#Supercomputers surprisingly link DNA crosses to cancer Supercomputers have helped scientists find a surprising link between cross-shaped (or cruciform) pieces of DNA and human cancer, according to a study at The University of Texas at Austin (UT Austin.
But scientists have suspected also these small cruciforms--a structure of DNA itself--to be linked to mutations that can elevate cancer risk.
altering DNA in a way that can increase risk of cancer in yeast, monkeys, and in humans.
and under in a reference database of mutations in human cancer that are somatic, meaning not inherited.
or translocations'can lead to cancer development.''We found that short inverted repeats are enriched indeed at translocation breakpoints in human cancer genomes,
'lead author Karen Vazquez said. Vasquez is the James T. Delucio Regents Professor in the Division of Pharmacology and Toxicology at The University of Texas at Austin.'
and potentially initiate cancer development.''Vasquez said, 'We have studied also the potential mechanisms that are involved in the interplays among alternative DNA structures and cancer development.
Our team has discovered at least two different mechanistic pathways: one involving DNA replication, where these unusual structures cause a roadblock to DNA replication;
'DNA double-strand breaks can increase the risk of cancer because they can result in translocations, deletions,
'These modifications of the DNA can lead to cancer, 'Vasquez said. According to Paul Okano, program director at the Division of Cancer Biology of the National Cancer Institute,
'The focus of Dr. Vasquez'research on the mechanisms of alternate DNA structure-induced mutations, DNA breaks,
Dr. Vasquez'studies on the role of non-B DNA sequences in these mechanisms can contribute to our knowledge of the etiology of human cancer.'
Then the number of these iterations needs to be multiplied by the length of the DNA, then by the number of the translocations in our cancer patients,
'COSMIC is maintained a database by the Sanger Institute in the U k. of mutations found in human somatic, or noninheritable cancer.'
'We had 20,000 translocations from human cancers from the COSMIC database; 200 bases of DNA for each translocation;
''With TACC's support, we were able to see that this is at least one plausible explanation in human cancer etiology,
'Our overarching interest is to understand how DNA structure can influence cancer development. With access to TACC, we are more confident that DNA sequences capable of forming particular unusual structures present a plausible explanation for how DNA breaks can lead to translocations in cancer,
'Vasquez said.''Our next steps are to go forward with a mouse model that can detect mutations
and translocations in the mouse genome using human sequences from these cancer breakpoints, 'Vasquez said.
'The long term goal for these studies is to develop better prevention or treatment strategies for cancer patients,
''If we can help clinical scientists apply mechanistic information such as we hope will be gained from our research to better cancer treatment and a cancer prevention strategies,
as well as in cancers, the researchers said. Traditional fate mapping, which is somewhat like developing a family tree for cells, labels cells based on the expression of a certain gene.
and even in cancer,"said Dr. Sadek, whose lab focuses on cardiac regeneration and stem cell metabolism m
'said Professor Shankar Balasubramanian of the Department of chemistry and the Cancer Research UK Cambridge Institute, who led the research.'
'The research was supported by Cancer Research UK, the Wellcome Trust and the Biotechnology and Biological sciences Research Council UK K
gastric cancer Researchers have devised a breath test that can help doctors diagnose the early signs of esophageal and gastric cancer in minutes.
They found that the test can discriminate between malignant and benign esophageal cancer in patients for the first time.
The test can also be applied to detect gastric (stomach) cancer tumours. According to the researchers, economic modelling showed that the test could save the NHS £145 million a year
Esophageal and gastric malignancies account for 15 per cent of cancer-related deaths globally. Both cancers are diagnosed usually in the advanced stages
because they rarely cause any noticeable symptoms when they first develop. As a result, the long-term survival rate is 13 per cent for esophageal cancer and 15 per cent for gastric cancer in the UK.
However diagnosis of these cancers at an early stage can improve survival rates. Doctors diagnose esophageal and gastric cancers by carrying out an endoscopy.
This is a procedure where the inside of the body is examined using a probe with a light source and video camera at the end via the mouth and down the gullet.
However, the procedure is invasive and costs the NHS around £400-£600 per endoscopy. Only two per cent of patients who are referred for an endoscopy by GPS are diagnosed with esophageal or gastric cancer.
The first study, published in the Annals of Surgery was carried out by an international team led by scientists at Imperial College London and clinicians at Imperial College Healthcare NHS Trust.
"Esophageal and gastric cancers are on the rise in the UK with more than 16,000 new cases diagnosed each year.
The current method for detecting these cancers is expensive, invasive and a diagnosis is made usually at a late stage
and often the cancer has spread to other parts of the body. This makes it harder to treat and results in poor long-term survival rates.
"The test looks for chemical compounds in exhaled breath that are unique to patients with esophageal and gastric cancer.
The cancers produce a distinctive smell of volatile organic compounds (VOC), chemicals that contain carbon and are found in all living things,
This quantitative technology identified VOCS that were present at significantly higher concentrations in patients with esophageal and gastric cancer than in non-cancerous patients.
The researchers used breath samples of patients with esophageal and gastric cancer at Imperial College Healthcare NHS Trust from 2011 to 2013.
Patients who are at risk of developing these cancers and those who had benign tumours were tested also.
#New mechanism that regulates tumor initiation, invasion in skin basal cell carcinoma Researchers at the Université libre de Bruxelles,
ULB uncover a new mechanism that regulates tumour initiation and invasion in skin basal cell carcinoma.
Basal cell carcinoma (BCC) is the most common cancer found in human with several million of new patients affected every year around the world.
directly controls skin cancer formation by regulating the expansion of tumor initiating cells and the invasive properties of cancer cells.
In collaboration with Pr Véronique Del Marmol (Department of Dermatology, Erasme Hospital, ULB) and the group of Pr François Fuks (Laboratory of cancer epigenetics, Faculty of medicine, ULB), Larsimont and colleagues demonstrated that
and is maintained in invasive tumors. Deletion of Sox9 prevents skin cancer formation demonstrating the essential role of Sox9 during tumorigenesis
"It was really exciting to see that the deletion of only one gene was sufficient to completely prevent tumor formation.
suggesting that we can eliminate oncogene expressing cells before cancer formation"comments Jean-Christophe Larsimont, the first author of this study.
as well as the gene network regulated by Sox9 during the early steps of skin tumor initiation
cell adhesion and cytoskeleton dynamics required for tumor invasion. These results have important implications for the development of novel strategies to block tumor formation and invasion in the most frequent cancer in humans."
"Given that the majority of human cancers express Sox9, it is likely that the results of this study will be relevant for other cancers in humans
and will help to define new strategies to prevent cancer formation and block tumor invasion"comments Cédric Blanpain, the last and corresponding author of this study.
This work was supported by the FNRS, Fondation Contre le Cancer, Foundation ULB, ERC the Fonds Gaston Ithier, the Fond Yvonne Boël, the foundation Bettencourt Schueller,
and the foundation Baillet-Latour. Cédric Blanpain is an investigator of WELBIO o
#X marks the spot: Novel method for controlling plasma rotation confirmed Such a method could prove important for future facilities like ITER,
the huge international tokamak under construction in France that will demonstrate the feasibility of fusion as a source of energy for generating electricity.
In rare instances, the internal chemical response of a cell can cause unregulated cell growth, leading to cancer.
or proteins that could be targeted by drugs, eventually leading to new medicines to fight cancer r
and may provide clues to the development of therapies for infectious diseases, cancers and immune diseases.,"
#Discovery could lead to personalized colon cancer treatment approach A UNC Lineberger Comprehensive Cancer Center discovery of just how a certain tumor suppressor molecule works to prevent tumor growth could lead to a personalized treatment
the researchers reported that the tumor-suppressing protein AIM2, or Absent in Melanoma 2, helps prevent colon cancer by restricting a signaling molecule called Akt.
With this finding, the researchers believe theye found a possible drug target for colon cancer patients who lack the tumor suppressor AIM2. everal studies
and clinical evidence suggest AIM2 functions as a tumor suppressor, but until now, wee had very little direct evidence to explains how this occurs,
said Justin E. Wilson, Phd, the study first author and a postdoctoral fellow at UNC Lineberger,
the UNC School of medicine Department of Microbiology and Immunology and the Department of Genetics. e found that AIM2 inhibits tumorigenesis in multiple animal models of colorectal cancer by restricting the pro-survival signaling molecule, Akt,
which is commonly hyperactive in many human cancers. The study builds on previous findings suggesting that AIM2 limits cancer cell growth in colon cancer cell lines,
Distinguished Professor in the UNC School of medicine Department of Genetics and a UNC Lineberger Comprehensive Cancer Center member.
And in mouse models lacking AIM2, the researchers found that they had smaller tumors and precancerous colon polyps when blocked Akt.
Wilson said the researchers believe their findings mean that drugs used to inhibit Akt could be used as a personalized therapy for people who don have AIM2. ur research paves the way for future clinical trials that screen for AIM2 expression in colon cancer
and possibly other cancers to identify patients who may potentially benefit from personalized anti-Akt therapy,
"This invention will allow us to detect anything we might be interested in, bacterial contamination or perhaps a protein molecule that is a cancer marker.
#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,
Similar results were obtained by the National Cancer Institute USA in tests conducted on 60 cell lines.
""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
"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.
"said co-author Bruce Hammock, distinguished professor at the UC Davis Department of Entomology and Nematology and the UC Davis Comprehensive Cancer Center."
"This search is already underway in a number of laboratories working on cancer and other diseases."
#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."
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."
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.
and is an area of great potential for the treatment of patients with cancer, "said Dr. Kim."
These types of clinical trials place the UH Seidman Cancer Center at the forefront of immune therapy of cancer."
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.
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."
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."
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.
it can be a source for triggering cancer, for example,"said Hickson. It is well known that microscopic cable-like structures,
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
#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,
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.
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.
the researchers analyzed 232 samples from prostate cancer patients for the amount of DNA-PKCS those cells contained
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,
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),
and will be available at multiple centers connected through the Prostate Cancer Clinical Trials Consortium, of which we are explained a member
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,
"Given the role of DNA-PKCS in DNA repair as well as control of tumor metastasis, there will be challenges in clinical implementation,
#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,
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,
The majority of clinical studies published on the use of DNA in blood to determine tumor genotype,
Arraytumor genotype plays an important role in drug resistance in patients with metastatic colorectal cancer,
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
and deliver targeted therapies tailored to the particularities of each tumor for an increasing number of patients.
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,
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
#Potential of blue LEDS as novel chemical-free food preservation technology A team of scientists from the National University of Singapore (NUS) has found that blue light emitting diodes (LEDS) have strong antibacterial
#Nanospheres shield chemo drugs, safely release high doses in response to tumor secretions Scientists have designed nanoparticles that release drugs in the presence of a class of proteins that enable cancers to metastasize.
so that the very enzymes that make cancers dangerous could instead guide their destruction.""We can start with a small molecule
and build that into a nanoscale carrier that can seek out a tumor and deliver a payload of drug,
The system takes advantage of a class enzymes called matrix metalloproteinases that many cancers make in abundance.
The shell fragments form a ragged mesh that holds the drug molecules near the tumor.
builds on his group's earlier sucess using a similar strategy to mark tumors for both diagnosis and precise surgical removal.
That means the drug was inactivated as it flowed through the circulatory system until it reached the tumor.
The protection allowed the researchers to safely give a dose 16 times higher than they could with the formulation now used in cancer clinics,
in a test in mice with grafted in fibrosarcoma tumors. In additional preliminary tests, Callmann and colleagues were able to halt the growth of the tumors for a least two weeks,
using a single lower dose of the drug. In mice treated with the nanoparticles coated with peptides that are impervious to MMPS or given saline,
the tumors grew to lethal sizes within that time. Gianneschi says they will broaden their approach to create delivery systems for other diagnostic and therapeutic molecules."
We'll test this in other models--with other classes of drug and in mice with a cancer that mimics metastatic breast cancer, for example."
"Additional authors include Matthew Thompson in Gianneschi's chemistry research group and Christopher Barback, David Hall and Robert Mattrey in UC San diego's Moores Cancer Center.
Callmann holds a fellowship through the Cancer Researchers in Nanotechnology Program at UC San diego. The National Institute of Biomedical Imaging
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