#Cancer drug 49 times more potent than Cisplatin Based on a compound of the rare precious metal osmium and developed by researchers at the University of Warwick's Department of chemistry and the Warwick Cancer Research Unit,
FY26 is able to shut down a cancer cell by exploiting weaknesses inherent in their energy generation. The researchers argue that the drug could be cheaper to produce,
Similar results were obtained by the National Cancer Institute USA in tests conducted on 60 cell lines.
This can lead to a wide-range of side-effects from renal failure to neurotoxicity, ototoxicity, nausea and vomiting.""
""Existing platinum-based cancer treatments often become less effective after the first course, as cancer cells learn how they are being attacked,
"The research could also lead to substantial improvements in cancer survival rates, suggests co-researcher Dr Isolda Romero-Canelon:"
"Current statistics indicate that one in every two people will develop some kind of cancer during their life time, with approximately one woman dying of ovarian cancer every two hours in the UK according to Cancer Research UK
and two deaths every hour from bowel cancer.""It is clear that a new generation of drugs is necessary to save more lives
"Arrayfollowing the successful test results the researchers have been awarded a Wellcome Trust Pathfinder grant to begin preclinical development of organo-osmium compounds s
In its absence, mice reproduce Seckel syndrome. The scientists rescued the microcephaly during mouse embryonic development by removing a protein that caused the loss of stem cells.
This defect in brain growth is present in several neurodevelopmental diseases, including Seckel syndrome.""There are diagnostic tests for some of these kinds of pathologies that can be performed during pregnancy,
but other than early detection, the expectant parents are limited to two choices, either to abort or to continue with the pregnancy,
being fully aware of the outcome, "explains the North american scientist Travis Stracker.""Our research paves the way to explore therapeutic approaches for microcephaly involving the inhibition of the protein p53,
"says the head of the Genomic Instability and Cancer Lab at IRB Barcelona. The scientists describe that this protein triggers the death of brain stem cells.
This occurs because cells without CEP63 have delayed cell division, leading them to enter programmed cell death through p53."
The discovery could eventually benefit millions of patients with chronic pain from trauma, diabetes, shingles, multiple sclerosis or other conditions that cause nerve damage."
"said co-author Bruce Hammock, distinguished professor at the UC Davis Department of Entomology and Nematology and the UC Davis Comprehensive Cancer Center."
"We can now specifically search for agents to control ER stress and its downstream pathways,
"This search is already underway in a number of laboratories working on cancer and other diseases."
"Working with Professor Fawaz Haj of the UC Davis nutrition department, Bettaieb found that key molecular signatures associated with diabetes
and diabetic pain were linked to ER stress. Neuropathic pain is a common consequence of both Type 1
and Type 2 diabetes, affecting up to 70 percent of patients. Inceoglu, working in Hammock's laboratory,
The team was able to show that blocking soluble epoxide hydrolase blocks ER stress and associated neuropathic pain.
With this knowledge, researchers can now test ER-stress blocking drugs in the clinic, and carry out fundamental research on how different types of pain grouped under the name"neuropathic"differ from each other
what causes neuropathic pain said John Imig, professor of pharmacology and toxicology at the Medical College of Wisconsin,
#Activated T cell therapy for advanced melanoma developed Published in the July/August issue of Journal of Immunotherapy,
these new findings demonstrate that T cells derived from lymph nodes of patients with melanoma can be expanded in number
Led by Julian Kim, MD, Chief Medical officer at UH Seidman Cancer Center, the research team has developed a novel technique to generate large numbers of activated T cells
which can be transferred back into the same patient to stimulate the immune system to attack the cancer."
"This study is unique in that the source of T cells for therapy is derived from the lymph node,
which is the natural site of the immune response against pathogens as well as cancer, "says Dr. Kim who is also Professor of Surgery at Case Western Reserve University School of medicine and the Charles Hubay Chair at UH Case Medical center."
"These encouraging results provide the rationale to start testing the transfer of activated T cells in a human clinical trial."
which have been exposed to growing melanoma in the patient's body. Rather than trying to activate the T cells while in the body,
This novel approach to cancer treatment, termed adoptive immunotherapy, is offered only at a few institutions worldwide.
These promising findings have led to the recent launch of a new Phase I human clinical trial at UH Seidman Cancer Center in patients with advanced melanoma.
The research leading to the clinical trial was funded by the National institutes of health and the Case Comprehensive Cancer Center.
The new Phase I clinical trial is being supported by University Hospitals as well as a significant philanthropic effort including the Immunogene Therapy Fund, Paula and Ronald Raymond Fund and the Kathryn and Paula Miller Family Fund."
and is an area of great potential for the treatment of patients with cancer, "said Dr. Kim."
Our goal is to eventually combine these T cells with other immune therapies which will result in cures.
These types of clinical trials place the UH Seidman Cancer Center at the forefront of immune therapy of cancer."
"Additionally, the research team has been researching the possibility of using lymph nodes from patients with pancreatic cancer to develop T cell therapy.
Their goal is to expand the program and eventually study other tumor types including lung, colorectal and breast cancers s
#Omnidirectional free space wireless charging of multiple wireless devices Scientists have made great strides in wireless-power transfer development.
University of Valencia and IGENOMIX have discovered that chromosomal abnormalities in human embryos created for in vitro fertilization,
because chromosomal abnormalities may not be identified until day five or six.""Many couples are choosing to have children later in life,
and assistant professor of Obstetrics and Gynecology, and Physiology and Pharmacology, in the OHSU School of medicine.""A failed IVF attempt takes an emotional toll on a woman who is anticipating a pregnancy as well as a financial toll on families, with a single IVF treatment costing thousands and thousands of dollars per cycle.
and make the connections needed for our collaborators to identify the genes that cause diseases
from which fifteen times more ips cells were produced by adding netrin-1. From a therapeutic point of view,
#Bonelike 3-D silicon synthesized for potential use with medical devices"Using bone formation as a guide,
"One of the major hurdles in the area of bioelectronics or implants is that the interface between the electronic device
#Gene therapy restores hearing in deaf mice Using gene therapy, researchers at Boston Children's 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."
"Our gene therapy protocol is not yet ready for clinical trials--we need to tweak it a bit more
--but in the not-too-distant future we think it could be developed for therapeutic use in humans,
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
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.
--and 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.
To deliver the healthy gene, the team inserted it into an engineered virus called adeno-associated virus 1,
In the recessive deafness model, gene therapy with TMC1 restored the ability of sensory hair cells to respond to sound--producing a measurable electrical current--and 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"startle box
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.
"Current therapies for profound hearing loss like that caused by the recessive form of TMC1 are hearing aids,
and cochlear implants,"says Margaret Kenna, MD, MPH, a specialist in genetic hearing loss at Boston Children's Hospital who is familiar with the work."
"Cochlear implants are great, but your own hearing is better in terms of range of frequencies, nuance for hearing voices, music and background noise,
and figuring out which direction a sound is coming from. Anything that could stabilize or improve native hearing at an early age is really exciting
"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.""I can envision patients with deafness having their genome sequenced and a tailored,
precision medicine treatment injected into their ears to restore hearing, "Holt says. Sound transducers: How TMC works Holt's team showed in 2013 that TMC1
and the related protein TMC2 are critical for hearing, ending a rigorous 30-year search by scientists.
a mutation in the TMC1 gene is sufficient to cause deafness. However, Holt's 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."
"This is a great example of how the basic science can lead to clinical therapies, "says Holt."
and can ultimately challenge, the burden of deafness in humans. The results are testament to the immense dedication of the research team
in order to specifically knock out the growth factors required by individual cancer types s
#Cell structure discovery advances understanding of cancer development A cell structure has been discovered that could help scientists understand why some cancers develop.
For the first time, a structure called'the mesh'has been identified which helps to hold together cells. This discovery changes our understanding of the cell's internal scaffolding.
which is found to change in certain cancers, such as those of the breast and bladder.
associate professor and senior Cancer Research UK Fellow at the division of biomedical cell biology at Warwick Medical school.
and support from Cancer Research UK and North West Cancer Research. Dr Royle said:""We had been looking in 2d
TACC3, is overproduced in certain cancers. When this situation was mimicked in the lab, the mesh and microtubules were altered
Dr Emma Smith, senior science communications officer at Cancer Research UK, said:""Problems in cell division are common in cancer-cells frequently end up with the wrong number of chromosomes.
and it might be a crucial insight into why this process becomes faulty in cancer
"North West Cancer Research (NWCR) has funded the research as part of a collaborative project between the University of Warwick and the University of Liverpool,
which could potentially better inform future cancer therapies.""As a charity we fund only the highest standard of research,
#Gene therapy advance thwarts brain cancer in rats Researchers funded by the National Institute of Biomedical Imaging
and Bioengineering have designed a nanoparticle transport system for gene delivery that destroys deadly brain gliomas in a rat model,
The nanoparticles are filled with genes for an enzyme that converts a prodrug called ganciclovir into a potent destroyer of the glioma cells.
Glioma is one of the most lethal human cancers, with a five year survival rate of just 12,
Advances in the understanding of the molecular processes that cause these tumors has resulted in therapies aimed at delivering specific genes into tumors--genes that make proteins to kill
or suppress the growth of the tumor. Currently this approach relies heavily on using viruses to deliver the anti-tumor genes into the target cancer cells.
Unfortunately, viral delivery poses significant safety risks including toxicity, activation of the patient's immune system against the virus,
and the possibility of the virus itself encouraging tumors to develop.""Efforts to treat glioma with traditional drug
and radiation therapies have not been very successful, "says Jessica Tucker, Ph d.,NIBIB Director for the Program in Gene and Drug Delivery Systems and Devices."
"The ability to successfully deliver genes using these biodegradable nanoparticles, rather than potentially harmful viruses, is a significant step that reinvigorates the potential for gene therapy to treat deadly gliomas as well as other cancers."
"Jordan Green, Ph d.,of the Johns hopkins university School of medicine Biomedical engineering Department and a senior author of the work,
The collaborators include colleagues from the Johns hopkins university School of medicine Departments of Neurosurgery, Oncology, Ophthalmology, and Pathology,
as well as Tang Du Hospital in China, University of the Negevin, Israel, and the Instituto Neurologico C. Besta in Italy.
Biodegradable nanoparticles have shown recently promise as a method to deliver genes into cells. Their use for delivery avoids many of the problems associated with viral gene delivery.
--which by itself has no effect on cancer cells--into a compound that is toxic to actively dividing brain cancer cells.
A number of polymer structures were tested for their ability to deliver DNA into two rat glioma cell lines.
Among the many polymers tried, the one known as PBAE 447 was found to be the most efficient in delivering the HSVTK gene into the cultured rat glioma cells.
the HSVTK-encoding nanoparticles were 100%effective in killing both of the glioma cell lines grown in the laboratory.
Next, the gene therapy system was tested in live rats with brain gliomas. Because it is important that the nanoparticles spread throughout the entire tumor,
they were infused into the rat gliomas using convection-enhanced delivery (CED). The method involves injection into the tumor and the application of a pressure gradient,
which efficiently disperses the nanoparticles throughout the tumors. To test the tumor-killing ability of the system,
the tumor-bearing rats were given systemic administration of ganciclovir for two days, then CED was used to infuse the HSVTK-encoding nanoparticles into the rat gliomas,
and systemic ganciclovir treatment continued for eight more days. The treatment resulted in shrinkage of the tumors
and a significant increase in survival when compared with control glioma-bearing animals that did not receive the combination treatment."
"The results provide the first demonstration of a successful non-viral nanomedicine method for HSVTK/ganciclovir treatment of brain cancer,"stated Green."
"Next steps will include enhancing the efficiency of this nanoparticle delivery system and evaluating the technology in additional brain cancer animal models."
"In the future, the investigators envision that doctors would administer this therapy during the surgery commonly used to treat glioma in humans.
They are interested also in testing the ability to deliver other cancer-killing genes and whether the nanoparticles could be administered successfully systemically
--which could broaden the use of the therapy for a wide range of solid tumors and systemic cancers s
#Ultrasound accelerates skin healing, especially for diabetics and the elderly Researchers from the University of Sheffield's Department of Biomedical science discovered the ultrasound transmits a vibration through the skin
and wakes up cells in wounds helping to stimulate and accelerate the healing process. More than 200,000 patients in the UK suffer with chronic wounds every year at a cost of over £3. 1 billion to the NHS.
The ultrasound treatment, which also reduces the chance of wounds getting infected, is particularly effective
when treating diabetics and the elderly. There are 11 million over-65s three million diabetics, and 10 million smokers in the UK--all of whom are likely to suffer problems with healing wounds.
A quarter of diabetics suffer from skin ulcers, particularly foot ulcers, due to the loss of sensation and circulation in the legs.
Lead author of the study Dr Mark Bass, from the University's Centre for Membrane Interactions and Dynamics (CMIAD), said:"
"Skin ulcers are excruciatingly painful for patients and in many cases can only be resolved by amputation of the limb."
"Using ultrasound wakes up the cells and stimulates a normal healing process. Because it is just speeding up the normal processes,
the treatment doesn't carry the risk of side effects that are associated often with drug treatments."
"Arraydr Bass added:""Now that we have proven the effectiveness of ultrasound we need to explore the signal further.
We have found that the ultrasound signal we currently use is effective, but it is possible that by refining the treatment we could improve the effects even further."
"Because ultrasound is relatively risk free we could expect to see it in broad clinical use within three or four years. s
#New cell division mechanism discovered Canadian and British researchers have discovered that chromosomes play an active role in animal cell division.
It was observed by a team of researchers including Gilles Hickson, an assistant professor at the University of Montreal's Department of Pathology and Cell biology and researcher at the CHU Sainte-Justine Research Centre, his assistant Silvana Jananji, in collaboration with Nelio
it can be a source for triggering cancer, for example,"said Hickson. It is well known that microscopic cable-like structures,
and to certain diseases,"said Hickson, who has devoted the last 15 years of his research life to cell biology.
In fact, all cancers are unchecked characterised by cell division, and the underpinning processes are potential targets for therapeutic interventions that prevent cancer onset and spread."
"But before we get there, we must continue to expand our knowledge about the basic processes
Ultimately, this could help the rational design of more specific therapies to inhibit the division of cancer cells,
#Lynchpin molecule for the spread of cancer found Cancer is a disease of cell growth,
but most tumors only become lethal once they metastasize or spread from their first location to sites throughout the body.
For the first time, researchers at Thomas Jefferson University in Philadelphia report a single molecule that appears to be the central regulator driving metastasis in prostate cancer.
The study, published online July 13th in Cancer cell, offers a target for the development of a drug that could prevent metastasis in prostate cancer,
and possibly other cancers as well.""Finding a way to halt or prevent cancer metastasis has proven elusive.
We discovered that a molecule called DNA-PKCS could give us a means of knocking out major pathways that control metastasis before it begins,
"says Karen Knudsen, Ph d.,Director of the Sidney Kimmel Cancer Center at Thomas Jefferson University, the Hilary Koprowski Professor and Chair of Cancer Biology, Professor of Urology, Radiation Oncology,
and Medical Oncology at Jefferson. Metastasis is thought of as the last stage of cancer. The tumor undergoes a number of changes to its DNA--mutations--that make the cells more mobile
able to enter the bloodstream, and then also sticky enough to anchor down in a new location,
such as the bone, the lungs, the liver or other organs, where new tumors start to grow.
Although these processes are characterized fairly well, there appeared to be many non-overlapping pathways that ultimately lead to these traits.
Now, Dr. Knudsen and colleagues have shown that one molecule appears to be central to many of the processes required for a cancer to spread.
In fact, previous studies had shown that DNA-PKCS was linked to treatment resistance in prostate cancer, in part because it would repair the usually lethal damage to tumors caused by radiation therapy and other treatments.
Importantly, Dr. Knudsen's work showed that DNA-PKCS has other, far-reaching roles in cancer.
The researchers showed that DNA-PKCS also appears act as a master regulator of signaling networks that turn on the entire program of metastatic processes.
In addition to experiments in prostate cancer cell lines, Dr. Knudsen and colleagues also showed that in mice carrying human models of prostate cancer,
And in mice with aggressive human tumors, an inhibitor of DNA-PKCS reduced overall tumor burden in metastatic sites.
In a final analysis that demonstrated the importance of DNA-PKCS in human disease the researchers analyzed 232 samples from prostate cancer patients for the amount of DNA-PKCS those cells contained
and compared those levels to the patients'medical records. They saw that a spike in the kinase levels was a strong predictor of developing metastases and poor outcomes in prostate cancer.
They also showed that DNA-PKCS was much more active in human samples of castrate-resistant prostate cancer, an aggressive and treatment-resistant form of the disease."
"These results strongly suggest that DNA-PKCS is a master regulator of the pathways and signals that lead to the development of metastases in prostate cancer,
and that high levels of DNA-PKCS could predict which early stage tumors may go on to metastasize,
"says Dr. Knudsen.""The finding that DNA-PKCS is a likely driver of lethal disease states was unexpected,
and the discovery was made possible by key collaborations across academia and industry,"explains Dr. Knudsen.
in addition to leaders of the Sidney Kimmel Cancer Center's Prostate Program, included the laboratories of Felix Feng (University of Michigan), Scott Tomlins (University of Michigan), Owen Witte (UCLA),
Cory Abate-Shen (Columbia University), Nima Sharifi (Cleveland Clinic) and Jeffrey Karnes (Mayo Clinic), and contributions from Genomedx.
"We are enthusiastic about the next step of clinical assessment for testing DNA-PKCS inhibitors in the clinic.
This new trial will be for patients advancing on standard of care therapies, and will be available at multiple centers connected through the Prostate Cancer Clinical Trials Consortium,
of which we are explained a member Dr. Knudsen.""Although the pathway to drug approval can take many years,
this new trial will provide some insight into the effect of DNAP-PKCS inhibitors as anti-tumor agents.
In parallel, using this kinase as a marker of severe disease may also help identify patients whose tumors will develop into aggressive metastatic disease,
so that we can treat them with more aggressive therapy earlier, "says Dr. Knudsen.""Given the role of DNA-PKCS in DNA repair as well as control of tumor metastasis,
there will be challenges in clinical implementation, but this discovery unveils new opportunities for preventing or treating advanced disease
#Wireless data delivery over active TV channels tested Rice university engineers have demonstrated the first system that allows wireless data transmissions over UHF channels during active TV broadcasts.
Today, injection and extrusion molding shape hot liquids into everything from car parts to toys.
As a result, patients often suffer for months before finding a medicine that makes them feel better.
The researchers tested the compounds in rats that were subjected to chronic mild stress that caused the animals to act in ways that resemble human depression.
who is also the vice president for Medical Affairs, University of Maryland, and the John Z. and Akiko K. Bowers Distinguished Professor and Dean of the School of medicine."
#Liquid biopsy identifies mutations in colorectal cancer undetected in tissue biopsy The results of the trial were twofold:
liquid biopsy effectively unmasked different tumor-related mutations. More specifically, in a subgroup of 41 patients who had received previously anti-EGFR therapy,
it was revealed that they had acquired KRAS mutations during the course of their disease. Such accurate information is difficult to obtain using tissue biopsy
which could, in the absence of this data, lead to a selection of therapy which may not be the most appropriate for these patients.
Moreover, the study concludes that regorafenib is effective in patients with KRAS and PIK3CA mutations."
"This is the first large clinical trial to compare liquid versus conventional tissue biopsy data, and the results show the former (BEAMING technology) obtain more data on tumor mutation throughout the course of the disease,
enabling us to better target therapy to the specificities of patient's tumor; this could have a considerable impact on clinical practice,
as novel applications of this technology could be investigated further and developed,"says Josep Tabernero, Head of the Medical Oncology Department of Hospital Universitario Vall d'Hebron, Director of VHIO,
and Co-Director of the study. The majority of clinical studies published on the use of DNA in blood to determine tumor genotype,
have enrolled only a relatively small number of patients which limits the significance of the findings as well as the ability to research possible correlations between genotype and clinical outcome.
Furthermore, most studies evaluated a single gene (such as KRAS) and used technologies that are not commercially available.
Arraytumor genotype plays an important role in drug resistance in patients with metastatic colorectal cancer,
but the genotype obtained at diagnosis can vary after different treatment lines. Therefore, DNA analysis using liquid biopsy has clear advantages over DNA analysis with tissue biopsy
and is rapidly gaining importance and momentum in the oncology field. Liquid biopsy, also known as a blood-based biomarker test, is a fast, simple method for detecting RAS (KRAS and NAS) mutation status in tumors
as it only requires a blood test rather than a tissue biopsy or surgical procedure. Further, it also provides mutation status results in a matter of days,
helping to determine the most specific, targeted treatment in each case. It represents one more important step in realizing the true promise of precision medicine in oncology--the main focus behind research at VHIO which aims to both advance
and deliver targeted therapies tailored to the particularities of each tumor for an increasing number of patients.
Although there are still some important questions that will need to be resolved concerning liquid biopsy for example, the possibility that not all tumors release enough DNA into the blood for it to be detected,
as well as the difficulty of assigning a particular genotype for each particular tumor in patients with multiple metastases,
the CORRECT study shows that liquid biopsy could become an essential tool in clinical practice.
Arraycolorectal cancer is the second most common cancer in the world, with an estimated incidence rate of more than 1. 36 million new cases per year.
Around 694,000 people die from colorectal cancer every year, accounting for 8. 5%of all cancer deaths
ranking as the fourth most common cause of death from cancer. Approximately 55%of all colorectal cancer cases are diagnosed in the world's developed regions,
and the incidence and mortality rates are considerably higher among men than in women e
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