Lawyers Push for Transplant Rule Exception to Save Girl

Lawyers for 10-year-old Sarah Murnaghan, who has been denied a lung transplant because of a controversial federal policy, say Health and Human Services' Secretary Kathleen Sebelius' decision to review the policy -- but not in time to save Sarah -- is unconstitutional.

Sarah would be at the top of the adult lung transplant list if she were 12, because she only has weeks to live and a lung transplant would as-good-as cure her of cystic fibrosis.

Organ Donation: Should Younger Patients Get Better Kidneys?

The Murnaghan family is fighting a little known organ transplant policy that is effectively pushing Sarah to the bottom of the adult transplant waiting list because it mandates that adult lungs be offered to all adult patients before they can be offered to someone under 12 years old.

Law firm Pepper Hamilton LLP wrote a letter to Sebelius on Monday calling the policy "unfair, arbitrary and capricious" and saying that Sebelius's failure to make an exceptionis is a violation of Sarah's constitutional rights to "due process" and "equal protection," according to a family statement.

Sarah's father, Fran Murnaghan, of Newtown Square, Pa., told ABC News Sunday that Sebelius' mandate for review of transplant policies would not deal with current cases in a timely manner, nor deal with what he characterized as an unequal system that discriminates against children younger than 12.

"Sarah is being left to die," Murnaghan said. "Not only Sarah, but there are many other children in the same situation.

"[Sebelius] clearly has the authority to do something now, and she has decided to do, to be honest, not much of anything," he said. "In my opinion, she has kicked the can down the political road."

"Secretary Sebelius' decision to not exercise her very clear authority under the law to intervene and mandate a variance that would help save Sarah's life is devastating," the family said in a prepared statement.

Sarah's family is asking the public to "consider naming our child an organ recipient should someone lose the life of a loved one in the very near future," they said in the statement.

"Our little girl, who loves writing music, making crafts, and playing with her siblings can honor someone's life by living on herself," they wrote.

Under the existing policy, children like Sarah are forced to wait for a lung transplant, despite her life-threatening illness.

In a letter sent Friday to the Organ Procurement and Transplantation Network, Sebelius asked for the review to consider changing the policy to make more transplants available to children, The Associated Press reported.

Sebelius called the incongruity between donors and children in need of transplants "especially stark."

There were only 11 lung donors between 6 and 10 years old and only two lung transplants in that age group in 2012, according to an Organ Procurement and Transplantation Network statement.

Patients with cystic fibrosis, a genetic condition that damages the lungs, have an average life expectancy of 31 years old, said Dr. Devang Doshi, a pediatric lung specialist at Beaumont Children's Hospital in Michigan who has not met Sarah. But if they get a lung transplant, the condition is essentially cured.

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Angelina Jolie's Mastectomy: What You Should Know

By going public with her prophylactic double mastectomy, actress Angelina Jolie has again shone the spotlight on breast cancer and the genetic mutation known to increase the risk of getting it by 60 percent.

(Jolie wrote that her doctor told her she had an increased risk of 87 percent, adding that the risk is different for each woman. An NIH?study?found this number to be too high.)

Although Jolie, 37, has the potential to save lives by raising awareness, facts about testing for the mutation and undergoing preventative care can be confusing. Here’s what you need to know:

The test for the genetic mutation, called BRCA, is a simple blood test, but it’s not for everyone. It’s not always covered by insurance and can cost about $3,000, so you should know whether you’re one of the 2 percent of women who have a family history that makes them more likely to have the BRCA mutation.

This is cancer.gov‘s list of family history to consider before undergoing BRCA testing:

For women who are not of Ashkenazi Jewish descent: two first-degree relatives (mother, daughter or sister) diagnosed with breast cancer, one of whom was diagnosed at age 50 or younger;three or more first-degree or second-degree (grandmother or aunt) relatives diagnosed with breast cancer regardless of their age at diagnosis;a combination of first- and second-degree relatives diagnosed with breast cancer and ovarian cancer (one cancer type per person);a?first-degree relative?with cancer diagnosed in both breasts (bilateral?breast cancer);a combination of two or more first- or second-degree relatives diagnosed with ovarian cancer regardless of age at diagnosis;a first- or second-degree relative diagnosed with both breast and ovarian cancer regardless of age at diagnosis; andbreast cancer diagnosed in a male relative.For women of Ashkenazi Jewish descent: any first-degree relative diagnosed with breast or ovarian cancer; andtwo second-degree relatives on the same side of the family diagnosed with breast or ovarian cancer.

In all, between 0.125 and 0.25 percent of women will test positive for the BRCA mutation, and it varies by ethnicity. These women have an increased risk of getting breast cancer and ovarian cancer.

If you do test positive for BRCA, you have options, and you don’t necessarily have to go the Jolie route.

Some women choose not to have surgery. Instead, they increase cancer surveillance with imaging tests. These include regular mammograms to test for breast cancer, and regular pelvic sonograms and blood-tests to watch for ovarian cancer.

It is important to note that surveillance or screening does not reduce risk, but rather potentially improves early detection of cancer should it occur.

Other options include chemo-prevention, or taking certain medications to reduce cancer risk. For example, some women take a drug called tamoxifen to prevent breast cancer and others take birth-control pills to prevent ovarian cancer.? These decisions are individual, highly personal and often times very difficult ones for a woman and her family to make.

Like Jolie, some women choose surgery when they learn they have the BRCA mutation. The decision to surgically remove the breasts and ovaries is an individual one and must take into account the woman’s age, fertility and reproductive wishes, psychological factors and cost. Her general medical condition for undergoing elective surgery should be taken into consideration, too.

Often, the reconstructive process is done in stages for a few months and can cost as much as $50,000. Fortunately, since 1998, women without medical insurance have increased options and mandatory coverage for undergoing breast reconstruction after mastectomy.

Because these decisions are complex, patients can seek consultations with oncologists, general gynecologists, gynecologic oncologists, breast surgeons and reconstructive plastic surgeons.

While studies have shown a significant risk reduction and likely survival benefit in women with a BRCA mutation who undergo preventive surgery, their risk does not drop to zero. There is still a low chance of developing breast cancer in the chest wall, and ovarian cancer in the pelvic cavity.

Men carry the BRCA mutation, too, so if a woman with a mutation has a son, he has a 50 percent chance of being a carrier and having the mutation.? Men with the mutation face increased risks of breast cancer, certain kinds of pancreatic cancer, testicular cancer and prostate cancer.

While the information presented here represents the medical tip of the iceberg, the hope is that? it can begin the process of informing, educating and empowering both women and men about this kind of genetic mutation and cancer risk.

Angelina Jolie revealed she had genetic testing and a double mastectomy. (Credit: Carlo Allegri/AP Photo)

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Kid's Hairdo Reveals Mom's Hang-ups

Jackie Morgan MacDougall struggled with her daughter's desire to cut her hair. (Image credit: psjackie.com)

Jackie Morgan MacDougall hoped the faux-hawk phase would be fleeting. Her 6-year-old daughter, Lucy, desperately wanted to chop her long black hair into the short, spiky style – a move the mother of two boys and a girl could hardly bear.

“She’s just so darn cute with this beautiful hair,” said Morgan MacDougall, who as a child lamented her own mousy brown mane, which she starting perming in the third grade. “But she’s very secure in herself and who she is, and she?didn’t?want the hair.”

Morgan MacDougall quickly realized that her own “appearance issues” were clouding her parental judgment.

“I thought, ‘Why am I doing this?’ It’s not for her,” she said. “How do I teach my only daughter not to look the way that other people tell her when that’s what she’s doing for me?”

That’s when Morgan MacDougall took Lucy to the nearest hair salon and asked a bewildered stylist to bring on the faux-hawk.

“She was very confused by the request,” said Morgan MacDougall, who documented the chop in a series of photos. “Then the woman next to us said, ‘Oh, you’re such a cool mom,’ – loosely translated to, ‘I would never do that to my kid.’”

Lucy during the haircut. (Image credit: psjackie.com)

But one look at Lucy’s face and Morgan MacDougall knew she had made the right decision.

“I can’t express how I felt seeing her with that smile,” she said. “I can say with words, ‘Whoever you are, whatever your choices, I love you,’ but that can never touch her the way driving her to the hair salon did.”

Alan Kazdin, a professor of psychology and director of the Yale Parenting Center, said parents should “let as many of these things go as they can in the spirit of compromise,” stressing that hairdos and clothing choices are temporary.

“Now, tattoos and weird orifices might be different,” he added. “But cutting one’s hair, maybe let that go.”

Morgan MacDougall said she’ll cross the tattoo bridge when she comes to it.

“I have two tattoos, not that one would ever know,” she said. “I would hope to teach her the permanence of it, but at same time, if that’s how she wants to express herself in creative ways, I think there are lot worse behaviors to have.”

Kazdin agreed, stressing that while compromise and flexibility are important, parents also need limits.

“You compromise because it makes you more powerful when you do make a claim that can’t be compromised,” he said. “So that you can say, ‘No, you can’t go to a home where there are no adults. No, you can’t have sex and birth control right now.’”

“The cliche is, ‘Pick your battles,’” he added. “But these?aren’t?battles. We’re all trying to raise our children into great adults. There are no sides.”

Kazdin said Morgan MacDougall should be praised for putting her daughter first despite her personal hang-ups.

“Child-rearing is about the child, not the parent,” he said.

Morgan MacDougall blogged?about her inner battle to see what other moms had to say: Some said they’d do the same, while others said there was just no way.

Tell us what you think in the comments section!

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Autistic Teen Has Off-the-Charts IQ

An Indiana mother said that her determination to find a niche for her autistic son, who doctors had little hope for, led him to flourish into a budding astrophysicist with an off-the-charts IQ, and he is now pursuing a PhD. in physics.

Kristine Barnett's son, Jacob, 15, was diagnosed with moderate to severe autism when he was 2. Because he had lost language, he was on the more severe end of the spectrum. Psychologists and teachers believed that the young boy may not ever speak again. As Barnett put it, they thought that he was lost.

"He was very precise," she told ABCNews.com. "He wasn't barreling through the world like other little boys. He lined cars up precisely. His mannerisms were precise.

"He seemed to like schedule and routine, even from infancy," she said.

After his diagnosis, Jacob was visited frequently by a number of psychologists under an Indiana program called First Steps, which included a developmental therapist, an occupational therapist, and a speech therapist, among others.

But early signs in Jacob's childhood hinted at an inner world that was harboring massive intelligence. At a very young age, he would carry a set of beloved alphabet cards with him wherever he'd go.

At one point, he took a bundle of crayons and arranged them across the living room floor in the color spectrum, which he had distinguished from light coming through the living room window and hitting glasses perched on a table.

As Barnett would run a daycare out of her home, she would play with other people's kids outside while Jacob was slumped over the table inside, where he would work with therapists. He was spending hours trying to put a ball in a cup.

One spring day, as the kids ran through a sprinkler, she decided to make a change.

"We were forgetting his childhood. His spirit was being crushed by the opinion that everything was wrong," she said. "I resolved to give it back to him."

That night, Barnett took Jacob out after dark, turned on fog lights of her car, put on some Louis Armstrong, laid on hood of the car with him and looked at the stars.

"Little did I know it would be those stars that would bring him back into our world," she said. "They were what we had. It was what we had to hold onto. It was the beginning with a relationship with my child."

In an attempt to connect with her son and nurture the spark of interest he showed when they would go look at the stars, she decided to take him to a planetarium.

"I didn't get it. They seemed like far-away dots to me," she said. "He then showed me a nebula on the computer, and it gave me a peek into his mind -- into the way he sees the world."

Barnett decided to stop having Jacob meet with therapists. She said that she was advised by everyone she knew, including her friends and her husband, not to remove Jacob from the system.

By the age of 3, Jacob began to talk again, and everyone was asking Barnett for the secret to the sudden recovery. Typically, it takes years for an autistic child to recover speech.

By the age of 3-and-a-half, Jacob had taught himself to read. This is what he'd been doing while taking books off to the corner, Barnett said she realized.

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Understanding of complex diseases likely to improve following the unexpected discovery of the ways Cells Move

Main category: Cancer / Oncology
Also included in: respiratory / asthma;??Biology / biochemistry
Article Date: June 25, 2013 - 1:00 PDT current ratings for:
Understanding of complex diseases likely to improve following the unexpected discovery of the ways Cells Move

A new discovery about how cells move within the organization can provide scientists with crucial information about the mechanisms of diseases such as the spreading of the cancer or constriction of the Airways caused by asthma. Led by researchers from the Harvard School of Public Health (HSPH) and the Institute for bioengineering of Catalonia (IBEC), investigators found that the epithelial cells - the type that form a barrier between the inside and the outside of the body, such as skin cells - move group, powered by forces both of in and from neighbouring cells - to fill the empty spaces that they encounter.

The study appears in Nature Materials advanced online edition.

"We have tried to understand the fundamental relationship between cellular movements collective and collective forces of cell phones, which may occur during the invasion of the cancer cells, for example. But, in so doing, we are fallen on a phenomenon that was totally unexpected, "said lead author Jeffrey Fredberg, Professor of Bioengineering and physiology to the investigator HSPH Department of Environmental Health and co-Minister of HSPH molecular laboratory and integrative cellular dynamics.

Biologists, engineers and physicists at HSPH and IBEC worked together to shed light on the collective cell movement because it plays a key role in functions such as the healing of wounds, organ development and tumor growth. Using a technique called stress monolayer microscopy--which they invented themselves - they have measured the forces affecting a single layer of epithelial cells in motion. They examined cells speed and direction as traction - how certain cells either pull or push themselves and thus force the collective movement.

As they expected, the researchers found that when an obstacle was placed in the path of a layer of advanced cell - in this case, a gel that provided no traction - cells settled around him, closely hugging the sides of the gel as they passed. However, the researchers also found something amazing - cells, in addition to moving forward, continued to collectively back to frost, as if the desire to fill the space empty. Researchers have dubbed this movement "kenotaxis", Greek words "keno" (empty) and "taxi" (arrangement), because it seemed that cells are trying to fill a void.

This new discovery could help researchers to better understand the behaviour of the cell - and evaluate the potential influence that behavior - in a variety of complex diseases, such as cancer, asthma, cardiovascular diseases, developmental anomalies and glaucoma. The findings could also help with regenerative medicine and tissue engineering, which rely on cell migration.

In carcinomas, for example - who represent 90% of all cancers and involve epithelial cells - new information on cell movement could improve understanding of how cancer cells migrate through the body. Research on asthma could also get a boost, because scientists believe the migration of epithelial cells damaged in the lungs are involved in narrowing of the Airways caused by the disease.

"Kenotaxis is a property of the cell collective, not the individual cell," said Jae Hun Kim, first author of the study. "It was amazing to us that the collective cell can organize itself draw systematically in one direction while moving consistently in a quite different direction. ''

Article adapted by Medical News Today press release original. Click on "references" tab above for the source.
Visit our cancer / Oncology section for the latest news on this subject. Other authors HSPH included James Butler, senior lecturer on physiology in the Department of health environmental and investigator co-Minister of the laboratory; and researchers Dhananjay Tambe, Enhua Zhou Chan Young Park, Monirosadat Sadati, Park Jin-Ah, Bomi Gweon and Emil Millet.

Support for the study came from the Spanish Ministry of Science and Innovation (BFU2012-38146 FPU fellowship XS) and the Swiss National Science Foundation (PBEZP2-140047), the National Research Foundation of Korea (2012R1A6A3A03040450), the European Research Council (Grant Agreement 242993) Parker B. Francis (RK Fellowship), American Heart Association (13SDG14320004) and the National Institutes of Health (R01HL102373, R01HL107561).

"Propulsion and navigation within the advanced single layer sheet," Jae Hun Kim, Xavier Serra-Picamal, Dhananjay T. Tambe, Enhua H. Zhou, Chan Young Park, Monirosadat Sadati, Park Jin-Ah, Krishnan Ramaswamy, Bomi Gweon, Emil Millet, James P. Butler, Xavier Trepat, Jeffrey J. Fredberg, Nature of materials, online, June 23, 2013

Harvard School of Public Health

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Vegetable Fats Reduce Prostate Cancer Death Risk

Editor's Choice
Academic Journal
Main Category: Prostate / Prostate Cancer
Also Included In: Nutrition / Diet;??Cancer / Oncology;??Neurology / Neuroscience
Article Date: 11 Jun 2013 - 0:00 PDT Current ratings for:
Vegetable Fats Reduce Prostate Cancer Death Risk

Prostate cancer patients who replace animal fats and some carbohydrates with vegetable fats have a lower risk of premature death, researchers from the University of California reported in JAMA Internal Medicine.

In the United States alone, nearly 2.5 million men currently live with prostate cancer. Not much is known about how diet may influence prostate cancer progression and death rates, the authors wrote as background information.

Erin L. Richman, Sc.D., and team carried out a study involving 4,577 men from the Health Professional Follow-up Study with non-metastatic prostate cancer between 1986 and 2010. They focused on the patients' dietary fat intake after diagnosis. Every four years, they completed questionnaires which asked how often they ate and drank over 130 different types of foods and drinks.

Over a follow-up period of 8.4 years, 315 men died from prostate cancer and 1,064 died from any cause. Those who replaced 10% of their dietary calorific intake of carbohydrates with vegetable fat had a 29% lower risk of lethal prostate cancer and a 26% lower risk of death from any cause.

The authors wrote:

"In this prospective analysis, vegetable fat intake after diagnosis was associated with a lower risk of lethal prostate cancer and all-cause mortality."

The results of this study go against what many doctors advise their recently diagnosed prostate cancer patients to do, which is "Cut out all fats from your diet". The right advice appears to be to tell the patient to consume more fat, fewer carbohydrates, and to make sure the fats come from plants and not animals.

The authors concluded:

"Overall, our findings support counseling men with prostate cancer to follow a heart-healthy diet in which carbohydrate calories are replaced with unsaturated oils and nuts to reduce the risk of all-cause mortality. ... The potential benefit of vegetable fat consumption for prostate cancer-specific outcomes merits further research."

Dr. Stephen J. Freedland, from Duke University Medical Center, Durham, North Carolina wrote in an invited Commentary:

"Using data from food frequency questionnaires completed every four years during follow-up, they found that men who consumed more vegetable fat had a lower risk of prostate cancer death.

Thus, in the absence of randomized trial data, it is impossible to use these data as 'proof' that vegetable intake lowers prostate cancer risk, and the authors have carefully avoided such statements.

Dr. Freedland says that the only modifiable risk factor associated with prostate cancer death risk is obesity. In other words, if you are diagnosed with prostate cancer, make sure you don't become obese, and if you are, lose weight.

How to avoid becoming or remaining obese remains unclear, although Richman and team's study suggests that switching from animal fats and some carbohydrates to vegetable fats may have some benefit.

Freedland concluded that "Determining whether this benefit is due to reduced consumption of carbohydrates or greater intake of vegetables will require future prospective randomized trials."

Low fat diet with fish oil supplements slow down prostate cancer progression

Scientists from UCLA's Jonsson Comprehensive Cancer Center reported in the American Association for Cancer Research that men who ate a low-fat diet with fish oil supplements had slower progressing prostate cancer compared to those on a traditional Western diet that was high in fat.

The researchers also found that the participants on a low-fat, fish oil supplement diet were able to change the structure of the cell membranes in both healthy and malignant cells in the prostate. They wrote "They had increased levels of omega-3 fatty acids from fish oil and decreased levels of omega-6 fatty acids from corn oil in the cell membranes, which may directly affect the biology of the cells, though further studies are needed."

When blood samples were tested in a test tube, the team found that the growth of prostate cancer cells was much slower among the men on the low-fat, fish oil supplement diet.

Mediterranean diet reduces prostate cancer risk

An article published in UroToday showed that a traditional Cretan Mediterranean diet may help reduce the risk of prostate cancer. A typical diet from Crete, a Greek island in the Mediterranean, is based on plenty of plant foods (vegetables, fruits, wholegrain cereals, legumes and nuts), olive oil as the main source of dietary fat, low red meat consumption, moderate to low consumption of dairy products, moderate to high fish intake, and moderate intake of wine (consumed mainly with meals).

The authors added that the Mediterranean diet has other health benefits and can help protect against cardiovascular and cancer mortality, as well as Parkinson's and Alzheimer's diseases.

Vegan diet plus exercise may halt/reverse prostate cancer progression

Men with early stage prostate cancer who adopted a vegan diet and did plenty of exercise were more likely to stop and even reverse their cancer progression, researchers from the Department of Urology, the University of California, San Francisco, and the Memorial Sloan-Kettering Cancer Center reported in the Journal of Urology (September 2005 issue).

The authors claimed that theirs was the first randomized, controlled trial that demonstrated clearly that lifestyle changes may influence the progression of any type of cancer.

Written by Christian Nordqvist
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our prostate / prostate cancer section for the latest news on this subject. "Fat Intake After Diagnosis and Risk of Lethal Prostate Cancer and All-Cause Mortality"
Erin L. Richman, ScD; Stacey A. Kenfield, ScD; Jorge E. Chavarro, MD, ScD; Meir J. Stampfer, MD, DrPH; Edward L. Giovannucci, MD, ScD; Walter C. Willett, MD, DrPH; June M. Chan, ScD
JAMA Intern Med. 2013;():1-8. doi:10.1001/jamainternmed.2013.6536

Invited Commentary
"Dietary Fat and Reduced Prostate Cancer Mortality: Does the Type of Fat Matter?Comment on “Fat Intake After Diagnosis and Risk of Lethal Prostate Cancer and All-Cause Mortality”
Stephen J. Freedland, MD
JAMA Intern Med. 2013;():1-2. doi:10.1001/jamainternmed.2013.7744

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Under-Use Of Genetic Testing Puts Health Of Entire Families At Risk

Main Category: Genetics
Also Included In: Cancer / Oncology;??Colorectal Cancer;??Breast Cancer
Article Date: 11 Jun 2013 - 0:00 PDT Current ratings for:
Under-Use Of Genetic Testing Puts Health Of Entire Families At Risk

A new study of the use of genetic testing for cancer-causing mutations in affected families in France has found that its take-up is very low. Professor Pascal Pujol, Head of the Cancer Genetics Department, Montpellier University Hospital, Montpellier, France told the annual conference of the European Society of Human Genetics that analysis of data from the French National Cancer Institute covering the years 2003 to 2011 showed that, although there had been a steady increase in tests performed for the breast and ovarian cancer-causing mutations BRCA1 and BRCA2, this was not the case with the MMR mutation, implicated in Lynch syndrome (a form of colorectal cancer). Only a third of relatives of individuals with either mutation underwent genetic testing themselves.

"Given that such testing can provide many options to enable individuals to manage their cancer risk, it is vital to encourage awareness and acceptance among both the public and medical professionals", he will say. "For example, removal of the ovaries in women over 40 years old who carry a BRCA mutation decreases their overall cancer mortality by 20% and prophylactic mastectomy can reduce the chances of breast cancer in women carrying such a mutation by around 90%. Those who are unwilling to undergo prophylactic surgery can benefit from increased surveillance, with regular MRI (magnetic resonance imaging) scans. For familial colon cancer, screening by colonoscopy has been shown to decrease mortality. It is therefore regrettable that so few people seem to be aware of the benefits of genetic testing in families with a history of breast, ovarian, or colorectal cancer."

Professor Pujol and colleagues from cancer centres across France analysed 240134 consultations and 134652 genetic tests from patients referred for a predisposition to breast or colorectal cancer. They found a substantial increase in tests for BRCA1/2 - from 2095 a year in 2003 to 7393 in 2011 - but for MMR mutations the increase was tiny - from 1144 to 1635 a year over the same period.

Mutations in BRCA1/2 genes are thought to be responsible for about 5% of all cases of breast and ovarian cancer. A woman with such a mutation has a risk of up to 87% of having breast cancer before she reaches the age of 80, as opposed to a risk of 8% in the general population. Such cancers are diagnosed at an average age of 43, as opposed to 60 in the general population, and are often more aggressive. In the case of ovarian cancer, a woman carrying a BRCA1 mutation has a risk of ovarian cancer of up to 63%.

Individuals with Lynch syndrome, or hereditary nonpolyposis colorectal cancer, have a 45% risk of developing colorectal cancer by the age of 70, and women with the syndrome are at increased risk of endometrial and ovarian cancers.

"While the increase in BRCA testing is encouraging, it is far from optimal. And the uptake of MMR testing for Lynch syndrome - responsible for 5% of all colorectal cancers - is frankly disappointing", says Professor Pujol. "And of course, positive test results may have implications for other family members.

"While we have only studied the situation in France, we believe that our findings would be likely to be replicated in many other countries across the world. It is extremely worrying that such a simple test, which has the potential to spare whole families from devastating illness, is being so under-used. We urgently need a major programme of awareness among all those concerned, involving medical education and training, information programmes for patients and their families, public health campaigning, and improved genetic counselling," he concluded.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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World's Oldest Human Tumor Discovered - Over 120,000 Years Old

Editor's Choice
Academic Journal
Main Category: Cancer / Oncology
Article Date: 07 Jun 2013 - 0:00 PDT Current ratings for:
World's Oldest Human Tumor Discovered - Over 120,000 Years Old

Researchers have just discovered the world’s oldest tumor, in the rib of a 120,000 year old Neanderthal in Croatia.

It is a very rare discovery considering that tumors were uncommon in prehistoric populations. Tumors in fleshy tissue decay quickly - making them difficult to identify.

Spelling: both "Neandertals" and "Neandertals" are correct.

The bone was originally excavated a hundred years ago and scientists have just found out that the it has a cavity, where a tumor, known as fibrous dysplasia, replaced what should have been inner bone structure.

Fibrous dysplasia is not considered to be cancerous, because the tumors do not spread to other tissues.

According to David Frayer, professor of anthropology at the University of Kansas, and co-author of the paper:

"It's evidence that Neanderthals suffered tumors - that they were susceptible to the same kinds of diseases that we see in modern humans. Before this, the earliest tumor in bone that we've seen goes back to an Egyptian mummy. So this is 100,000 years older than the previous tumor that has been found. There is no evidence of cancer older than this in the human fossil record."

The 30-millimeter-long left rib fragment was unearthed between 1899 and 1905 in a Croatian cave that contained around 900 Neanderthal bones - hundreds of thousands of years old.

Back in the 1980s, all the bones from the cave were x-rayed and published in a book which showed each radiogram, with the exception of the rig fragment - which appeared burned out in the x-ray image.

Finally, using new high quality X-rays, researchers have been able to look at the bone more clearly.

They found that the rib contained a cavity 18 millimeters in length and 7.6 millimeters wide. After thorough analysis with radiograph and CT scans, the scientists concluded that the cavity was the site of a benign tumor associated with Fibrous dysplasia, which "is a developmental disorder of bone in which lesions develop fibrous tissue and spicules of woven bone."

Frayer said:

"It wasn't a small tumor. It was a fairly large one, probably bulging at the base of the rib. We're not sure how far along it was, but it was well-expressed in the bone. It was in the upper third of the back, and muscles attach there that are associated with raising the arm."

Frayer also mentioned that there may have been other bones involved, but they have not been identified. Adding that, although the site contained more than 900 bones "very few of them are associated one with the other. And while there are other pathologies, none of the others show evidence of a tumor."

Neanderthals are more similar to modern day humans than previously thought.

Scientists were once sure that Neanderthals had no influence on the evolutionary line of modern day humans., However, although Neanderthals died out 30,000 years ago and were a different species of human compared to modern day homo sapiens, we share much of the same DNA.

Frayer concluded:

"We have actual nuclear DNA from a number of different Neanderthals - not complete sequences - but segments of nuclear DNA. So we know that Neanderthals have a set of unique genes that were passed on to modern humans. It's about 4 percent of our genetic makeup."

By analyzing DNA extracted from three Neanderthal bones over 40,000 years old, European and the US researchers revealed that some Neanderthal DNA were passed on to humans.

Written by Joseph Nordqvist
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our cancer / oncology section for the latest news on this subject. "Fibrous Dysplasia in a 120,000+ Year Old Neandertal from Krapina, Croatia"
Janet Monge, Morrie Kricun, Jakov Radov?i?, Davorka Radov?i?, Alan Mann, David W. Frayer
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'Undruggable' To Druggable: A New Target For Cancer Drug Development

Main Category: Stem Cell Research
Also Included In: Cancer / Oncology;??Lymphoma / Leukemia / Myeloma;??Genetics
Article Date: 19 Jun 2013 - 1:00 PDT Current ratings for:
'Undruggable' To Druggable: A New Target For Cancer Drug Development

Harvard Stem Cell Institute (HSCI) researchers have identified in the most aggressive forms of cancer a gene known to regulate embryonic stem cell self-renewal, beginning a creative search for a drug that can block its activity.

The gene, SALL4, gives stem cells their ability to continue dividing as stem cells rather than becoming mature cells. Typically, cells only express SALL4 during embryonic development, but the gene is re-expressed in nearly all cases of acute myeloid leukemia and 10 to 30 percent of liver, lung, gastric, ovarian, endometrial, and breast cancers, strongly suggesting it plays a role in tumor formation.

In work published in the New England Journal of Medicine, two HSCI-affiliated labs - one in Singapore and the other in Boston - show that knocking out the SALL4 gene in mouse liver tumors, or interfering with the activity of its protein product with a small inhibitor, treats the cancer.

"Our paper is about liver cancer, but it is likely true about lung cancer, breast cancer, ovarian cancer, many, many cancers," said HSCI Blood Diseases Program leader Daniel Tenen, who also heads a laboratory at the Cancer Science Institute of Singapore (CSI Singapore). "SALL4 is a marker, so if we had a small molecule drug blocking SALL4 function, we could also predict which patients would be responsive."

Studying the therapeutic potential of a transcription factor is unusual in the field of cancer research. Transcription factors are typically avoided because of the difficulty of developing drugs that safely interfere with genetic targets. Most cancer researchers focus their attention on kinases.

The HSCI researchers' inquiry into the basic biology of the SALL4 gene, however, revealed another way to interfere with its activity in cancer cells. The gene's protein product is responsible for turning off a tumor-suppressor gene, causing the cell to divide uncontrollably. Using this knowledge, the researchers demonstrated that targeting the SALL4 protein with druglike molecules could halt tumor growth. "The pharmaceutical companies decided that if it is not a kinase and it is not a cell surface molecule, then it is 'undruggable,' " Tenen said. "To me, if you say anything is 'undoable,' you are limiting yourself as a biomedical scientist."

Earlier this year, Tenen's co-author, HSCI-affiliated faculty member Li Chai, a Harvard Medical School assistant professor of pathology at Brigham and Women's Hospital, published a paper in the journal Blood, reporting that a SALL4 inhibitor has similar treatment potential in leukemia cells.

Chai took blood samples from patients with acute myeloid leukemia, treated the leukemic cells with the inhibitor that interferes with SALL4 protein activity, and then transplanted the blood into mice. The result was a gradual regression of the same cancer in mice.

"I am excited about being on the front line of this new drug development," Chai said. "As a physician-scientist, if I can find a new class of drug that has very low toxicity to normal tissues, my patients can have a better quality of life."

Chai and Tenen are now working with HSCI Executive Committee member Lee Rubin, the Harvard Institute of Chemistry and Cell Biology, and James Bradner of Dana-Farber Cancer Institute, another HSCI-affiliated faculty member, to overcome the technical challenges of drug development and demonstrate the potential of SALL4 interference to treat other forms of cancer.

"I think as academics, we seek to engage drug companies because they can do these types of things better than we can," Tenen said. "But, also as an academic, I want to go after the important biologic targets that are not being sought after by the typical drug company - because if we do not, who will?"

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our stem cell research section for the latest news on this subject. The basic research that explored the biology of SALL4 was financed by a 2007 seed grant from HSCI, with more recent funding provided by a Singapore Translational Research Award from the Singapore National Medical Research Council, and grants from the Singapore Ministry of Education and National Research Foundation, and the National Institutes of Health. Kol Jia Yong, Chong Gao, and Henry Yang, among others, contributed to this work.
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''Undruggable' To Druggable: A New Target For Cancer Drug Development'

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Virus Combination Effective Against Deadly Brain Tumor, Moffitt Cancer Center Study Shows

Main Category: Cancer / Oncology
Also Included In: Neurology / Neuroscience
Article Date: 24 Jun 2013 - 1:00 PDT Current ratings for:
Virus Combination Effective Against Deadly Brain Tumor, Moffitt Cancer Center Study Shows

A combination of the myxoma virus and the immune suppressant rapamycin can kill glioblastoma multiforme, the most common and deadliest malignant brain tumor, according to Moffitt Cancer Center research. Peter A. Forsyth, M.D., of Moffitt's Neuro-Oncology Program, says the combination has been shown to infect and kill both brain cancer stem cells and differentiated compartments of glioblastoma multiforme.

The finding means that barriers to treating the disease, such as resistance to the drug temozolomide, may be overcome. The study, by Forsyth and colleagues in Canada, Texas and Florida, appeared in a recent issue of Neuro-Oncology.

"Although temozolomide improves survival for patients with glioblastoma multiforme, drug resistance is a significant obstacle," said Forsyth, the study lead author. "Oncolytic viruses that infect and break down cancer cells offer promising possibilities for overcoming resistance to targeted therapies."

The authors note that oncolytic viruses have the potential to provoke a multipronged attack on a tumor, with the potential to kill cancer cells directly through viral infection and possibly through inducing the immune system to attack the tumor. The multipronged approach might get around some of the classical resistance mechanisms that have plagued both targeted therapies and conventional chemotherapies.

Several oncolytic viruses, both alone or in combination with small molecule inhibitors, have been tested and show promise for malignant gliomas. However, most have not been effective in killing cancer cells. Two likely obstacles may be the patient's own anti-viral immune response and limited virus distribution.

"Based on our previous work with myxoma virus, we considered it to be an excellent oncolytic virus candidate against brain cancer stem cells," explained Forsyth.

The researchers found that brain cancer stem cells were susceptible to myxoma virus in the laboratory cultures (in vitro) and in animal models (in vivo), including in temozolomide-resistant cell lines.

"We also found that myxoma virus with rapamycin is a potentially useful combination. The idea that cancer cells can be killed by a harmless virus is an exciting prospect for therapy," Forsyth said.

The precise mechanism rapamycin uses to enhance infection in brain cancer stem cells is unknown, and the combination therapy does not result in cures. However, researchers are investigating other drugs that may improve the effectiveness of myxoma virus when used in combination, and they are evaluating the use of other strains of myxoma virus that might be more effective.

"Although our study adds myxoma virus to the list of oncolytic viruses capable of infecting and killing these cells, which strengthens its candidacy for clinical application, our model will need clinical application to determine its safety for patients," concluded the authors. "We expect that intracranial injections of myxoma virus will be safe based on our extensive preclinical work and the demonstrated safety of other oncolytic viruses in clinical trials."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject. This study was supported by grants from the National Institutes of Health (R01 AI080607, R21 CA149869, and R01 CA138541).

Researchers from the University of Florida, University of Calgary, University of Texas and Ottawa Regional Cancer Centre Research Laboratories contributed to this work and publication.

H. Lee Moffitt Cancer Center & Research Institute

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Why Does Promising Anti-Cancer Therapy Suddenly Stop Working?

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Academic Journal
Main Category: Cancer / Oncology
Article Date: 24 Jun 2013 - 9:00 PDT Current ratings for:
Why Does Promising Anti-Cancer Therapy Suddenly Stop Working?

Why does anti-cancer therapy stop working at a specific stage? Scientists in Israel and the USA believe they have made a breakthrough in understanding why a hopeful anti-cancer therapy fails to destroy tumor cells successfully.

The researchers, whose study is published in PNAS (Proceedings of the National Academy of Sciences), believe their findings may lead to new approaches in overcoming this cul-de-sac.

Suppressing the mTOR (mammalian target Of Rapamycin) protein has been extremely challenging for oncologists.

mTOR plays a key role in regulating vital cell growth processes - it is a bit like a communications command center, receiving external signals from hormones, growth factors and proteins. It then sends out "on" or "off" signals for the cell to grow and divide, seek nutrition, or use that nutrition. mTOR is strongly activated in several solid cancers.

While drugs have been shown to suppress mTOR and have been successful in causing the death of cancer cells in the outer layers of malignant tumors, in clinical trials they have failed in destroying the core of those tumors.

Hypoxia (lack of oxygen) is an almost-universal characteristic of solid tumors that can affect how tumors respond to therapies. Scientists know that the condition of hypoxia affects the behavior of mTOR signaling, but nobody knew what the mechanism was.

Prof. Emeritus Raphael D. Levine, from the Institute of Chemistry at the Hebrew University of Jerusalem, Israel, and scientists from the David Geffen School of Medicine at UCLA and the California Institute of Technology set out to determine what role hypoxia plays on mTOR signaling in model brain cancer systems and whether this could explain why promising mTOR drugs fail.

They used a new microchip technology to measure the mTOR protein-signaling network in cancer cells. They also used a new set of theoretical tools derived from the physical sciences to interpret the results. This dual approach simplified an otherwise extremely complex biological system.

The mTOR biochemical pathway is a complex one

The investigators found that at a specific level of hypoxia, which is typical in solid tumors, the mTOR signaling network switches between two sets of properties. At exactly the moment when the switching over takes places, the theoretical models predicted that mTOR would not respond to mTOR-inhibiting medications.

According to the combined experiment finding, the researchers believe that the switching over might be a kind of phase transition, something not observed before in biological systems.

This phase transition happened very suddenly, and cells being studied stopped responding like they had done before. The authors wrote "In the case of the tumor, the 'drugging' of the mTOR ceased, meaning that the tumor was no longer inhibited."

These results: explain why promising mTOR-inhibiting drugs stop working at a specific stage"indicate that certain complex biological behaviors, which often confound scientists who are seeking to find effective therapies for human diseases, may be understood by the effective application of experimental and theoretical tools derived from the physical sciences."Levine wrote in the PNAS Abstract:

"We find a hypoxia-induced switch within a mammalian target of rapamycin (mTOR) signaling network. At the switching point, mTOR is predicted, and then shown by experiment, to be unresponsive to inhibition. These results may help explain the undistinguished performance of mTOR inhibitors in certain clinical trials."

In an animal study, scientists from the University of California San Diego, La Jolla, found that mTOR-inhibitors may have adverse effects on heart function in patients with ongoing heart problems.

Written by Christian Nordqvist
Copyright: Medical News Today
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posted by Greg Pawelski on 24 Jun 2013 at 12:17 pm

One of the themes at the 103rd Annual American Association of Cancer Research was the growing recognition that human tumors exist as microenvironments and not isolated single cells. The tumor microenvironment is characterized by regions of fluctuating hypoxia, low pH, and nutrient deprivation. Each of these microenvironment factors has been shown to cause severe disturbance in cell metabolism and physiology.

By examining drug-induced cell death events in native-state 3D (three dimensional) microclusters, the functional profiling platform has the unique capacity to capture stromal, cytokines (chemokines), macrophages, lymphocytes, vascular and inflammatory cell interactions with tumor cells, known to be crucial for clinical response prediction.

The microclusters recapitulate the human tumor environment, while the "3D" advancement recreates the extracellular matrix (metalloproteinases). The platform studies cancer response to drugs within this microenvironment, enabling it to provide clinically relevant predictions to cancer patients. It is this capacity to study human tumor microenvironments that distinguishes it from other platforms in the field.

Tumors are very complex organisms. Ignoring this complexity, most studies of human cancer in culture have focused upon individual tumor cells that have been removed from their complex microenvironment.

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'Why Does Promising Anti-Cancer Therapy Suddenly Stop Working?'

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Tumour "Tweets" Influence Other Cells

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Main Category: Biology / Biochemistry
Also Included In: Cancer / Oncology;??Neurology / Neuroscience
Article Date: 24 Jun 2013 - 2:00 PDT Current ratings for:
Tumour "Tweets" Influence Other Cells

Groundbreaking research from Australia reveals that brain tumours release small bits of information, rather like "tweets", that interact with blood vessel cells in a way that causes them to undergo significant changes. The researchers believe the discovery may lead to new treatments.

Writing in the 17 June online issue of RNA Biology, Michael Buckland, associate professor in the University of Sydney's Brain and Mind Research Institute (BMRI), and colleagues, describe how they found brain tumours release microvesicles containing new forms of RNA, and these interact with nearby brain blood vessel cells.

RNA (short for ribonucleic acid), a close cousin of DNA, is a group of long-chained molecules that among other things, control gene expression and help transfer the genetic code held in DNA to make proteins.

Microvesicles are tiny pockets of cell plasma, enclosed in a membrane. They are released by cells and were once considered to be junk, or debris.

Buckland says scientists are just becoming aware of the significance of microvesicles, and how they may be important for health and disease.

For instance, there have been suggestions that microvesicles may have potential as clinical biomarkers for individual cancers.

"It seems that many cells release microvesicles allowing them to communicate and influence other cells nearby and in distant parts of the body in real-time - much like tweeting," Buckland says in a statement.

Tumours thrive in different environments to healthy tissue. As the tumour grows it interacts with its environment, for instance changing the blood supply to suit its own needs.

To do this the tumour must interact with other cells, and modify their gene expression so they make the proteins that suit the tumour rather than those that suit healthy tissue.

The team had a hunch that one way brain tumour cells (gliomas) do this is via the microvesicles.

So they designed a study that took an "unbiased approach to identifying RNAs in glioma-derived microvesicles, and explored their potential to regulate gene expression in recipient cells".

For the study, the team grew brain tumour cells (gliomas) in culture and harvested the microvesicles they released into the culture medium.

When they added the glioma-produced microvesicles to cultures of brain blood vessel cells, they triggered significant changes in the cells, including many changes in gene expression.

On closer examination they found that the glioma microvesicles contained complex populations of coding and non-coding RNA, and the proportions of these populations were different to those from the cells they came from.

Compared to the glioma cells that made them, glioma microvesicles had lower levels of microRNA and higher levels of unusual or new non-coding RNA, most of which "have no known function", write the authors, who conclude:

"Our data suggest that the scope of potential actions of tumor-derived microvesicles is much broader and more complex than previously supposed, and highlight a number of new classes of small RNA that remain to be characterized."

Buckland says their findings suggest microvesicles "likely to play an important role in the changes to blood vessels seen in high grade brain tumours, the most common form in Australian adults".

They present a new target for treatment against brain tumours, he says, adding that:

"Furthermore, they can be detected in the blood of patients with brain tumours, and may be an important diagnostic tool in the future."

A biosciences company has also suggested, at a scientific meeting in 2011, that the fact circulating microvesicles have different RNA profiles highlights their potential use in cancer detection and monitoring.

Written by Catharine Paddock PhD
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our biology / biochemistry section for the latest news on this subject. "Glioma microvesicles carry selectively packaged coding and noncoding RNAs which alter gene expression in recipient cells"; Cheryl C.Y. Li, Sally Eaton, Paul E. Young, Maggie Lee, Rupert Shuttleworth, David T. Humphreys, Georges E. Grau, Valery Combes, Mary Bebawy, Joyce Gong, Susan Brammah, Michael E. Buckland, and Catherine M. Suter; RNA Biology, Volume 10, Issue 8, published online 17 June 2013; Link to Abstract.
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Three Important Studies Published In The June Issue Of Neurosurgery

Main Category: Neurology / Neuroscience
Also Included In: Cancer / Oncology
Article Date: 24 Jun 2013 - 0:00 PDT Current ratings for:
Three Important Studies Published In The June Issue Of Neurosurgery

The results of three important studies have been published in the June issue of Neurosurgery, official journal of the Congress of Neurological Surgeons. The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health.

One study indicates that continuous "machine learning" using artificial neural networks (ANNs) may improve the ability to predict survival in patients with advanced brain cancers. Another study in the June Neurosurgery supports increased use of stereotactic biopsy for obtaining samples of brainstem tumors; while another calls for medical professionals and specialty societies to play an increased role in evaluating "off label" uses of medications.

Artificial Neural Networks Predict Brain Cancer Prognosis

Dr. Matthew Ewend of University of North Carolina and colleagues evaluated the use of ANNs to predict the chances of survival for patients with brain cancer. Based on the biological functioning of brain cells, ANNs are computer programs designed "to learn patterns within a data set and then apply that learning for recognition and prediction."

The researchers performed a pilot study of ANNs using data on patients treated for advanced brain cancer at several hospitals. The results showed that ANNs beat standard prediction models for predicting patient survival. "Pooled voting" of five ANNs correctly predicted the risk of death within one year in 84 percent of patients, compared to 78 percent with a single ANN and 74 percent using standard statistical techniques.

The predictive power of ANNs would likely increase over time, providing a "facile and powerful means or predicting survival" in patients with brain cancers or other conditions. The researchers conclude, "With the explosion in clinical data over the past few years....we anticipate a growing need for modern machine learning techniques such as ANNs to properly make use of the information at our disposal and realize its full benefit for clinical care."

New Proposal for Evaluating 'Off Label' Uses of Medications

An improved process for evaluating "off label" use of drugs - using medications for purposes other than those for which they were approved - is described by Donlin Long, MD, PhD, of Johns Hopkins School of Medicine and Clark Watts, MD, JD, of University of Texas School of Law. They cite the example of bone morphogenetic protein-2 (BMP-2), a product approved to promote bone growth in one specific type of spinal fusion surgery.

After approval, surgeons started using BMP-2 for various other types of spinal surgery - leading to complications in some cases. The authors believe that problems resulting from "uncontrolled" off-label use have had a chilling effect, leading to missed opportunities to develop effective uses of BMP-2.

In the proposed approach, medical specialty societies such as the Congress of Neurological Surgeons would play a leading role in setting parameters for off-label use of new products, and in systematically gathering evidence of effectiveness. Drs. Long and Watts write, "Our goal is to challenge our professional societies to take a leadership role in the study of valid uses of new drugs and devices in a cooperative, constructive relationship with government regulators and industry."

Stereotactic Biopsy for Brainstem Tumors

Dr. Philipp Kickingereder of University Hospital of Cologne and colleagues present a review of research evidence on stereotactic biopsy - using triangulation techniques to precisely localize tumors - to obtain samples of uncommon brainstem cancers. While stereotactic biopsy is not a new technique, surgeons may hesitate to use it for brainstem tumors because of the perceived risks of the procedure.

But the available data show a diagnostic success rate of 96 percent, with a relatively low complication rates. Dr. Kickingereder and coauthors conclude that stereotactic biopsy is a safe and valuable procedure that provides samples for simultaneous tissue and genetic analysis - which may allow more individualized treatment. They recommend its use in all adult patients with brainstem cancers, as well as in certain groups of children.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Whole Exome Sequencing Seeks Out Adenoid Cystic Carcinoma

Main Category: Cancer / Oncology
Also Included In: Dentistry;??Genetics
Article Date: 19 Jun 2013 - 0:00 PDT Current ratings for:
Whole Exome Sequencing Seeks Out Adenoid Cystic Carcinoma

Adenoid cystic carcinoma (ACC) is a slow-growing and often fatal malignancy that can occur at multiple organ sites, but is most frequently found in the salivary glands. The primary treatment is surgical removal; however, the majority of patients develop metastatic disease.

In this issue of the Journal of Clinical Investigation, researchers led by Andrew Futreal at the Wellcome Trust Sanger Institute in Cambridge, MA, performed a type of genetic sequencing known as whole exome sequencing of 24 ACC cases. They identified a genetic translocation that can precipitate disease and determined that a large number of disease-associated mutations occurred in genes that modify DNA.

In the accompanying commentary, Henry Frierson, Jr. of the University of Virginia emphasizes that identifying individual mutations will aid the development of personalized therapy.

TITLE: Whole exome sequencing of adenoid cystic carcinoma

View this article at: http://www.jci.org/articles/view/67201?key=d9e8a757b7c521272b6f

ACCOMPANYING COMMENTARY TITLE: Mutation signature of adenoid cystic carcinoma: evidence for transcriptional and epigenetic reprogramming

View this article at: http://www.jci.org/articles/view/69070?key=b1da65c50c2dc7a2e200

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60 Years Of Data Suggest A Link Between Obesity And Height In Childhood And Endometrial Cancer In Adulthood

Main Category: Obesity / Weight Loss / Fitness
Also Included In: Cancer / Oncology
Article Date: 14 May 2013 - 1:00 PDT Current ratings for:
60 Years Of Data Suggest A Link Between Obesity And Height In Childhood And Endometrial Cancer In Adulthood

New research presented at the European Congress in Liverpool (ECO) beginning today (Sunday 12 May) shows a possible link between obesity and height in childhood and endometrial cancer in adulthood. The research* is by Julie Aarestrup, Institute of Preventive Medicine, Copenhagen University Hospital, Copenhagen, Denmark, and colleagues.

Endometrial cancer is in Europe the fourth most common cancer in women with more than 90,000 new cases diagnosed each year. In adult women, a high body mass index (BMI) is associated with an increased risk of endometrial cancer, whereas associations with height are limited. It is largely unknown, however, whether any of the risk originates in childhood. In this new study, the researchers investigated if childhood BMI and height at each age from 7-13 years were associated with risk of endometrial cancer in adulthood.

The total cohort consisted of 158,459 women from the Copenhagen School Health Records Register with data on measured heights and weights at 7-13 years who were born from between 1930 and 1989. BMI and height were transformed into age-specific z-scores, a method for comparing how large or tall a child is compared to a reference population. Follow-up occurred by linkage via a personal identification number to the Danish Cancer Registry, the Hospital Discharge Register (hysterectomy information), and the vital statistics register. Subjects were followed until a diagnosis of endometrial cancer, hysterectomy, death, emigration, loss-to-follow-up, or December 31, 2010; whichever came first.

The researchers found 940 diagnoses of endometrial cancer occurred during follow-up. At age 7 the risk of endometrial cancer in adulthood increased 18% per increase in BMI z-score and by 12% per increase in height z-score. To put this in perspective, compared to an average height and weight girl born in the late 1950s (122.4 cm, 22.9kg), another girl of the same height but who weighed 3.3 kg more would have an 18% higher risk of endometrial cancer. Further, height also increased the risk; compared to the same average girl, another girl of the same age but who was 5.2cm taller had a 12% increased risk of endometrial cancer. When looking at a girl aged 13 years born in the late 1950s compared to an average height and weight girl (156.7cm, 44.6 kg), another girl of the same height but who weighed 6.8kg more had a 24% increased risk of endometrial cancer; and another girl of the same age but who was 6.9cm taller had a 15% increased risk of endometrial cancer.

The peak age of endometrial cancer diagnosis is approximately 65 years. Therefore girls born in the 1950s are approaching their highest risk years. As the cohort members from later birth years continue to age, the study will continue to follow them in order to assess their risk of endometrial cancer.

Aarestrup concludes: "Higher BMI and height during childhood are associated with an increased risk of endometrial cancer in adulthood. These results suggest that some risk of endometrial cancer observed in adult women has its origins in childhood."

Research is ongoing to refine these results by subtypes of endometrial cancer. This project forms part of a series of studies led by Dr. Jennifer L. Baker, also of the Institute of Preventive Medicine, that are exploring associations between childhood body size and the later risk of cancers including those of the liver, prostate and thyroid. *This study is part of the European Research Council (ERC) project 'Childgrowth2cancer: Childhood body size, growth and pubertal timing and the risk of cancer in adulthood' which is run by Associate Professor Jennifer L. Baker.

Article adapted by Medical News Today from original press release. Source: Source: European Congress on Obesity (ECO)
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Avastin Can Lengthen The Lives Of Advanced Cervical Cancer Patients

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Main Category: Cervical Cancer / HPV Vaccine
Also Included In: Cancer / Oncology
Article Date: 03 Jun 2013 - 10:00 PDT Current ratings for:
Avastin Can Lengthen The Lives Of Advanced Cervical Cancer Patients

The addition of targeted therapy Avastin (bevacizumab) with chemotherapy can significantly lengthen the lives of women with advanced cervical cancer by close to 30%, according to research presented at the 2013 American Society of Clinical Oncology Congress.

The finding is an important discovery in the fight against cervical cancer - the most common cancer in women under the age of 35.

More than 3,000 women in the UK are diagnosed with cervical cancer annually, while 1,000 will die from it. Cervical cancer is normally treated with surgery, radiotherapy, and chemotherapy. If the cancer is detected early and treated promptly, the prognosis is generally good.

Screening and vaccination against the human papilloma virus is crucial in preventing cervical cancer altogether, as well as keeping it from reaching an advanced stage if it does develop. For those patients who are diagnosed at an advanced stage, it becomes harder to treat the disease.

The research presented from this study is known as GOG 240. GOG 240 is an independent, National Cancer Institute (NCI) -sponsored phase III trail examining the effectiveness and safety of Avastin with chemotherapy (paclitaxel and topotecan or cisplatin) to treat women with recurrent, persistent, or advanced cervical cancer (stage IVb), that was not cured by standard treatment methods.

The study consisted of 452 women in the U.S. and Spain who were randomly assigned to one of four treatment schedules: paclitaxel and cisplatinpaclitaxel, cisplatin and Avastin (15 mg/kg every three weeks)paclitaxel and topocetan paclitaxel, topotecan and AvastinThe research revealed that the women who underwent combination treatment with chemotherapy and Avastin lived almost 30% longer, and when compared to those who were just treated with chemotherapy alone: the median overall survival was of 17 months compared to 13.3 months, respectively.

Also, the percentage of patients who responded positively to therapy increased by a third from 36% to 48%. The participants who received bevacizumab had more side effects than those who did not, however, these side effects were consistent with those previously known to be linked to bevacizumab.

Professor Stan Kaye, Head of Clinical Studies at The Institute of Cancer Research, London, and Consultant Medical Oncologist in the Gynaecology Unit at The Royal Marsden Hospital, said:

"The improvements in overall survival achieved for women with advanced cervical cancer treated with Avastin are extremely encouraging. Thousands of women are diagnosed with cervical cancer every year in the UK and for those with recurrent disease there is a desperate need for more treatment options."

Bevacizumab has a well-confirmed tolerability profile with the most frequently seen adverse effects in clinical trials listed as: hypertensionpainproteinuria (abnormal amount of protein in the bloodneutropeniaThese side effects are generally easy to take care of. The study did not find any new adverse effects. Bevacizumab was also associated with higher rates of grade 3 bleeding, thrombosis embolism, and gastrointestinal fistula.

Robert Music, Director of Jo's Cervical Cancer Trust, said:

"For women who receive a late stage diagnosis of cervical cancer the prognosis can often be poor. The results of this research look promising and if this work can go some way in improving outcomes and overall survival rates in women with advanced cervical cancer then that is a positive step."

Bevacizumab is not currently licensed for the treatment of advanced cervical cancer.

Avastin is approved for four different types of cancers in the United States: mCRC (metastatic Colorectal Cancer), NSCLC (Non-Small Cell Lung Cancer), rGBM (recurrent Glioblastoma Multiforme) and RCC (Renal Cell Cancer).

In 2011, the FDA removed the approval of Avastin for the treatment of breast cancer. The regulating body explained that Avastin is not effective or safe for that type of cancer.

Written by Kelly Fitzgerald

Copyright: Medical News Today
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Shared Decision Making And How Decision Aids Help Guide Choices For Cancer Screening

Main Category: Cancer / Oncology
Also Included In: Primary Care / General Practice;??Public Health
Article Date: 14 May 2013 - 1:00 PDT Current ratings for:
Shared Decision Making And How Decision Aids Help Guide Choices For Cancer Screening

When it comes to a cancer diagnosis, timing can be everything - the sooner it's found, the more treatable it is. But when and how often should someone get screened?

A growing number of educational, interactive tools known as "decision aids" - such as videodiscs, audiotapes, workbooks and pamphlets - are intended to supplement patient-doctor discussions on the pros and cons of timing, methods and frequency for different types of cancer screening.

A University of Michigan study found that despite strong recommendations from the medical community to use these aids to help patients make more well-informed decisions, there is lack of evidence on whether they work - which may lead to fewer doctors using them.

"We continue to see more cancer screening options and also conflicting recommendations on whether to get screened, which method to use and how often it should be done," says lead author Masahito Jimbo, M.D., Ph.D., M.P.H., associate professor in family medicine and urology at the U-M Medical School.

"Our goal was to determine whether decision aids could potentially lead to better shared decision-making regarding screening between the patient and the clinician. There is evidence that decision aids are fairly effective in improving patient knowledge but we found that they may not be used as well and effectively as they could be."

The study appears in CA: A Cancer Journal for Clinicians, a medical journal published for the American Cancer Society.

Decision aids are delivered as self-administered or practitioner administered tools designed to help patients understand the disease, associated tests and treatments and the risks versus benefits of different types of screening. They are designed to help address such issues as whether to get a stool blood test versus a colonoscopy for colon cancer screening or whether women under the age of 50 should get screened for breast cancer at all.

Researchers reviewed 73 decision aids for breast, cervical, colon and prostate cancers. Just half of the decision aids, 36, were evaluated for subsequent screening behavior. Only a quarter of the decision aids, 18, had been assessed for their effect on shared decision making. Little information was available on the feasibility and outcomes of integrating decision aids into actual practice.

"These decision aids are designed as tools to improve communication between patients and clinicians, so it's surprising that there is so little data to support claims that they improve shared decision making," Jimbo says.

With the push towards more sophisticated electronic health records, decision aids may become more available to patients looking for additional guidance on health decisions, authors note.

Certain screening options also continue to be debated among the medical community. The U.S. Preventive Services Task Force, for example, recommended against routine screening for prostate cancer, while other guidelines encourage doctors and patients to weight the risks and benefits. Decision aids may assist patients and doctors work through those conflicting recommendations together.

"Do decision aids help improve communication between a patient and physician and can that improved communication lead to better outcomes - those are the broader questions we need to answer," Jimbo says.

"There is also some disconnect between how decision aids can help if they're actually applied and physicians actually using them. As we see an increased emphasis on the importance of shared decision making between patients and doctors, we need to better understand what the most valuable tools are in aiding this goal."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject. Additional Authors: Gurpreet K. Rana, MLIS; Sarah Hawley, Ph.D., M.P.H.; Margaret Holmes-Rovner, Ph.D.; Karen Kelly-Blake, Ph.D.; Donald E. Nease, Jr., M.D.; Mack T. Ruffin IV, M.D., M.P.H.
Disclosure: Dr. Jimbo receives funding from the National Cancer Institute (Grant RO1CA152413).
Funding: National Cancer Institute (Grant RO1CA152413).
Reference: "What is Lacking in Current Decision Aids on Cancer Screening," American Cancer Society, Inc., doi:10.3322/caac.21180.
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