Now, new research from the Sehgal lab is taking a peek inside, describing a molecular pathway and its inner parts that connect the well-known clock neurons to cells governing rhythms of rest and activity in fruit flies. Sehgal is also an investigator with the Howard Hughes Medical Institute.

The other co-author on the study is Wenyu Luo, PhD, a Penn doctoral student who recently defended her dissertation. The findings, which will be featured on the cover of the February 17th issue of Cell, are published on-line this week.

“Most colleagues would state that we have some understanding of how the clock works and how it is synchronized with light,” states Sehgal. “But we are just beginning to get a glimpse of how the clock drives behavior in the rest of an organism’s systems.”

Normally, flies have a robust rhythm of being active during daylight hours and quiet during the night. Sehgal and Luo essentially found that a microRNA (miRNA) named miR-279 acts through the JAK/STAT pathway to regulate locomotor activity rhythms through a daily cycling of proteins.

An miRNA is a tiny piece of RNA — a tiny over 20 bases (DNA building blocks) in length — that binds to matching pieces of messenger RNA, thereby tying it up and decreasing the production of the corresponding protein.

They found that in mutant flies in which miR-279 was either overexpressed or deleted — causing high levels or low levels of JAK/STAT signaling — the flies wake and sleep at random intervals. The flies showed no discernible pattern of activity. Therefore, the investigators concluded that a mid-range level of JAK/STAT activity is necessary to maintain the flies’ normal pattern. In fact, they found that STAT activity displays a daily rhythm.

Oscillations of the clock protein PERIOD are normal in clock pacemaker neurons lacking miR-279, suggesting that miR-279 acts downstream of the clock neurons. The team identified the JAK/STAT partner, a protein called Upd, as a target of miR-279. They also showed that knocking down Upd rescues the off-rhythm behavior of the miR-279 mutant flies.

In addition, in brains of mutant flies stained to identify circadian proteins, they found that the central clock neurons project their axons into the vicinity of Upd-expressing neurons, providing a possible physical connection by which the central clock could regulate JAK/STAT signaling to control rest and activity rhythms.

With these findings, the team proposed a model in which the central clock affects the cycle of secretion of the Upd protein from cells. “Upd may act like a time-release capsule,” explains Sehgal. “To maintain a typical rest:activity rhythm, the level of Upd has to be just right.”

The mRNA levels of Upd in neurons are kept low by miR-279. Upd may rhythmically activate a receptor, Dome, in a third cell, which would lead to daily oscillations of JAK/STAT activity and ultimately to the rest:activity rhythm.

The direct clinical implications of knowing the players in this complicated pathway are not yet clear. But we might be able to conclude, suggests Sehgal, that, if these mechanisms are conserved in humans, then disorders in which the JAK-STAT pathway is not working properly, as in some immune disorders, doctors might also see problems with patients’ sleep-wake cycle. These findings also provide researchers with a handle on the neural circuit that generates rest:activity behavior in Drosophila. The ultimate goal of many neurobiologists is to trace the entire molecular and cellular pathway that produces a specific behavior. This study is a step towards that goal.

The work was supported by NIH allows 1-R560NS-048471 and 2R01NS04847.

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source : www.sciencedaily.com

The provincial government states 8,000 New Brunswickers are getting their medicare cards late because of a money-saving Christmas shut down that is now being reassessed for next year.

The office that processes the cards for the Department of Health closed for an extra five days over the holidays and many peoples’ cards expired before their new ones arrived.

“We think that that may have caused a bit of backlog for us, so we have been really catching up,” stated Lyne St-Pierre-Ellis, the assistant deputy minister for medicare.

People who have not received their cards will get them soon, she said.

In the meantime, they will either get medical care without charge, or will be reimbursed, stated St-Pierre-Ellis.

‘We may have to go to government and say, ‘We cannot do that next year because it causes too much problems.”—Lyne St-Pierre-Ellis, assistant deputy minister for medicare

The department is also re-evaluating whether to shut down the office for five days again this Christmas, she said.

“We may have to look at the impact that the closure did have and see if we can do that again next year. We may have to go to government and say, ‘We cannot do that next year because it causes too much problems.’ So we are going to be looking at it over the next 11 months.”

St-Pierre-Ellis was responding to concerns raised by a Fredericton woman and her husband about why the government is months behind schedule in renewing their medicare cards.

The Department of Health announced last March that it was experiencing delays in processing new medicare cards, but almost a year later, Glennis Arsenault and her husband, Terry, are still experiencing delays.

Arsenault stated she, her husband and son all sent in the paper work to have their cards renewed in November. Their son received his new card in December, but their cards still have not shown up.

Glennis Arsenault stated her card is now expired and she’s left questioning what will happen if she has to suddenly go to the hospital or a health-care clinic.

“It just leaves a lot of uncertainty there as to if something comes up, what will happen. And just because the way the process has gone, am I even going to get it in two or three weeks?” she said.

“This has been going on for over two months and if there is that backlog, then maybe somebody should be looking into this and finding out, and I don’t know, are we the only ones?”

Arsenault stated a department official told her that her card was being produced outside of the province and it should arrive in the mail in the next few weeks.

Delays ‘unacceptable,’ states Opposition

Opposition health critic Bill Fraser calls the delays “unacceptable.”

“We raised this issue in the legislature almost a year ago and the minister of health stated it would only be a matter of weeks before it was resolved,” Fraser stated in a news release. “Ten months later and people are still experiencing delays, but to make matters worse, the government is offering tiny help, support, or even information to people in the meantime,” he said.

Last March, Health Minister Madeleine Dubé estimated that 1,500 people did not get renewal forms for their medicare cards when the Department of Health moved to a new computer system.

At the time, Dubé stated anyone who is asked to pay for services should keep their receipts or invoices so they can apply for reimbursement. The provincial government also brought on additional staff to reduce the backlog.

“Given how long this has been going on, you’d think the government could deal with it more proactively,” stated Fraser. “Why wouldn’t you just automatically send a letter to everyone affected that they could then present to health-care providers in lieu of a card?

“My main concern is that people will select to go without treatment because they don’t have the cash on hand or because they simply don’t have the right information,” he said.

Arsenault stated the government official she spoke to gave her very few details about what was causing the on-going problems.

“Quite honestly there has been no explanation whatsoever. The only thing they mentioned is they changed their system over and that was last year in March. But that is almost a year ago since the system has been changed, but that is the only information that they would say,” she said.

source : www.cbc.ca

Published in the Feb. 3 early on-line issue of EMBO Molecular Medicine, the study explored an inherited mutation located in part of the KRAS gene, which leads to abnormal endometrial growth and endometrial risk. In endometriosis, uterine tissue grows in other parts of the body, such as the abdominal cavity, ovaries, vagina, and cervix. The condition is often hereditary and is found in 5%-15% of women of reproductive age, affecting over 70 million women worldwide.

Although the disorder has been studied for many years, its exact cause and how it develops remained unclear. It was previously shown that activating the KRAS gene caused mice to develop endometriosis. However, no mutations in this gene have been identified in women with endometriosis.

Led by senior author Dr. Hugh S. Taylor, professor and chief of the Division of Reproductive Endocrinology and Infertility in the Department of Obstetrics, Gynecology & Reproductive Sciences, the authors studied 132 women with endometriosis and evaluated them for a newly identified mutation in the region of the KRAS gene responsible for regulation. This mutation was previously linked to an increased risk of lung and ovarian cancer by study co-author Joanne Weidhaas, M.D., assistant professor of therapeutic radiology.

“We found that 31% of the women with endometriosis in the study carried this mutation, compared to only 5.8% of the general population,” stated Taylor. “The presence of this mutation was also linked to higher KRAS protein levels and associated with an increased capacity for these cells to spread. It also may explain the higher risk of ovarian cancer in women who have had endometriosis.”

The Yale team is the first to identify a cause of this common and previously tiny understood disease. “This mutation potentially represents a new therapeutic target for endometriosis as well as a basis of potential screening methods to determine who is at risk for developing endometriosis,” stated Taylor.

Other authors on the study include Olga Grechukhina, Rafaella Petracco, Shota Popkhadze, Trupti Paranjape, Elcie Chan, Idhaliz Flores, and Joanne Weidhaas.

The National Institutes of Health supported the study.

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source : www.sciencedaily.com

Royal Caribbean’s Voyager of the Sea left a couple of hours late on Saturday because of the norovirus outbreak, Port of New Orleans spokesman Chris Bonura stated Sunday.

About 200 passengers became ill with the gastrointestinal illness, which causes vomiting and diarrhea. The company did not immediately return a call and email seeking further details.

Earlier in the weekend, two Princess cruise ships were forced to undergo a complete disinfection at their home port of Fort Lauderdale, Fla., after dozens of passengers and crew fell ill.

The Crown Princess has already headed back to sea. About 158 people were infected by the virus on that ship.

In a statement issued Sunday, Princess Cruises, a unit of Carnival, stated the Ruby Princess, which had set sail for the Caribbean from Fort Lauderdale on Jan. 29 had returned to port for a sanitizing process after 90 passengers and 13 crew were struck with the highly contagious virus.

Vacation-goers were told their cruise would be delayed a few hours while the ship was being cleaned.

Norovirus, which usually lasts from one to three days, can be debilitating for the very young, the very old and those with weakened immune systems. It is easily spread through contact with infected people, items they touch, such as food in buffets, and human waste.

source : www.cbc.ca

The discovery of the role played by the molecule CD74 could help immunologists investigate treatments that offer better immune responses against cancers, viruses and bacteria, and lead to more efficient vaccines.

The findings were recently published in Nature Immunology.

“This could ultimately lead to a blueprint for improving the performance of a variety of vaccines, including those against HIV, tuberculosis and malaria,” states UBC biologist Wilfred Jefferies, whose lab conducted the study. “This detailed understanding of the role of CD74 may also start to explain differences in immune responses between individuals that could impact personalized medical options in the future.”

CD74 is an important piece of cellular machinery inside dendritic cells — which regulate mammalian primary immune responses. Dendritic cells possess specialized pathways that enable them to sense and then respond to foreign threats. Until now no one has been able to piece together the circuitry which enables a cellular receptor — Major Histocompatability Class I (MHC I) — inside the cells to find and ‘collide’ with foreign invaders.

The key finding of this work is the discovery of the guiding role played by CD74 to link MHC I receptors to compartments containing invading pathogens within the immune cell. This sophisticated circuit grants the immune cell to recognize and signal the presence of a pathogen in the body and to alert T immune fighter cells. The T-cells respond by dividing and attacking infected cells, destroying the pathogen.

Jefferies’ team used ‘knock-out’ mice that had been genetically altered to lack the CD74 function to uncover the role of the molecule. The team-which includes research associate Genc Basha, postdoctoral fellow Anna Reinicke, graduate students Kyla Omilusik and Ana Chavez-Steenbock1, undergraduate student Nathan Lack, and technician Kyung Bok Choi -then confirmed their findings using biochemical analysis.

Jefferies is a professor with UBC’s departments of Microbiology and Immunology, Zoology, and Medical Genetics and with UBC’s Michael Smith Laboratories and Biomedical Research Centre. He is also a member of the Centre for Blood Research and the Brain Research Centre at UBC.

The research was supported by the Canadian Institutes of Health Research and the Michael Smith Foundation for Health Research.

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Genc Basha, Kyla Omilusik, Ana Chavez-Steenbock, Anna T Reinicke, Nathan Lack, Kyung Bok Choi, Wilfred A Jefferies. A CD74-dependent MHC class I endolysosomal cross-presentation pathway. Nature Immunology, 2012; DOI: 10.1038/ni.2225

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Canadian Blood Services is calling on people of African and Caribbean heritage to register as blood and stem donors through its OneMatch Stem Cell and Marrow Network.

Sickle cell disease is an inherited disease of red blood cells, predominantly affecting people of African descent. In people with sickle cell disease, the red blood cells are abnormally shaped and starve tissues of oxygen.

The lifespan of affected people is about three decades shorter than average, stated Dr. Isaac Odame, medical director of the Global Sickle Cell Disease Network at the Hospital for Sick Children in Toronto.

Complications can include infections, extreme bone pain and damage to the brain, lungs, heart and kidneys, Odame said.

Kynan Jackson, 7, of Halifax struggles with painful sickle cell disease. He takes medication twice a day, has had blood transfusions and been admitted to the hospital a few times since he was diagnosed at age four.

“It is stressful,” stated his mother, Winnell Jackson. “It’s nearly like a waiting game. The medication will not ever stop him from getting crisis again, so I know it’s coming.”

A stem cell transplant replaces the bad, misshapen ones with normal ones, stated Odame.

Sickle cell disease can be cured with stem cell transplants, states Dr. Issac Odame. (CBC)

“The only way to give him [Kynan] a chance is to cure it,” Odame said. “We know that it can be cured through stem cell transplantation.”

Stem cell transplants require a close match from a donor of the same ethnic background, which narrows Kynan’s odds of getting one.

“If you are Caucasian and you are looking for an unrelated match, probably 75 per cent chance you will find one. If you are of African descent, your odds are far, far, far less,” Odame said.

Canada’s blacks represent about 2.5 per cent of the population, based on the 2006 census. But of the 300,000 on the blood agency’s stem cell and marrow registry, only 0.7 per cent are of African descent.

“Sometimes people wait six months to years to find a match and they may end up passing away in that time period because we cannot find a match in Canada or around the world,” stated Sue Smith, executive director of One Match.

During Black History Month, Canadian Blood Services is appealing for young, black male donors in particular to donate blood and be registered. Men tend to be bigger and deliver a bigger volume of stem cells without the complications of an over-reactive immune system that can occur during pregnancy.

Currently, the bureau stated there is a waiting list of 36 African Canadians with cancer who could be cured with a stem cell transplant. Kynan’s mother hopes the campaign is a success and she is able to see him grow up.

It would “be really nice to know that, you know what, he does have a match out there. There’s somebody out there wherever they may be, that would match him and be able to take that pain, help ease that pain in his life.”

The blood agency’s theme this year, “Our Canadian Story: Making Community Engagement a Priority,” emphasizes community.

With files from CBC’s Pauline Dakin

source : www.cbc.ca

It’s believed to be the first-ever transplant of an esophagus and the largest number of organs transplanted at one time in New England.

Spunky and bright-eyed as she scampered around her family’s farmhouse outside Portland, Alannah Shevenell stated Thursday that she is glad to be feeling well again and able to go sledding, make a snowman, work on her scrapbooks and give her grandmother a tiny good-humoured sass.

The ideal part, though? “Being home,” she said. “Just being home.”

It was 2008 when Alannah, then 5, began running a fever and losing weight while her belly swelled. Doctors discovered the tumour that year and twice attempted to remove it, as it made its way like octopus legs from organ to organ. But it was difficult to access what turned out to be a rare form of sarcoma, stated Debi Skolas, Alannah’s grandmother, and chemotherapy did not do the trick, either.

All the time, the growth — known as an inflammatory myofibroblastic tumour — continued to grow in her abdomen, causing pain, making it hard to eat and swelling her up with fluid. Surgery was the last resort to save her life, and Alannah spent more than a year on a waiting list for the organs, stated Dr. Heung Bae Kim, the lead surgeon on the procedure at Children’s Hospital Boston.

The family was told there was a 50 per cent chance Alannah would not survive the procedure. But without it, she had no chance whatsoever.

Things were more tense than celebratory in October when physicians prepared to remove the growth and the organs in one fell swoop and replace them with organs transplanted in one tangled piece from another child of similar size.

The hardest part was taking out her organs and the tumour, Kim said, calling it a difficult operation with lots of blood loss.

Being home is the ideal part of having the transplants, Alannah Shevenell says. (Robert F. Bukaty/Associated Press)

“It’s probably one of the most extensive tumour removals ever done,” the surgeon said.

Dr. Allan Kirk, professor of surgery at Emory University in Atlanta and the editor-in-chief of The American Journal of Transplantation, stated no other esophageal transplant has been reported in medical literature.

After the surgery, Alannah spent three more months at the hospital, with her grandmother sleeping every night in a lounge chair by her bed. She battled infections and complications from the surgery before finally being given the OK to leave.

She arrived back home Wednesday in the 192-year-old house on a country road where she lives with her grandmother and grandfather, Jamie Skolas, in Hollis, a town of 4,500 residents about 20 miles west of Portland.

But just because she is home doesn’t mean she is out of the woods. Alannah has to take nine medications each day, some two, three or four times. Her grandparents have to precisely measure what goes in and comes out of her body, and check her blood sugar.

She has an ostomy pouch and feeding tube attached to her for nutrition as she slowly gets used to eating again. Scars from her surgeries look like a roadmap on her stomach. A tutor comes to the home 20 hours a week for her schooling.

Thankful for 2nd chance at life

Her immune system is so weak that she cannot go to places with massive numbers of other people, such as school, church or a mall. She cannot eat raw vegetables or fruits unless they have thick skins because of concerns over germs, and she will never be able to swim in a lake because of the bacteria. The Skolases installed ultraviolet lights in their heating ducts to kill mould, mildew and bacteria that might sicken Alannah.

Alannah is aware of her limitations and what she is been through.

“Don’t even ask,” she states when the subject of the medical costs, which have been covered by MaineCare — Maine’s version of Medicaid — come up.

She’s talkative and enjoys bantering with her grandparents.

“Grammy, you are not always right,” she stated to end a conversation.

Friends have organized a fundraiser to help raise money to offset the costs.

More than anything, though, the family is thankful for the girl’s second chance at life and to the family that went through the pain of losing a child and before deciding to donate the organs to help Alannah.

“That was a courageous decision,” Debi Skolas said. “I still cry when I think about it.”

source : www.cbc.ca

A case report, published this week in the American Journal of Human Genetics, shows how researchers can combine a easy blood test with an “executive summary” scan of the genome to diagnose a type of severe metabolic disease.

Researchers at Emory University School of Medicine and Sanford-Burnham Medical Research Institute used “whole-exome sequencing” to find the mutations causing a glycosylation disorder in a boy born in 2004. Mutations in the gene (called DDOST) that is responsible for the boy’s disease had not been previously seen in other cases of glycosylation disorders.

Whole-exome sequencing is a cheaper, faster, but still efficient strategy for reading the parts of the genome scientists believe are the most important for diagnosing disease. The report illustrates how whole-exome sequencing, which was first offered commercially for clinical diagnosis in 2011, is entering medical practice. Emory Genetics Laboratory is now gearing up to begin offering whole exome sequencing as a clinical diagnostic service.

It is estimated that most disease-causing mutations (around 85 percent) are found within the regions of the genome that encode proteins, the workhorse machinery of the cell. Whole-exome sequencing reads only the parts of the human genome that encode proteins, leaving the other 99 percent of the genome unread.

The boy in the case report was identified by Hudson Freeze, PhD and his colleagues. Freeze is director of the Genetic Disease Program at Sanford-Burnham Medical Research Institute. A team led by Madhuri Hegde, PhD, associate professor of human genetics at Emory University School of Medicine and director of the Emory Genetics Laboratory, identified the gene responsible. Postdoctoral fellow Melanie Jones is the first author of the paper.

“This is part of an on-going effort to develop diagnostic strategies for congenital disorders of glycosylation,” Hegde says. “We have a collaboration with Dr. Freeze to identify new mutations.”

Glycosylation is the process of attaching sugar molecules to proteins that appear on the outside of the cell. Defects in glycosylation can be identified through a relatively easy blood test that detects abnormalities in blood proteins. The sugars are important for cells to send signals and stick to each other properly. Patients with inherited defects in glycosylation have a broad spectrum of medical issues, such as developmental delay, digestive and liver problems and blood clotting defects.

The boy in this case report was developmentally delayed and had digestive problems, vision problems, tremors and blood clotting deficiencies. He did not walk until age 3 and can’t use language. The researchers showed that he had inherited a gene deletion from the dad and a genetic misspelling from the mother. “Over the years, we have come to know many families and their children with glycosylation disorders. Here we can tell them their boy is a true ‘trail-blazer’ for this new disease,” Freeze said. “Their smiles — that is our bonus checks.”

The researchers went on to show that introducing the healthy version of the DDOST gene into the patient’s cells in the laboratory could restore normal protein glycosylation. Thus, restoring normal function by gene therapy is conceivable, if still experimental. However, restoration of normal glycosylation would be extremely difficult to achieve for most of the existing cells in the body.

The research was supported by the National Institutes of Health and by the Rocket Fund.

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British drug maker AstraZeneca announced Thursday plans to cut costs by closing its Quebec research and development facility, eliminating 132 jobs.

It’s just the latest to make such a move. French pharmaceutical company Sanofi-Aventis laid off 100 workers last month at its R&D centre in Laval. Johnson & Johnson also announced the closure of its research centre and the layoff of 126 workers.

The shut down announcement comes some 18 months after Merck & Co. cut 200 jobs by closing its Montreal lab, which was once the largest research facility in Canada.

“Unfortunately, Montreal is caught up in these global shifts in the pharmaceutical industry,” stated Robert David, associate professor of strategy at McGill University’s Desautels Faculty of Management.

He stated Montreal is being caught in a storm because pharmaceutical multinationals that bulked up through acquisitions decades ago now have to prepare for the loss of billions of dollars in revenue as drugs lose patent protection.

Pfizer faced that problem with Lipidor last year. AstraZeneca’s revenues have continued to decline. It faces a huge hit beginning later this year with the gradual loss of protection of Crestor, Seroquel and Nexium.

Each of the three blockbuster drugs has netted around US$5-billion in annual global revenues.

AstraZeneca’s Montreal closure will cut almost 17 per cent of its Canadian workforce of 800 and leave a few marketing and sales people in the St. Laurent borough of Montreal.

The facility is one of the company’s main neuroscience sites focused on the discovery and development of new medicines to treat neuropathic pain.

“Sadly we have to wonder whether Montreal will on an on-going basis have a very strong pharmaceutical research cluster,” stated David.

London-based AstraZeneca is reducing its global workforce by 7,300, including 1,800 at 14 research and development sites around the world.

It will also stop R&D activities at its sites in Sodertalje, Sweden, where there is a focus on neuroscience research.

The company is creating a new virtual Neuroscience Innovative Medicines organization in Boston and Cambridge, U.K.

Communications director Jennifer Robinson stated the R&D changes are designed to reduce costs and improve productivity.

“The thinking is what we will do going forward is to manage this portfolio of projects with external partners,” she stated in an interview.

In addition to lost revenues from patented drugs, companies face challenges in finding new medicines to treat complex ailments such as cancer, Alzheimer’s and Parkinson’s.

“Our capability to find new medicines has not been as great as we would have hoped, so the number of new medicines coming onto the market is in decline and has been for years.”

Regulators are also raising the hurdles to approve drugs in light of failures such as Vioxx while insurers and government are reducing how much they pay for drugs.

Quebec Premier Jean Charest stated his economic development minister has been given a mandate to develop a plan to address the shift from internal research to pharma partnerships with academia and small companies.

“What I plan to do is adjust and work with the pharmaceutical sector to adjust the intervention and presence of the Quebec government in this sector of research,” he told reporters in Ottawa.

David stated the shift to personalized medicine based on genetics will require governments to target investments to university medical labs and small startup biotech firms with 10 to 20 workers.

“The problem with that is that doesn’t happen in the short-term,” the academic said.

“That’s something that really takes a decade to foster and in the meantime I think it’s going to be really rough but now’s the time to start.”

Montreal InVivo general manager Michelle Savoie stated the latest closure announcement is disappointing, but the life sciences and health technologies cluster has been undergoing deep changes for about three years.

“The massive pharma companies are not leaving Montreal. There are some activities that are leaving but the sector will survive,” she said.

The nonprofit represents some 620 organizations, including 150 research organizations, and 80 subsidiaries of foreign companies. In 2010, it employed 41,000 people in the greater Montreal area, including 31,000 in the private sector.

While layoffs have resulted in a brain drain, many skilled employees have joined small local firms, where they increasingly need both scientific skills the capability to manage the research process.

Savoie stated the federal government needs to ensure the regulatory environment is competitive by adopting intellectual property measure to protect companies internationally.

source : www.cbc.ca

“It’s a next-generation technology,” stated Scripps Research Associate Professor Peter Kuhn, PhD, senior investigator of the new studies and primary inventor of the high-definition blood test. “It significantly boosts our capability to monitor, predict, and comprehend cancer progression, including metastasis, which is the major cause of death for cancer patients.”

The studies were published February 3, 2012, in the journal Physical Biology.

The new test, called HD-CTC, labels cells in a patient’s blood sample in a way that distinguishes possible CTCs from ordinary red and white blood cells. It then uses a digital microscope and an image-processing algorithm to isolate the suspect cells with sizes and shapes (“morphologies”) unlike those of healthy cells. Just as in a surgical biopsy, a pathologist can analyze the images of the suspected CTCs to eliminate false positives and note their morphologies.

Kuhn emphasizes that this basic set-up can be easily altered with different cell-labeling and image-processing techniques.

Five New Studies, Five Steps Forward

To test the new technology, members of the Kuhn lab at Scripps Research teamed up with pathologists and oncologists at Scripps Health in La Jolla, California; UC San Diego Moores Cancer Center at the University of California, San Diego; the Billings Clinic in Billings, Montana; the Division of Medical Oncology at the University of California, San Francisco; the Center for Applied Molecular Medicine at the University of Southern California, in Los Angeles; and the Netherlands Cancer Institute-Antoni van Leeuwenhoek Hospital in Amsterdam, the Netherlands.

The five new studies that resulted from the collaboration not only demonstrate the accuracy and effectiveness of the new test for a number of different cancer types, but also start to explore the utility of the technology for diagnosing and monitoring patients and improving cancer research in the lab. While other tests for CTCs typically use “enrichment” steps in which suspected CTCs are concentrated — and these methods inadvertently exclude some types of CTCs — the new studies show HD-CTC works well as a no-cell-left-behind process and enables a more complete analysis.

Also striking is the quality of the images. “The high definition method gives a detailed portrait of these elusive cells that are caught in the act of spreading around the body,” stated diagnostic pathologist Kelly Bethel, MD, of Scripps Health, Scripps Research, and UC San Diego School of Medicine, who is the senior clinical investigator on Kuhn’s team. “It’s unprecedented — we have never been able to see them routinely and in high definition like this before.”

In the first study, the research team analyzed 83 advanced cancer patients using HD-CTC to document the test’s sensitivity and accuracy for different cancer types. The scientists found that the test detected five or more CTCs per milliliter of blood in 80 percent of patients with metastatic prostate cancer, 70 percent of those with metastatic breast cancer, 50 percent of those with metastatic pancreatic cancer, and no healthy subjects. The current gold-standard CTC test, known as CellSearch, was notably less sensitive in detecting tumor cells in these samples.

Most patients whose CTC counts surpassed the detection threshold also showed small aggregates of CTCs, which cancer biologists term “microtumor emboli.” These are widely suspected to be incipient metastatic tumors, as well as triggers for the blood clots that often kill advanced cancer patients. In the second study, the scientists showed that HD-CTC could detect these aggregates in 43 percent of 71 patients with advanced prostate, lung, pancreas, and breast cancers, and in none of a group of 15 healthy subjects. “This tells us that HD-CTC could be helpful in studying the origins of cancer metastases and related blood clots, and for predicting them, too,” Kuhn said.

In the third study, the team used HD-CTC to compare circulating tumor cells from prostate cancer patients with cells from prostate cancer cell lines that researchers often use as convenient models for prostate cancer biology in the lab. The team found significant differences between the two classes of cells, in their cell morphology and in the way they were labelled by HD-CTC’s fluorescent tags. “This underscores the need for studying cancer cells from patients, not just model cancer cells that in some ways may be utterly different from the real thing,” Kuhn said.

In the fourth study, the researchers performed HD-CTC tests on 28 patients with advanced non-small-cell lung cancer over periods of up to a year. The team was able to detect CTCs in 68 percent of samples, and found that the numbers of detected CTCs tended to go up as other measures showed cancer progression.

In the fifth and final paper of the series, the team used HD-CTC in 78 patients who had just been diagnosed with various stages of non-small-cell lung cancer. “We demonstrated that we could sensitively detect CTCs even in patients with early-stage cancer,” Kuhn said.

This result points to the possibility of using the HD-CTC blood test not only to evaluate already-diagnosed cancer, but also to help detect cancer in people who are unaware they have it. “If HD-CTC works on the day after cancer diagnosis, as we have shown, then one can easily imagine that it would work the day before diagnosis, too,” Kuhn said.

Kuhn and his colleagues now intend to study the use of HD-CTC as a potential screening test and to develop it further for use in clinical monitoring and cancer research. Kuhn has founded a San Diego-based biotechnology company, Epic Sciences, Inc., to develop HD-CTC commercially for companion diagnostic products in personalized cancer care.

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