people and affects up to 18 million people worldwide annually.
The electrical and mechanical malfunctions of the heart have been understood poorly in sepsis, with underdeveloped clinical management strategies,
as a consequence. This new discovery, however, promises to benefit a high number of patients with heart failure or rhythm abnormalities that complicate sepsis.
Extensive cell damage The team discovered that nuclear proteins called histones, induce damage to heart muscle cells when released into the blood circulation following extensive cell damage in sepsis.
Blood levels of histones, however, are robust biomarkers that can predict which patients are more likely to develop heart complications.
Dr Yasir Alhamdi, from the University Institute of Infection and Global Health, said: his new discovery has important clinical implications.
Firstly, we now provide a much-needed explanation for why cardiac injury markers are high in sepsis. econdly,
histone levels in the blood can potentially be used at an early stage to predict which septic patients are at highest risk of developing deadly heart complications.
This can improve overall management of patients with sepsis worldwide. Toxic effects The research team has developed also
and found that their use can significantly prevent the development of heart complications in sepsis.
from the University Institute of Infection and Global Health, said: he translational impact to patients with sepsis can extend beyond biomarker prediction of heart complications,
to novel targeted treatment for improved survival. his discovery could therefore enable us to better stratify patients for more precise and personalised treatment in sepsis
#Bonelike 3-D silicon synthesized for potential use with medical devices Semiconducting silicon spicules engage tissue like a bee stinger.
#Gene therapy restores hearing in deaf mice Proof-of-principle study takes a step toward precision medicine for genetic hearing loss.
researchers at Boston Children Hospital and Harvard Medical school have restored hearing in mice with a genetic form of deafness.
Their work, published online July 8 by the journal Science Translational Medicine, could pave the way for gene therapy in people with hearing loss caused by genetic mutations. ur gene therapy protocol is not yet ready for clinical trialse need to tweak it a bit moreut in the not-too-distant
More than 70 different genes are known to cause deafness when mutated. Holt, with first author Charles Askew and colleagues at École Polytechnique Fédérale de Lausanne in Switzerland, focused on a gene called TMC1.
because it is a common cause of genetic deafness, accounting for 4 to 8 percent of cases,
Children with two mutant copies of TMC1 have profound hearing loss from a very young age, usually by around 2 years.
The other type of mouse, called Beethoven, has a specific TMC1 mutation change in a single amino acidnd is a good model for the dominant form of TMC1-related deafness.
In this form, less common than the recessive form, a single copy of the mutation causes children to gradually go deaf beginning around the age of 10 to 15 years.
In the recessive deafness model, gene therapy with TMC1 restored the ability of sensory hair cells to respond to soundroducing a measurable electrical currentnd also restored activity in the auditory portion of the brainstem.
Most importantly, the deaf mice regained their ability to hear. To test hearing, the researchers placed the mice in a tartle boxand sounded abrupt,
In the dominant deafness model, gene therapy with a related gene, TMC2, was successful at the cellular and brain level,
and is already in use in human gene therapy trials for blindness, heart disease, muscular dystrophy and other conditions.
Holt hopes to partner with clinicians at Boston Children Department of Otolaryngology and elsewhere to start clinical trials of TMC1 gene therapy within 5 to 10 years. urrent therapies for profound hearing loss like that caused by the recessive
a specialist in genetic hearing loss at Boston Children Hospital who is familiar with the work. ochlear implants are great,
Holt believes that other forms of genetic deafness may also be amenable to the same gene therapy strategy.
Overall, severe to profound hearing loss in both ears affects 1 to 3 per 1, 000 live births. can envision patients with deafness having their genome sequenced and a tailored,
precision medicine treatment injected into their ears to restore hearing, Holt says. Holt team showed in 2013 that TMC1
a mutation in the TMC1 gene is sufficient to cause deafness. However, Holt study also showed that gene therapy with TMC2 could compensate for loss of a functional TMC1 gene,
restoring hearing in the recessive deafness model and partial hearing in the dominant deafness model. his is a great example of how the basic science can lead to clinical therapies,
and can ultimately challenge, the burden of deafness in humans. The results are testament to the immense dedication of the research team
which may one day allow them to be programmed to detect and ultimately treat diseases such as colon cancer and immune disorders.
with future applications that might include the early detection and treatment of inflammatory bowel disease or colon cancer.
and report on pathologies in the gut, including signs of bleeding or inflammation, the bacteria will need to remember this information and report it externally.
To enable them to do this, the researchers equipped B. thetaiotaomicron with a form of genetic memory.
and respond to signs of disease could also be used elsewhere in the body, he adds.
and specificity when diagnosing disease with engineered bacteria, Lu says. o achieve this, we could engineer bacteria to detect multiple biomarkers,
#Tumor-suppressing gene lends insight to cancer treatment Cell duplication and growth is essential to sustaining life,
a known tumor-suppressor gene, has mutated or is absent, this delicate replication process derails and can lead to cancer development.
The study, published in Nature Communications, could influence how future cancer patients are treated based on their genetic makeup. umors without PTEN are more sensitive to chemotherapies that work by targeting DNA replication,
while normal cells or cancers with active PTEN resist these treatments, said Dr. Wen H. Shen, the study lead investigator and an assistant professor of cell biology in radiation oncology at Weill Cornell. ased on our research,
knowing PTEN status is critical for guiding treatment choices. n the late 1990s, scientists discovered the PTEN gene,
and growing evidence has shown that PTEN is a powerful tumor suppressor. Less clear, however, has been whether
and if loss of PTEN could impact this central process of genome transmission to allow development and progression of cancer.
and Edward Meyer Cancer Center at Weill Cornell. s the DNA double helix unwinds and separates, forming A y-shaped open structure,
leading the cell to produce stress signals. Cancer can result when the stress signals accumulate
or when cells with unreplicated DNA rush into cell division prematurely to produce an abnormal number of chromosomes in a cell, a condition called aneuploidy.
PTEN function is absent in a wide variety of cancers for example, 70 percent of prostate cancers have PTEN mutation or deletion.
Because of this, researchers are testing PTEN to see if it a marker of aggressive cancer
and for personalized cancer treatment. atients whose cancers have lost PTEN or harbor mutations in the gene are known to have poorer outcomes than patients with active PTEN,
Shen said. ur expectation is that a PTEN blood test in the near future will help clinicians decide on the right therapies for each cancer patient,
and in particular, to benefit this subgroup of cancer patients carrying PTEN mutations. ource: Cornell Universit u
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