Medicine  

Nanotechnology research is making exciting advances in a number of different academic fields, but it is in medicine where the tiniest particles can make the biggest differences. Treating cancer has always been a challenge, but one type of cancer is especially difficult, aggressive, and most often terminal.

Mesothelioma is a type of cancer that mostly affects the tissue that lines the lungs and the chest cavity. It is associated with exposure to asbestos and has affected thousands of people. Now, advances in the use of nanoparticles are giving these patients new hope.

Nanoparticles and Targeted Treatment

There are many different forms that nanotechnology can take, but in medicine and cancer treatment, tiny biomolecules, termed nanoparticles are proving to be useful in a number of treatments. For cancer and mesothelioma, nanoparticles can be used to encapsulate and then deliver medications or other factors directly to a tumor and directly into cancer cells.

Medicinal nanoparticles may range in size from just ten nanometers to 200 nanometers. The surfaces can be designed for different uses and to minimize the chances that they will be destroyed by a patient’s immune system. In targeting nanoparticles to cancer cells, antibodies can be used on the surface. Researchers doing this work select an antibody that matches receptors on the surfaces of cancer cells in the target tumor. This allows the nanoparticle to be directed right to the tumor and the cells of interest.

What makes targeted nanoparticles such an important achievement in cancer treatment is that it could replace systemic chemotherapy, which is the administration of chemotherapeutic drugs intravenously. It is systemic because the drugs spread throughout the body and act on any fast growing cells, not just cancer cells. This is what makes chemotherapy so uncomfortable for patients. It causes painful side effects, as well as hair loss. If those same drugs can be targeted at tumors specifically, side effects could be avoided and that would be a big deal for cancer patients.

Using Nanoparticles to Deliver Genetic Material

Nanoparticles that are targeted to strike tumors in the body can encapsulate chemotherapy drugs, but also genetic factors. These factors can be used to insert, delete, or change genes in cancer cells to direct them to slow their growth, to stop dividing, or to die. Research into this use for nanoparticles is already underway and has shown some promising and hopeful results for mesothelioma patients.

A group of researchers in Australia recently eliminated nearly all the cancer cells from a patient with late-stage mesothelioma. This is a huge achievement because mesothelioma in its later stages is very difficult to treat and is considered, short of a miracle, impossible to cure. One patient out of a group of six in this research saw almost complete remission after treatment with nanoparticles containing genetic factors. This was after the patient had failed to respond to several rounds of conventional chemotherapy.

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The genetic material used in the nanoparticles is called microRNA, or miRNA. These small pieces of genetic material were used in the study to insert a gene into the cells of mesothelioma tumors. Research had previously found a gene missing from the cancer cells, and by inserting this missing gene, the miRNA acted like a tumor suppressant, slowing and stopping the growth of tumors.

Nanotechnology is leading a revolution in science, but in medicine the use of nanoparticles means so much more. It means that patients who had previously had no hope of surviving a difficult cancer like mesothelioma, now can dream of a day when this cancer and others may be treatable and even curable.

By  Virgil Anderson	Embed
Virgil Anderson is a mesothelioma cancer survivor. He was treated by the carer network at mesothelioma.net, and wants more cancer patients find this information.

Nanotechnology  

Nanotechnology is the technology and science of extremely small things that are typically less than 100 nanometers (nm) long. A nanometer is 10-9 long or about as long as three atoms sitting side by side. The technologies being developed at nanoscales will have major impacts on our future.

Nanotechnology is the technology and science of extremely small things that are typically less than 100 nanometers (nm) long. A nanometer is 10-9 long or about as long as three atoms sitting side by side. Things that small have different properties than do larger things, and nanotechnology has many different possible applications:

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Treating cancer

Last year, scientists developed “nanocarriers” that can directly deliver cancer drugs to the patient’s tumor and thus reduce the damage to neighboring healthy cells. Some of them are so tiny they can slip through the walls of blood vessels on their way to the tumor.

Scientists are currently working on nanoparticles that will be able to recognize cancerous cells by their molecular structure. A variant nanoparticle called a nanoshell will be able to absorb light and then generate sufficient heat to kill the cancer cells.

Improving solar cells

Improving the efficiency of solar power has long been a challenge. Even today, a solar cell converts only about 20 percent of visible light—like that from the sun—into electricity.

Researchers at the Kyoto Institute announced in January 2017 that have built a “nano-sized” semiconductor with a narrower bandwidth concentrated on the shorter wavelengths that produce more heat and energy. The new semiconductor proved able to convert at least 40 percent of light into energy.

Veelo

Veelo is a class of nanotubes made by the company General Nano. The nanotubes are lightweight with conductive properties and can therefore be used in both airplanes and spacecraft. One type, called Veelo Blac, is described as “super-black” and can absorb over 99.6 percent of visible light. It can therefore absorb reflection and interference from light produced by stars, the moon and other sources. NASA will be using it on the mini-satellites or CubeSats that will be launched in 2018.

Wearable electronics

Wearable electronics like the Apple Watch aren’t just a fashion statement. They can be used as medical monitors, military GPS trackers and many other things. To fulfill their potential, wearable electronics need better energy sources, sensors and other devices—and those components have to be small. The various makers of wearable electronics are exploring the possibilities of using nanomaterials like silver nanowires graphene or carbon nanotubes.

Ultimate waterproofing

A company based in Britain called P2i has developed a nanotechnology called Aridion that can repel any liquid. It’s a polymer coating that can be sprayed on an object like a smartphone. If the smartphone gets wet, the liquid simply forms beads on its surface. Since the coating is less than 50 nm thick, the smartphone won’t look any different from an unprotected phone. The phone’s innards can also be sprayed and protected. Aridion was originally developed to protect soldiers’ uniforms from poisonous or corrosive chemicals.

By  Dixie Somers	Embed
Author Bio - Dixie is a freelance writer who loves to write about business, finance and self improvement. She lives in Arizona with her husband and three beautiful daughters.

Artificial Intelligence  

Charlie Rose from 60 Minutes recently reported on how it might not be long before machines begin thinking for themselves—creatively, independently and with judgment sometimes better than ours. The exploration follows progress in AI over the last five years since Watson's win on Jeopardy!

In a recent piece for 60 Minutes, Charlie Rose undertook to look at the rise of artificial intelligence in the past five years. Five years ago, IBM's Watson won on the game show, Jeopardy! AI is making important strides in areas like medicine and military technology.  What was once in the realm of science fiction has become day-to-day reality.

Starting with a review of Watson's win, Rose shows how the system is now being used in the fight against cancer.

Watson has now been used on over 2,000 cancer patients, and the doctors feel that their work has forever been changed with the tool. IBM has partnered with 20 top-cancer institutes to tutor Watson in genomics and oncology.

"To me like a very comprehensive tool," says Dr. Ned Sharpless in the program. "Imagine doing clinical oncology up in the mountains of western North Carolina by yourself, you know, in a single or one-physician-- two-physician practice and 8,000 papers get written a day. And, you know-- and you want to try and provide the best, most cutting-edge, modern care for your patients possible. And I think Watson will seem to that person like a lifesaver."

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What Watson’s AI technology does is essentially what Dr. Sharpless and his team of experts do every week at this molecular tumor board meeting. They come up with possible treatment options for cancer patients who already failed standard therapies. They try to do that by sorting through all of the latest medical journals and trial data, but it is nearly impossible to keep up. Watson is used to read all of the up-to-the-minute research available and help guide the doctors.

Sharpless has started using Watson as part of University of North Carolina’s standard of care so it can help patients.

Watson is also shown in a research lab, embedded onto a Softbank Pepper robot.

Many other companies are trying to create artificial intelligence that’s closer to human intelligence, and one that is working towards the goal is featured on the show, Hanson Robotics. Rose sits down and interviews David Hanson and his latest humanoid robot, Sophia.

Unfortunately the clear leader in the pursuit of artificial general intelligence, DeepMind did not participate in the 60 Minutes piece, but their work was largely featured.

SOURCE  CBS News

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Cancer  

A team of researchers has identified a non-coding RNA, NEAT1 as a potential therapeutic target in the fight against cancer. They have shown that NEAT1 plays an important role in the survival of highly dividing cells, in particular of cancer cells. These findings can help develop new drugs that target NEAT1, in order to kill cancer cells more effectively.

"Our findings can help develop new drugs targeting NEAT1 in order to kill cancer cells more effectively."

A team of researchers led by professor Jean-Christophe Marine at the Flanders Institute for Biotechnology in Belgium(VIB-KU Leuven) has identified NEAT1, a non-coding RNA, as a potential therapeutic target in the fight against cancer. In collaboration with the Cédric Blanpain lab at the Université libre de Bruxelle (ULB), the researchers have shown that NEAT1 plays an important role in the survival of highly dividing cells—in particular of cancer cells. These findings can help develop new drugs that target NEAT1, in order to kill cancer cells more effectively.

The research has been published in the journal Nature.

As a non-coding RNA, NEAT1 is not translated into a protein. It does however contribute to the formation of so-called 'paraspeckles', subnuclear particles that can be found in the cell nuclei of cancer cells. The function of these particles has remained incompletely understood. Although highly conserved through evolution, NEAT1 appears to be dispensable for normal embryonic development and adult life as mice lacking NEAT1 are viable and healthy.

PhD student Carmen Adriaens stated: "In our study, we have found that the expression of NEAT1 in the cell nucleus is regulated by p53. This protein plays an important role in protecting people against cancer and is known as 'the guardian of the genome'. When a cell is stressed or damaged, p53 will upregulate the expression of NEAT1, which leads to the formation of paraspeckles. This has two possible outcomes: the cell can either go into transient cell cycle arrest, giving it time to deal with the stress and repair the damage before continuing cell division. If the stress or damage is too high, however, p53 will instruct the cell to commit suicide and die."

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The key observation made by the VIB researchers is that NEAT1/paraspeckles are required for the survival of highly dividing cancer initiating cells and that mice lacking NEAT1 are protected from developing skin cancer. This means that cancer cells can 'hijack' the survival principle of NEAT1 for their own good.

Marine states, "We expected NEAT1 to be a tumor suppressor, since it is regulated by p53. Instead, it turned out that NEAT1 helps cancer cells in growing opportunistically. They use the survival mechanisms put in place by NEAT1 to survive standard chemotherapeutics. Our research shows that cancer cells die more effectively after removing NEAT1/paraspeckles from the cell nucleus. In other words: the loss of NEAT1 leads to increased chemosensitivity and cell death. Therefore, our findings can help develop new drugs targeting NEAT1 in order to kill cancer cells more effectively."

As normal cells do not rely on NEAT1/paraspeckles, these nuclear bodies may be promising therapeutic targets. The researchers will now try to get a better understanding of how exactly NEAT1 applies its survival functions to cells. The ultimate goal of the Jean-Christophe Marine Lab is to find out how this knowledge can be harnessed to help cure cancer.

SOURCE  Flanders Institute for Biotechnology (VIB)

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Artificial Intelligence  

Pathologists have been largely diagnosing disease the same way for the past 100 years, by manually reviewing images under a microscope. Now, new research suggests that computers can help doctors improve accuracy and significantly change the way cancer and other diseases are diagnosed. 

A group of researchers from Beth Israel Deaconess Medical Center (BIDMC) and Harvard Medical School (HMS) recently developed artificial intelligence (AI) methods aimed at training computers to interpret pathology images, with the long-term goal of building AI-powered systems to make pathologic diagnoses more accurate.

"Our AI method is based on deep learning, a machine-learning algorithm used for a range of applications including speech recognition and image recognition," explained pathologist Andrew Beck, MD, PhD, Director of Bioinformatics at the Cancer Research Institute at Beth Israel Deaconess Medical Center (BIDMC) and an Associate Professor at Harvard Medical School. "This approach teaches machines to interpret the complex patterns and structure observed in real-life data by building multi-layer artificial neural networks, in a process which is thought to show similarities with the learning process that occurs in layers of neurons in the brain's neocortex, the region where thinking occurs."

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The Beck lab's approach was recently put to the test in a competition held at the annual meeting of the International Symposium of Biomedical Imaging (ISBI), which involved examining images of lymph nodes to decide whether or not they contained breast cancer. The research team placed first in two separate categories, competing against private companies and academic research institutions from around the world. The research team today posted a technical report describing their approach to the arXiv.org repository, an open access archive of e-prints in physics, mathematics, computer science, quantitative biology, quantitative finance and statistics.

"Our AI method is based on deep learning, a machine-learning algorithm used for a range of applications including speech recognition and image recognition."

"Identifying the presence or absence of metastatic cancer in a patient's lymph nodes is a routine and critically important task for pathologists," Beck explained. "Peering into the microscope to sift through millions of normal cells to identify just a few malignant cells can prove extremely laborious using conventional methods. We thought this was a task that the computer could be quite good at -- and that proved to be the case."

In an objective evaluation in which researchers were given slides of lymph node cells and asked to determine whether or not they contained cancer, the team's automated diagnostic method proved accurate approximately 92 percent of the time, explained Khosla, adding, "This nearly matched the success rate of a human pathologist, whose results were 96 percent accurate."

"But the truly exciting thing was when we combined the pathologist's analysis with our automated computational diagnostic method, the result improved to 99.5 percent accuracy," said Beck. "Combining these two methods yielded a major reduction in errors."

The team trained the computer to distinguish between cancerous tumor regions and normal regions based on a deep multilayer convolutional network.

"In our approach, we started with hundreds of training slides for which a pathologist has labeled regions of cancer and regions of normal cells," said the lab's post-doctoral fellows Dayong Wang, PhD. "We then extracted millions of these small training examples and used deep learning to build a computational model to classify them." The team then identified the specific training examples for which the computer is prone to making mistakes and re-trained the computer using greater numbers of the more difficult training examples. In this way, the computer's performance continued to improve.

"There have been many reasons to think that digitizing images and using machine learning could help pathologists be faster, more accurate and make more accurate diagnoses for patients," Beck added. "This has been a big mission in the field of pathology for more than 30 years. But it's been only recently that improved scanning, storage, processing and algorithms have made it possible to pursue this mission effectively. Our results in the ISBI competition show that what the computer is doing is genuinely intelligent and that the combination of human and computer interpretations will result in more precise and more clinically valuable diagnoses to guide treatment decisions."

SOURCE  Science Daily

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Medicine  

Human papillomavirus, or HPV is a group of more than 150 related viruses. Each HPV virus in this large group is given a number which is called its HPV type. HPV is named for the warts (papillomas) some HPV types can cause. Some other HPV types can lead to cancer, especially cervical cancer.

One of the most common infections when it comes to Sexually transmitted diseases is HPV or Human Papilloma Virus. It has been proven that a huge percentage of young adults have contracted a strain of HPV through sexual contact. HPV is transmitted through skin contact. It shows up in forms of rings that create a cauliflower shape like formation on the pubic area. Some will experience bumps on the same area. One of the most worrying factors about HPV is that it provides a ripe ground for cervical cancer. Most of the patients that have ended up with cervical cancer have more often than not contracted HPV at some point in their lives. This doesn’t mean however that all HPV infections will lead to cancer.

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The virus provides a higher risk in this situation. There are more than one hundred types of HPV with more than a dozen strains in the mix. It is proven that more than two-thirds of all cervical cancer cases were initiated by HPV 16 and 18 strains. HPV affects cervical cells causing them to mutate and multiply. It is, however, impossible to test for HPV through a pap smear. This will only detect the presence of cancer. Screening for abnormal cells will, however, give a clear indication of the presence of HPV.

HPV does not entirely in itself cause cancer. HIV will easily do the same thanks to the lowered CD4+ count. A lower immunity will expose the body to diseases that would easily be averted. The human immune system is the first frontier when it comes to dealing with cancer. It is good to note that most cancers are dealt with by the body’s immune system. Cancers are mostly opportunistic diseases. They will develop fast and easy as long as there is a helping agent.

Smoking also increases the risk of cervical cancer through HPV. One of the most disturbing findings is that tobacco by-products can be found along the cervical mucus lining of smokers. This causes damage to the cells lining the cervix exposing it to cancerous growths. The tobacco by products are designed for maximum absorption in the blood. They travel through the bloodstream to settle on these areas increasing the risk of cervical cancer.

You can now safeguard your children from cervical cancer and HPV thanks to the HPV vaccine. Gardasil, also known as Silgard was developed for teens for the purpose of preventing HPV through sexual contact. The vaccine also prevents cervical cancer through keeping all forms of HPV at bay. It also decreases the chances of penile and oral cancer in sexually active teens.

PCR kits are used to detect high-risk HPV strains that would lead to cervical cancer. There are a number of kits all specialized in detecting different types of high-risk HPV. Protecting yourself from HPV not only safeguards you from STDs but keeps cancer away. It is important that you have all the necessary tests. It is even more important that you protect yourself by avoiding multiple sexual partners and using protection when engaging in intercourse. This may not help much with HPV but is still better than nothing. It will help keeping clean knowing the high risks involved.

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SOURCES  

• http://www.cancer.gov/about-cancer/causes-prevention/risk/infectious-agents/hpv-fact-sheet#q1
• http://www.cdc.gov/cancer/hpv/ http://www.who.int/mediacentre/factsheets/fs380/en/
• http://www.cancer.net/navigating-cancer-care/prevention-and-healthy-living/hpv-and-cancer

By Maggie Martin

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Author Bio: Maggie Martin is completing her PhD in Cell Biology, works as a lab tech for Mybiosource.com and contributes content on Bio-tech, Life Sciences, and Viral Outbreaks. Follow on Twitter @MaggieBiosource

Cancer Research  

Researchers have, for the first time, visualized the origins of cancer from the first affected cell and watched its spread in a live animal. Their work could change the way scientists understand melanoma and other cancers and could lead to new, early treatments before the cancer has taken hold.

For the first time researchers hav visualized the origins of cancer from the first affected cell and watched its spread in a live animal. The work undertaken at Boston Children's Hospital, was published recently in the journal Science. It could change the way scientists understand melanoma and other cancers and could lead to new, early treatments before the cancer has taken hold.

"An important mystery has been why some cells in the body already have mutations seen in cancer, but do not yet fully behave like the cancer," says the paper's first author, Charles Kaufman, MD, PhD, a postdoctoral fellow in the Zon Laboratory at Boston Children's Hospital. "We found that the beginning of cancer occurs after activation of an oncogene or loss of a tumor suppressor, and involves a change that takes a single cell back to a stem cell state."

That change, Kaufman and colleagues found, involves a set of genes that could be targeted to stop cancer from ever starting.

The study imaged live zebrafish over time to track the development of melanoma. All the fish had the human cancer mutation BRAFV600E -- found in most benign moles -- and had also lost the tumor suppressor gene p53.

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Kaufman and colleagues engineered the fish so that individual cells would light up in fluorescent green if a gene called crestin was turned on -- a "beacon" indicating activation of a genetic program characteristic of stem cells. This program normally shuts off after embryonic development, but occasionally -- for reasons not yet known -- crestin and other genes in the program turn back on in certain cells.

"Every so often we would see a green spot on a fish," says Leonard Zon, MD, director of the Stem Cell Research Program at Boston Children's and senior investigator on the study. "When we followed them, they became tumors 100 percent of the time."

When Kaufman, Zon and colleagues looked to see what was different about these early cancer cells, they found that crestin and the other activated genes are the same ones turned on during zebrafish embryonic development -- specifically, in the stem cells that give rise to the pigment cells known as melanocytes, within a structure called the neural crest.

"What's cool about this group of genes is that they also get turned on in human melanoma," says Zon, who is also a member of the Harvard Stem Cell Institute and a Howard Hughes Medical Institute investigator. "It's a change in cell fate, back to neural crest status."

Finding the cancer-originating cells was tedious work, with the researchers wearing goggles and using a microscope with a fluorescent filter. They examined the fish as they swam, shooting iPhone video.

Scanning the fish took hours each day. In 30 fish, Kaufman spotted a small cluster of green-glowing cells about the size of the head of a Sharpie marker -- and in all 30 cases, these grew into melanomas. In two cases, he was able to see a single green-glowing cell and watch it divide and ultimately become a tumor mass.

"It's estimated that only one in tens or hundreds of millions of cells in a mole eventually become a melanoma," says Kaufman, who is also an instructor at Dana-Farber Cancer Institute. "Because we can also efficiently breed many fish, we can look for these very rare events. The rarity is very similar in both humans and fish, which suggests that the underlying process of melanoma formation is probably much the same in humans."

The research team believe that their findings could lead to a new genetic test for suspicious moles to see whether the cells are behaving like neural crest cells, indicating that the stem-cell program has been turned on. They are also investigating the regulatory elements that turn on the genetic program (known as super-enhancers). These DNA elements have epigenetic functions that are similar in zebrafish and human melanoma and could potentially be targeted with drugs to stop a mole from becoming cancerous.

Zon and Kaufman posit a new model for cancer formation, going back to a decades-old concept of "field cancerization." They propose that normal tissue becomes primed for cancer when oncogenes are activated and tumor suppressor genes are silenced or lost, but that cancer develops only when a cell in the tissue reverts to a more primitive, embryonic state and starts dividing. They believe this model may apply to most if not all cancers, not just melanoma.

SOURCE  Boston Children's Hospital via EurekAlert

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Medicine  

3D printing technology has helped save a Spanish cancer patient, who received a 3D printed titanium sternum and rib cage.

A cancer patient in Spain has received a 3D printed titanium sternum and rib cage that looks like a part from the T-800 cyborg.

Suffering from a chest wall sarcoma (a type of cancerous tumor that grows, in this instance, around the rib cage), the 54 year old man needed his sternum and a portion of his rib cage replaced. This part of the chest is notoriously tricky to recreate with prosthetics, due to the complex geometry and design required for each patient.

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So the patient’s surgical team determined that a fully customized 3D printed sternum and rib cage was the best option.That’s when they turned to Melbourne, Australia-based medical device company Anatomics, who designed and manufactured the implant.

Twelve days after the surgery the patient was discharged and has recovered well.

This isn’t the first time surgeons have turned the human body into a titanium masterpiece. Thoracic surgeons typically use flat and plate implants for the chest. However, these can come loose over time and increase the risk of complications. The patient’s surgical team at the Salamanca University Hospital thought a fully customised 3D printed implant could replicate the intricate structures of the sternum and ribs, providing a safer option for the patient.

Using high resolution CT data, the Anatomics team was able to create a 3D reconstruction of the chest wall and tumour, allowing the surgeons to plan and accurately define resection margins. 

A typical 3D printer like the MakerBot Replicator wasn't really adequate for this work. Instead, we relied on our $1.3 million Arcam printer to build up the implant layer-by-layer with its electron beam, resulting in a brand new implant which was promptly couriered to Spain.

The advantage of 3D printing is its rapid prototyping. When you’re waiting for life-saving surgery this is the definitely the order of the day.

When it comes to using 3D printing for biomedical applications, it seems that we are just scratching the surface of what’s possible.

SOURCE  CSIRO

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 Imaging  

Tumors are often surrounded and invaded by bone marrow-derived cells. Imaging the infiltration of such immune cells into tumors may therefore be an attractive means of detecting tumors or of tracking the response to anticancer therapy. A new imaging technique may now make this possible.

Using a new approach has allowed real-time imaging of the immune system’s response to the presence of tumors—without the need for blood draws or invasive biopsies. The method offers a potential breakthrough both in diagnostics and in the ability to monitor efficacy of cancer therapies.

The method, developed in the lab of Whitehead Institute Member Hidde Ploegh and reported in the Proceedings of the National Academy of Sciences (PNAS), harnesses the imaging power of positron emission tomography (PET), which is normally used to monitor cancer metabolism, to identify areas of immune cell activity associated with inflammation or tumor development.

“Every experimental immunologist wants to monitor an ongoing immune response, but what are the options?” Ploegh asks rhetorically. “One can look at blood, but blood is a vehicle of transport for immune cells and is not where immune responses occur. Surgical biopsies are invasive and non-random, so, for example, a fine-needle aspirate of a tumor could miss a significant feature of that condition.”

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In search of a better monitoring approach Ploegh leveraged two research tools that have become staples in his lab in recent years. The first exploits so-called single-domain antibodies known as VHHs, derived from the heavy chain-only antibodies made by the immune systems of animals in the camelid family. Ploegh’s lab immunizes alpacas to generate VHHs specific to immune cells of interest. The second tool, known as sortagging, labels the VHHs in site-specific fashion to enable the tracking of the VHHs and their targets in a living animal.

"We’re very excited about this because it’s a powerful approach to pick up inflammation in and around the tumor."

Knowing that the tissue around tumors often contains immune cells such as neutrophils and macrophages, Ploegh and his lab members hypothesized that appropriately labeled VHHs might allow them to pinpoint tumor locations by finding the tumor-associated immune cells. Ploegh notes that VHHs’ extremely small size—approximately one-tenth that of conventional antibodies—are likely responsible for their superior tissue penetration and thus makes them particularly well suited for such use.

For the current research, the lab generated VHHs that recognize mouse immune cells, then labeled these VHHs with radioisotopes, and injected them into tumor-bearing mice. Subsequent PET imaging detected the location of immune cells around the tumor quickly and accurately.

“We were able to image tumors as small as one millimeter in size and within just a few days of their starting to grow,” says Mohammad Rashidian, a postdoctoral researcher in Ploegh’s lab and first author of the PNAS paper. “We’re very excited about this because it’s a powerful approach to pick up inflammation in and around the tumor.”

Rashidian and Ploegh believe that with further refinement, the method could be used to monitor response to—and perhaps modify—cancer immunotherapy, which, though quite promising, has thus far met with great success in some cases, but has failed in others.


SOURCE  Whitehead Institute

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 Aging  

A study tying the aging process to the deterioration of tightly packaged bundles of cellular DNA could lead to methods of preventing and treating age-related diseases such as cancer, diabetes and Alzheimer's disease.

Astudy tying the aging process to the deterioration of tightly packaged bundles of cellular DNA could lead to methods of preventing and treating age-related diseases such as cancer, diabetes and Alzheimer’s disease, as detailed in Science.

In the study, scientists at the Salk Institute and the Chinese Academy of Science found that the genetic mutations underlying Werner syndrome, a disorder that leads to premature aging and death like progeria, resulted in the deterioration of bundles of DNA known as heterochromatin.

The discovery, made possible through a combination of cutting-edge stem cell and gene-editing technologies, could lead to ways of countering age-related physiological declines by preventing or reversing damage to heterochromatin.

The top image shows normal human cells (left) and genetically modified cells developed by the Salk scientists to model Werner syndrome (right), which showed signs of aging, including their large size.

“Our findings show that the gene mutation that causes Werner syndrome results in the disorganization of heterochromatin, and that this disruption of normal DNA packaging is a key driver of aging,” says Juan Carlos Izpisua Belmonte, a senior author on the paper. “This has implications beyond Werner syndrome, as it identifies a central mechanism of aging–heterochromatin disorganization–which has been shown to be reversible.”

Werner syndrome is a genetic disorder that causes people to age more rapidly than normal. It affects around one in every 200,000 people in the United States. People with the disorder suffer age-related diseases early in life, including cataracts, type 2 diabetes, hardening of the arteries, osteoporosis and cancer, and most die in their late 40s or early 50s.

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The disease is caused by a mutation to the Werner syndrome RecQ helicase-like gene, known as the WRN gene for short, which generates the WRN protein. Previous studies showed that the normal form of the protein is an enzyme that maintains the structure and integrity of a person’s DNA. When the protein is mutated in Werner syndrome it disrupts the replication and repair of DNA and the expression of genes, which was thought to cause premature aging. However, it was unclear exactly how the mutated WRN protein disrupted these critical cellular processes.

"Accumulated alterations in the structure of heterochromatin may be a major underlying cause of cellular aging. This begs the question of whether we can reverse these alterations–like remodeling an old house or car–to prevent, or even reverse, age-related declines and diseases."

In their study, the Salk scientists sought to determine precisely how the mutated WRN protein causes so much cellular mayhem. To do this, they created a cellular model of Werner syndrome by using a cutting-edge gene-editing technology to delete WRN gene in human stem cells. This stem cell model of the disease gave the scientists the unprecedented ability to study rapidly aging cells in the laboratory. The resulting cells mimicked the genetic mutation seen in actual Werner syndrome patients, so the cells began to age more rapidly than normal. On closer examination, the scientists found that the deletion of the WRN gene also led to disruptions to the structure of heterochromatin, the tightly packed DNA found in a cell’s nucleus.

This bundling of DNA acts as a switchboard for controlling genes’ activity and directs a cell’s complex molecular machinery. On the outside of the heterochromatin bundles are chemical markers, known as epigenetic tags, which control the structure of the heterochromatin. For instance, alterations to these chemical switches can change the architecture of the heterochromatin, causing genes to be expressed or silenced.

The Salk researchers discovered that deletion of the WRN gene leads to heterochromatin disorganization, pointing to an important role for the WRN protein in maintaining heterochromatin. And, indeed, in further experiments, they showed that the protein interacts directly with molecular structures known to stabilize heterochromatin–revealing a kind of smoking gun that, for the first time, directly links mutated WRN protein to heterochromatin destabilization.

“Our study connects the dots between Werner syndrome and heterochromatin disorganization, outlining a molecular mechanism by which a genetic mutation leads to a general disruption of cellular processes by disrupting epigenetic regulation,” says Izpisua Belmonte. “More broadly, it suggests that accumulated alterations in the structure of heterochromatin may be a major underlying cause of cellular aging. This begs the question of whether we can reverse these alterations–like remodeling an old house or car–to prevent, or even reverse, age-related declines and diseases.”

Izpisua Belmonte added that more extensive studies will be needed to fully understand the role of heterochromatin disorganization in aging, including how it interacts with other cellular processes implicated in aging, such as shortening of the end of chromosomes, known as telomeres. In addition, the Izpisua Belmonte team is developing epigenetic editing technologies to reverse epigenetic alterations with a role in human aging and disease.

SOURCE  Salk Institute for Biological Studies

By 33rd Square

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 Cancer  

A new breakthrough study has shown that pancreatic cancer cells can be reverted back to normal cells by introducing a controlling protein. The work may open the door to controlling the deadly disease.

Anew research study has shown that pancreatic cancer cells can be coaxed to revert back toward normal cells by introducing a protein called E47. E47 binds to specific DNA sequences and controls genes involved in growth and differentiation.

"For the first time, we have shown that overexpression of a single gene can reduce the tumor-promoting potential of pancreatic adenocarcinoma cells and reprogram them toward their original cell type. Thus, pancreatic cancer cells retain a genetic memory which we hope to exploit," said Pamela Itkin-Ansari, Ph.D., adjunct professor in the Development, Aging, and Regeneration Program at Sanford-Burnham and lead author of the study published in the journal Pancreas.

"For the first time, we have shown that overexpression of a single gene can reduce the tumor-promoting potential of pancreatic adenocarcinoma cells and reprogram them toward their original cell type."

In vivo studies showed that when the reprogrammed cancer cells were introduced into mice, their ability to form tumors was greatly diminished compared to untreated adenocarcinoma cells.

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"Presently, pancreatic adenocarcinoma is treated with cytotoxic agents, yet the average survival for patients post-diagnosis is merely six months, and the improvements in therapies are measured in days," said Andrew M. Lowy, M.D., professor of surgery at the UC San Diego Moores Cancer Center and co-chair of the National Cancer Institute's Pancreatic Cancer Task Force.

"The finding that we can differentiate these cancer cells back to a non-threatening phenotype is encouraging. Indeed, there is a precedent for cell differentiation therapy in that the approach has been used to treat acute promyelocytic leukemia (APL) and some neuroblastomas successfully."

"Our next step is to test primary patient-derived tumor tissue to determine whether E47 can produce similar results, potentially providing a novel therapeutic approach to combat this highly lethal disease," said Itkin-Ansari. "Additionally, we are screening for molecules—potential drugs—that can induce overexpression of E47."

Pancreatic adenocarcinoma is the most common form of pancreatic cancer. It's primarily caused by a mutation in the oncogene called Kras that causes the digestive enzyme-secreting cells (acinar cells) to differentiate into a destabilized duct-like cell type, which is cancerous. The disease is often called a "silent" cancer because it rarely shows early symptoms—it tends to be diagnosed at advanced stages when it causes weight loss, abdominal pain, and jaundice.


SOURCE  Sanford-Burnham Medical Research Institute via NewsWise

By 33rd Square

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Medicine  

A new cancer treatment shows great promise as an alternative cancer surgery. The Edge Radiosurgery Suite offers an equal or greater accuracy level in targeting tumors, but with the ability to treat multiple tumors simultaneously.

A

n exciting new cancer treatment has been developed that shows great promise as an alternative cancer surgery. The Edge Radiosurgery Suite offers an equal or greater accuracy level in targeting tumors, but with the ability to treat multiple tumors simultaneously and with greater comfort to patients.

High Precision

The Edge Radioactive Suite is able to perform cutting edge, non-invasive procedures on any part of the body--including the brain, head and neck, spine, adrenal gland, pancreas, liver, and lung—with a high degree of precision and very low toxicity. The Edge, developed by Varian Medical Systems, employs tumor tracking capability in real time to improve safety and comfort for patients. The technology is safer and more comfortable because of the precise way it targets tumors, while sparing healthy surrounding tissue.

Targeted Treatment

Stereotactic radiation delivers a precision dose of intense radiation to targeted tumors in up to five treatments. The goal is to render the tumor inactive or destroyed, while minimizing exposure to healthy, neighboring tissue. The Edge offers patients faster treatment using dose rates up to 2,400 monitor units each minute. It also delivers rapid stereotactic treatments in only 15 minutes, in contrast to other techniques that may take over one hour per session.

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Greater Patient Comfort

Increased comfort for patients is achieved using a six degrees of freedom treatment couch and offering the flexibility and precision to precisely adjust and position patients. An imaging specialist with a degree in Radiology says the Edge has an advanced imaging system which compensates for any tumor movement in the course of the treatment. Additionally, the Edge can do most of what a proton beam treatment method is able to do, at a fraction of the cost.

Test Driving the System

Henry Ford Hospital in Detroit was the first in North America to have the Edge. The hospital tested the procedure by comparing it to frame-based radiosurgery systems. All components of the system were utilized to localize targets. The study found that the locational accuracy was inside 0.9 mm for one target and 1.2 mm for multiple targets.

The Edge is a novel platform for radiosurgery that offers a technique for providing a completely integrated solution for administering and planning radiosurgery treatments. Since accuracy matters greatly in this field, The Edge suite is groundbreaking in calibrating for sub-millimeter accuracy and precisely targeting cancerous tumors, while leaving surrounding healthy tissue untouched. The result is a lower-cost treatment that also reduces patient recovery times.

By Emma Sturgis

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Author Bio - Emma is a freelance writer currently living in Boston, MA. She writes most often on education and technology. When not writing, she enjoys watching old movies and indoor rock climbing.