Category Archives: Press Releases

First proven ovarian cancer origin could unlock earlier detection in many human cancers

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A very large ovarian cancer as seen on CT

The most common and aggressive type of ovarian cancer, ovarian carcinoma, leaves a dark trail. Science has learned too little and most women learn too late to treat the deadly disease.

Cornell scientists have found ovarian carcinoma’s first proven origin cells and uncovered clues for finding similar sources of other cancers. Published in Nature in March 2013, the study opens paths for new screening methods to detect cancer earlier and increase treatment chances in the ovaries and beyond.

Most organs have stem-cells, which help healing and development, but many cancers start when such cells go astray. Using a novel cell location technique never before used in ovaries, the Cornell study uncovered a nest (niche) of particularly cancer-prone stem cells at an area in the ovaries where different tissue types meet. It provides the most direct proof yet that vulnerable stem cells can nest near such tissue junctions, which occur throughout the body.

“Poor understanding of ovarian cancer’s development has posed the biggest roadblock to helping its victims,” said Dr. Alexander Nikitin, pathology professor at Cornell’s College of Veterinary Medicine and leader of the Cornell Stem Cell Program. “We have found what is very likely to be the source of cells from which ovarian carcinoma arises, as well as the strongest suggestion yet that cancer-prone stem cells can nest in tissue junctions. This could spur new discoveries of cancer-prone stem cell niches throughout the body, revealing new ways to screen for and diagnose several different cancers.”

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Stem cells expressing stem cell marker ALDH1 (red) and retaining proliferation label BrdU (green) in the hilum region of the ovary

A woman’s risk of getting aggressive ovarian cancer in her lifetime is about 1 in 72, according to the American Cancer Society. Once diagnosed, 70% will die within five years. No good screening tests exist, but uncovering a specific location that seeds it could let people catch it earlier and change those chances for the better.

Nikitin’s lab found the new cancer-prone stem cell niche using direct lineage tracing, a new technique that labels and tracks cells. The niche, found near the junction of the ovaries and the uterine tube (also known as the Fallopian tube), houses stem cells that regenerate the ovarian surface epithelium, a cover that opens when females ovulate and must grow back each time.

But Nikitin’s team found that these cells turned cancerous when two important tumor suppressor genes p53 and Rb were deleted. These genes have been shown to be inactive in human ovarian carcinoma. Nikitin’s lab had previously proven that properly functioning p53 and Rb protected against ovarian carcinoma development in the mouse.

The new study showed that newly discovered stem cells without p53 and Rb grew faster and showed more aggressive metastatic behavior compared to more mature cells. Nikitin is now working on leveraging his lab’s discoveries to find cancer-prone stem cells at similar junction areas in human ovaries and other places where two different types of tissue converge, such as the esophagus and stomach, anus and rectum, and different parts of the uterus. Such junctions are breeding grounds for tumors.

“Until now, we have had no explanation for why so many tumors form at junction sites,” said Nikitin. “Our study suggests new undiscovered stem cell niches might occur beyond the ovaries. It’s likely to lead scientists to search for similar cancer-prone stem cell niches at other junctions, which could lead to specific diagnostic screening tests to detect cancers earlier.”

Published 3/7/13

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New Salmonella Dublin test for milk and cattle available for first time in US

Salmonella can cause serious disease on cattle farms, killing calves, causing cows to abort, contaminating raw milk, and harming humans along the way. While the cattle-adapted strain Salmonella Dublin creeps into the Northeastern US, veterinarians and farmers struggle to catch the bacteria in time to protect livestock because these bacteria often hide dormant in carrier animals, making the strain particularly hard to diagnose.

For the first time in the US, a more useful test for Salmonella Dublin is now available exclusively at the Cornell University College of Veterinary Medicine’s Animal Health Diagnostic Center (AHDC). Cheaper, quicker, safer, and more sensitive, the test detects antibodies rather than bacteria. Traditional bacteriological tests could only identify S. Dublin organisms in sick or deceased animals, missing up to 85% of infections in carrier cattle. The new test reveals carriers, helping farmers and veterinarians monitor infection spread over time and track the impact of control measures in ways that were previously impossible.

Dairy-cows-Pavement“We’re very concerned about this disease spreading east because it could severely harm animal and human health, as well as the livelihoods of dairies in the region,” said Dr. Belinda Thompson, senior extension associate at the AHDC. “Salmonella Dublin is already common west of the Mississippi River, but it’s only recently being recognized in the Northeastern US. We want to be pro-active now to keep it out of our farms.”

In recent years the AHDC has dealt with several high-morbidity and high-mortality outbreaks of Salmonella Dublin in New York and other states. To address the problem before it grows further, Dr. Bettina Wagner, director of the Serology and Immunology Section of the AHDC laboratory, secured the nation’s first USDA permit to import and use the enhanced test.

While Salmonella Dublin usually doesn’t make adults cows very sick, it can wreak havoc on young and unborn calves, particularly in populations like those in the East Coast that haven’t been exposed. Its resistance to many common antibiotics severely limits treatment options and, to make matters even worse, it often presents as respiratory disease, throwing off track veterinarians trained to recognize diarrhea as salmonella’s telltale sign.

“Infected calves often look fine the day before a sudden rapid onset, the next day they look depressed, and the next day they die,” said Dr. Paul Virkler, senior extension associate at the AHDC. “Veterinarians often think it’s something else-. We’ve seen newly infected herds in which every single calf in a particular age group dies. We’re trying to keep this from getting to baby calves, the life and future of a farm, and the animals most at risk.”

People working with cattle are also at risk. All Salmonella strains affect most vertebrates and can jump between species. Even carriers that don’t seem sick can shed bacteria, and people, companion animals, and other livestock can pick up the infection through contact with any bodily excretion.

“People have died drinking raw milk with Salmonella Dublin,” said Virkler. “It’s one of the bad players in raw milk. Pasteurizing milk will kill the bacteria.”
Prior to the new test’s release, testing had to be done animal by animal. The new antibody test can use milk samples straight from bulk milk tanks to find whether a herd has been exposed. It can also work with blood samples and diagnose individuals, helping keep unexposed herds infection-free by removing infected animals and pre-screening new animals farmers are considering buying.

“Herd managers can take preventative measures and help control the infection’s spread by isolating sick calves, pasteurizing milk, managing cattle movement, and improving hygiene,” said Thompson. “But to see if any of this is working, they need a tool to monitor success. We didn’t have that until now. This test will let us learn about the prevalence of Salmonella Dublin on the East Coast and hopefully nip it in the bud.”
cows in field

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http://vet.cornell.edu/news/Dublin.cfm

Media Hits:

Cornell Chronicle

http://www.news.cornell.edu/stories/Oct12/SalmonellaDublin.html

Meat Trade News Daily

http://www.meattradenewsdaily.co.uk/news/291112/usa___a_lack_of_understanding_over_salmonella_.aspx

MyScience

http://www.myscience.us/wire/cornell_offers_only_u_s_salmonella_dublin_test_for_cattle-2012-cornell

The Post Standard: Syracuse.com

http://blog.syracuse.com/farms/2012/11/better_test_for_cattle_disease.html

Phys.org

http://phys.org/news/2012-11-cornell-salmonella-dublin-cattle.html

Drovers CattleNetwork.com

http://www.cattlenetwork.com/cattle-news/Cornell-offers-only-US-salmonella-dublin-test-for-cattle-176821551.html?ref=551

Bovine Veterinarian Online

http://www.bovinevetonline.com/news/industry/Cornell-offers-only-US-salmonella-dublin-test-for-cattle-176821551.html

USAgNet

http://www.usagnet.com/story-national.php?Id=2486&yr=2012

Dairy Herd Network

http://www.dairyherd.com/dairy-news/latest/Cornell-offers-only-US-salmonella-dublin-test-for-cattle-176821551.html

Food Safety News

http://www.foodsafetynews.com/2012/11/cornells-new-test-spots-salmonella-in-cattle/

Ithaca Journal

http://www.theithacajournal.com/article/20121111/NEWS01/311110027/Cornell-test-detects-salmonella-cattle?odyssey=mod|newswell|text|FRONTPAGE|p

Before It’s News

http://beforeitsnews.com/food-and-farming/2012/11/cornells-new-test-spots-salmonella-in-cattle-2446024.html

Healthy Cooking News

http://healthycookingnews.blogspot.com/2012/11/cornells-new-test-spots-salmonella-in.html

Beef Cattle News

http://savant7.com/beefcattlenews/

Stop Foodborne Illness

http://www.stopfoodborneillness.org/content/cornell%E2%80%99s-new-test-spots-salmonella-cattle

MeatingPlace

http://webcache.googleusercontent.com/search?q=cache:lnLu6SjDDeMJ:www.meatingplace.com/Industry/News/Details/37578+&cd=2&hl=en&ct=clnk&gl=us

Highbeam Business

http://business.highbeam.com/409224/article-1G1-310739927/cornell-offers-new-salmonella-test-cattle

CABI.org VetMed Resource

http://www.cabi.org/VetMedBeta/news/22617

The Meat Site

http://www.themeatsite.com/meatnews/19365/cornell-offers-us-salmonella-dublin-test-for-cattle

Surprise packages sent by cancer cells can turn normal cells cancerous

Surprise packages sent by cancer cells can turn normal cells cancerous, but Cornell scientists have found a way to keep their cargo from ever leaving port. Published in Oncogene in January 2012, their study demonstrates the parcels’ cancer-causing powers, describes how they are made, and reveals a way to jam production. Treatments that follow suit could slow tumor growth and metastasis, the spread of cancer to new parts of the body.

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A cancer cell (bottom right) producing and shedding microvesicles, which travel between cells and attach to a normal cell (upper left) to unload cancerous cargo

Remote recruiting through inter-cellular mail lets cancer cells grow their ranks without having to move. While most cells communicate through a standard postal system of growth factors and hormones, cancer cells and stem cells use bulkier parcels called microvesicles. These big packages are stuffed with unconventional cargo that boosts the survival and growth rates of recipient cells and can dramatically alter their behavior and surrounding environment. The cargo of microvesicles includes unique sets of proteins that often reflect their cell of origin and are capable of completely changing a cell’s form and function.

“Stem cells make microvesicles containing one set of proteins that can help heal damaged tissue, while cancer cells make malignant microvesicles called oncosomes that contain another set of proteins which facilitate the growth and spread of tumors,” said Dr. Richard Cerione, professor at the College of Veterinary Medicine and co-author.

Dr. Marc Antonyak and graduate student Bo Li, co-authors and researchers in Cerione’s lab, examined cells in culture to observe the effects of oncosomes on normal cells. They focused on fibroblasts, a normal cell type that is often found associated with human tumors and helps to facilitate tumor growth.
“We incubated healthy fibroblasts together with aggressive breast cancer cells,” said Antonyak. “Although we’d disabled the cancer cells from forming tumors on their own, they kept pumping out oncosomes. The fibroblasts that were bathed in these oncosomes began turning cancer-like, living longer, growing faster, and forming tumors.”

Using a variety of techniques to parse out participating proteins, including immunoblot analysis, immunofluorecence, and electron microscopy imaging, Antonyak identified each link in this pathway and traced it back to the first: a protein called RhoA that acts like a lever initiating microvesicle production. Cancer cells crank production into overdrive, said Antonyak, but jamming the lever could stop the whole assembly line.

“Even if we immobilize cancer cells, as long as they can make these microvesicles they can continue spreading vital components for the development of cancer,” said Cerione. “It’s clear that microvesicles can change the behavior of cells and play an important part in cancer progression. Treatments targeting the microvesicle production pathway we’ve outlined could have a real impact on slowing cancer progression.”

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http://vet.cornell.edu/news/CancerCargo.cfm

 

First total knee-replacement surgery restores young dog’s active life at Cornell

jake-copy_000James Gillette has two passions: hunting and his dog. In an effort to spend time with both, he has dedicated years to training Jake, his chocolate lab, how to retrieve game. Often described as inseparable, Gillette and Jake were just as likely to be wandering through wetlands as they were to be at home until travesty hit both.

In the summer of 2010, Gillette fell so ill that when Jake ran in front of a truck and fractured his knee, it was several weeks before Gillette was well enough to get Jake to a veterinarian. When Jake later arrived at the Cornell University Hospital for Animals (CUHA), he was unable to put any weight on the leg and it looked like it might have to be amputated.
In a first-ever surgery at Cornell, Assistant Professor of Surgery Dr. Ursula Krotscheck and an orthopedic surgeon from Ohio State University led a team of CUHA residents in a total knee replacement surgery, a relatively novel procedure never before performed at Cornell. The surgery team removed pieces of bone around Jake’s knee and constructed components to recreate the joint, giving Jake a second chance at an active life.

jakedog055-copySoon after the surgery in Spring 2011, Jake walked home by Gillette’s side using all four legs.

“Jake has recovered extremely well from what in most cases would have been a crippling injury,” said Krotscheck. “We are one of only five teaching hospitals that have performed this procedure. Our team and Jake’s resilience all contributed to making our first canine knee replacement a success.”

Now a year post-surgery, Jake recently passed his first anniversary check-up with flying colors.

“Look at him run!” said Gillette as he tossed Jake’s favorite toy, spurring the eager retriever into a full sprint. “He’s happy as ever and his leg is like new. Before the surgery he wasn’t using it at all. Now we’re playing and hunting together again.”

jakedog035-copy_000jakedog096_000

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College of Veterinary Medicine News
http://vet.cornell.edu/news/Jake.cfm

First discovery of cells expelling mitochondria uncovers newfound survival tactic

An ancient union between cell and organelle has shown the first sign of fracture, challenging common conceptions of a primordial partnership all multicellular organisms rely on to live. Cornell researchers have recorded the first direct evidence of cells expelling intact mitochondria, the cellular machinery responsible for energy production.

AAAmitochondria B

An illustrated mitochondrion

Malfunctioning mitochondria produce free-radicals that damage cells, contributing to aging, mitochondrial myopathies, and disorders ranging from schizophrenia, bipolar disorder, and dementia to Parkinson’s disease and multiple sclerosis. The newfound breakup behaviour, described in Mitochondrion 2011 Nov.11(6), may be an early cell-survival strategy to escape the toxic effects of damaged mitochondria.

“It is very surprising to see living cells actively jettisoning vital parts of themselves,” said Dr. Theodore Clark, immunologist at the College of Veterinary Medicine. “This is the first time full mitochondria have been found outside cells and it may account for 15 years’ worth of unexplained data showing mitochondrial DNA and protein in extracellular spaces. We think these cells’ behaviour reveals a newfound survival tactic deeply rooted in evolution.”

Today’s mitochondria evolved from freewheeling bacteria that settled down in other cells two billion years ago. In exchange for food and shelter, the bacteria helped cells break nutrients into energy. These helpful tenants became modern mitochondria: the power-plants inside all cells of nearly every animal, plant, fungus, and protozoan.

Yet domestic disputes over cellular housekeeping may spur divorce, according to findings from Clark’s lab showing mitochondria moving out.

Graduate student Yelena Bisharyan discovered this while studying an unrelated phenomenon: escape stunts of the fish parasite Ichthyophthirius multifiliis. Clark’s lab had observed these parasitic protozoa avoiding destruction by shaking off attacking antibodies and exiting their hosts and wanted to see how they escaped.

“Attacking antibodies bind to the parasite’s cell surface,” said Clark. “We suspected that when antibodies attach, the parasite can shed them by breaking off its surface proteins – sort of like a lizard shedding its tail.”

tetrehymena 2

Tetrahymena, a protozoan, sheds proteins and mitochondria in response to attacking antibodies

Applying antibodies to parasites in culture, Bisharyan observed the reactions of Ichtyophthirius and Tetrahymena, another ciliated protozoan used as a model system to study fundamental biological principles across species.

Using negative staining and electron microscopy techniques, Bisharyan recorded parasites sacrificing their surface proteins to rid themselves of attached antibodies. Yet her images also captured something completely unexpected: intact and fragmented mitochondria coming out of the parasite’s cells.

This surprising finding won Bisharyan an invitation to present at one of the 2011 Gordon Research Conferences, a prestigious international forum showcasing major discoveries across scientific fields.

“Mitochondria experts were very excited to see this,” said Clark. “Over the past 15 years several papers have reported mitochondrial DNA and proteins floating outside mammalian cells. No one knew how or why they got there. What we’ve found in protozoa may help explain similar processes in mammals.”

Mitochondria (m) are pushed to the surface and jettisoned from the cell

mitochondria shed

Mitochondria (red) discovered outside cells

Certain cellular stressors can trigger mitochondrial expulsion, according to Bisharyan’s study. In protozoa, for example, not only antibodies but also heat shock can induce this effect. These stressors elevate calcium levels within the cell, possibly damaging mitochondria and causing them to produce toxic free-radicals.

“Our hypothesis is that mitochondria become poisoned and these protozoa have found a way to rid themselves of the damaged powerplants before they can cause further harm,” said Clark. “We think their behaviour reveals an early adaption to cellular stress that other species may share.”

Mammals and fish parasites may bear little family resemblance these days, but a common ancestor may have equipped both with emergency mitochondria-removal systems. Understanding this process could illuminate new approaches to reducing mitochondria-induced damage in humans and other animals.

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Cornell University College of Veterinary Medicine news

http://vet.cornell.edu/news/Mitochondria.cfm

Researchers discover what cancer cells need to travel

Feb. 21, 2012

Cancer cells must prepare for travel before invading new tissues, but new Cornell research has found a possible way to stop these cells from ever hitting the road.

Researchers have identified two key proteins that are needed to get cells moving and have uncovered a new pathway that treatments could block to immobilize mutant cells and keep cancer from spreading, says Richard Cerione, Goldwin Smith Professor of Pharmacology and Chemical Biology at Cornell’s College of Veterinary Medicine.

The study, co-authored by graduate student Lindsey Boroughs, Jared L. Johnson, Ph.D. ‘11, and Marc Antonyak, senior research associate, is published in the Journal of Biological Chemistry (286:37094-37107)

Most adult cells stay stationary, but the ability for some to move helps embryos develop, wounds heal and immune responses mobilize. When migrating cells go astray they can cause developmental disorders, ranging from cardiovascular disease to mental retardation. Metastasis (the spread of cancer from one part of the body to another) also relies on cell migration. How exactly cancer cells migrate
and invade tissues continues to be a mystery. However, Cerione’s lab uncovered a potentially important clue when it noticed that cancer cells gearing up to move would collect a protein called tissue transglutaminase (tTG) into clusters near the cell membrane.

meta“TTG is turning up in many aspects of human cancer research and seems to be contributing to the process that turns cells cancerous,” said Cerione. “Lindsey and Marc discovered that cells must gather tTG into a specific place in their membrane before they can move. But tTG is usually inactive, and we’ve been trying to understand how a cell gets this protein to the exact right place so that it can be activated to stimulate cell migration.”

Observing breast-cancer cells in culture, Cerione’s lab found a missing link in our understanding of cell migration: Cancerous cells become hyperactive invasion vehicles by using tTG together with other proteins like wheels, poking them through the surface to form a “leading edge” that pulls the cell forward. But to get the wheels to the leading edge, it turns out they need another protein to roll them there – a “chaperone” protein called heat-shock-protein-70 (Hsp70).

“We’ve known for years that Hsp70 acts as a chaperone to other proteins, ensuring that they assume the right structure and behave properly when a cell is under stress,” said Cerione. “Heat shock proteins have also been implicated in cancer, although scientists have been trying to understand their exact role in cancer. Our research has uncovered a previously unknown role for these chaperones – helping tTG get to the leading edge. TTG must be in this location for cancer to spread.”

migrating cervical cancer cell

A migrating cervical cancer cell stained for tissue transglutaminase (green). Cells must gather this protein at their leading edge in order to move.

When cells become stressed, Hsp70 influences the behavior of their “client” proteins, ensuring they keep the right shape. Cells need chaperones like Hsp70 to ensure that various proteins work correctly and don’t warp, but these same chaperones can help cancer cells spread by helping move tTG to the membrane surface. Using inhibitors that block the function of chaperones, Cerione and his team paralyzed Hsp70s and stopped breast cancer cells in culture from gathering tTG into a leading edge, effectively immobilizing them.

Exactly how Hsp70 gets tTG going remains unknown, but Cerione believes other proteins are involved.

“If we can better understand how Hsp70 influences tTG, we can figure out ways to modulate that interaction to immobilize cancer cells and keep them from becoming invasive,” said Cerione. “We suspect Hsp70 is using a third kind of protein to move tTG, and that’s what we’re trying to figure out now. Finding the next link in this chain of events could have important consequences for preventing cancer migration and metastasis.”

Carly Hodes ’10 is a communication specialist at the College of Veterinary Medicine.

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Original Press Release:

Cornell University College of Veterinary Medicine news

http://www.vet.cornell.edu/news/Migration.cfm

Media Hits:

Cornell Chronicle

http://www.news.cornell.edu/stories/Feb12/CancerMovers.html

Ithaca Journal

http://www.theithacajournal.com/article/20120222/LIFE/202220336/Cornell-scientists-find-cancer-cells-need-travel?odyssey=mod|newswell|text|Life|s

PhysOrg

http://www.physorg.com/news/2012-02-cancer-cells.html

ECNMag

http://www.ecnmag.com/News/Feeds/2012/02/blogs-the-cutting-edge-researchers-discover-what-cancer-cells-need-to-tra/

Zeit News

http://www.zeitnews.org/biotechnology/researchers-discover-what-cancer-cells-need-to-travel.html

My Science

http://www.myscience.cc/news/2012/what_cancer_cells_need_to_travel-2012-cornell

Reddit

http://www.reddit.com/r/science/comments/q0swt/cancer_cells_must_prepare_for_travel_before/

Laboratory Equipment

http://www.laboratoryequipment.com/news-Proteins-Key-to-Stopping-Cancer-from-Spreading-022312.aspx

How unchecked alarms can spark autoimmune disease

November 29, 2011

A white blood cell engulfs an invading Bacillus anthracis

A neutrophil (yellow), the most abundant white blood cell type and the first line of defense against invading microbes, engulfs Bacillus anthracis (orange), the agent of anthrax. The bacteria break down, releasing DNA that triggers an immune response.

One in five Americans suffers from autoimmune disease, in which the immune system goes off-track and attacks the body’s own cells. Cornell researchers have identified a signaling mechanism in immune-system cells that may contribute to this mistake, opening the door for possible new therapies for autoimmune diseases such as lupus and arthritis.

Cynthia Leifer, assistant professor of microbiology and immunology in the College of Veterinary Medicine, and colleagues described the mechanism in the August issue of the European Journal of Immunology. The problem lies in what are called innate immune cells, the first responders to infection.

“Innate immune cells have internal watchdogs called TLR-9 receptors that set off alarms whenever they encounter invaders,” said Leifer. “They look for general classifying patterns [in DNA] to determine whether something is a virus, bacterium, protozoan, or part of self.”

However, some of these patterns exist both in invading organisms and the body’s own cells, so mistakes can arise.

Cynthia Leifer

Leifer

“We are mapping the critical regulatory mechanisms that keep these receptors from responding to self-DNA so that we can know if and how they predispose people to autoimmune disorders when they fail,” Leifer said.

Innate immune cells engulf things that look dangerous, tear them open, and release their components, including DNA. When TLR-9 receptors see DNA that identifies microbes, they send a signal to fire up more immune-system activity, including inflammation and the creation of antibodies. But before a receptor can work, enzymes in the cell must prepare it by chopping off part of the receptor molecule and leaving a part that can bind to microbe DNA.

From there, Leifer believes it’s a numbers game. If too many receptors are prepared, they may respond to the small amount of self-DNA that makes its way into immune cells, triggering an autoimmune response. So the immune cell has a regulatory mechanism, an enzyme pathway that cuts prepared receptors in a second place.

Working with cells in culture, Leifer identified this second chopping event, which cuts TLR-9 at a different site. This produces a molecule that binds to DNA, blocking it from reaching the prepared receptors, and does not send a signal.

“People without autoimmune diseases have the right balance of these two chopping events,” Leifer said. “Our studies suggest that people with a propensity for these diseases might have a defect in this pathway that allows more prepared receptors to signal for immune responses. This may be a potential target for therapies designed to help quiet those alarms.”

A second but interrelated problem Leifer has tackled involves how TLR-9 moves through an immune cell from the placewhere it is created to its working site. In earlier work she described the protein sequences in TLR-9 that act as address labels guiding where the receptor travels.

“We think they’re interrelated because if you don’t travel properly you don’t get chopped properly,” she said. “If TLR-9 ends up in the wrong place at the wrong time, it can sound a false alarm.

Leifer’s research is supported by the National Institutes of Health.

Carly Hodes ’10 is a communication specialist at the College of Veterinary Medicine.

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Original Press Release:

Cornell University College of Veterinary Medicine news

http://www.vet.cornell.edu/news/leifer.cfm

 

Media Hits:

Cornell Chronicle

http://www.news.cornell.edu/stories/Nov11/LeiferDNA.html

Medical Xpress (PhysOrg)

http://medicalxpress.com/news/2011-11-unchecked-alarms-autoimmune-disease.html

MyScience

http://www.myscience.us/wire/how_unchecked_alarms_can_spark_autoimmune_disease-2011-cornell

Bionity

http://www.bionity.com/en/news/135431/how-unchecked-alarms-can-spark-autoimmune-disease.html

R&D Mag

http://www.rdmag.com/News/Feeds/2011/11/general-sciences-how-unchecked-alarms-can-spark-autoimmune-disease/

ECN

http://www.ecnmag.com/News/Feeds/2011/11/blogs-the-cutting-edge-how-unchecked-alarms-can-spark-autoimmune-disease/

Futurity

http://www.futurity.org/top-stories/false-alarm-can-spark-autoimmune-disease/