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Precision Medicine: What Is Cancer, Really? Scientists overview here.

May 22nd, 2017

The men and women who are trying to bring down cancer are starting to join forces rather than work alone. Together, they are winning a few of the battles against the world’s fiercest disease. For this unprecedented special report, we visited elite cancer research centers around the country to find out where we are in the war.

I. Precision Medicine: What Is Cancer, Really?

When you visit St. Jude Children’s Research Hospital in Memphis, Tennessee, you expect to feel devastated. It starts in the waiting room. Oh, here we go with the little red wagons, you think, observing the cattle herd of them rounded up by the entrance to the Patient Care Center. Oh, here we go with the crayon drawings of needles. The itch begins at the back of your throat, and you start blinking very fast and mentally researching how much money you could donate without starving. Near a row of arcade games, a preteen curls his face into his mother’s shoulder while she strokes his head. Oh, here we go.

But the more time you spend at St. Jude, the more that feeling is replaced with wonder. In a cruel world you’ve found a free hospital for children, started by a Hollywood entertainer as a shrine to the patron saint of lost causes. There is no other place like this. Corporations that have nothing to do with cancer—nothing to do with medicine, even—have donated vast sums of money just to be a part of it. There’s a Chili’s Care Center. The cafeteria is named for Kay Jewelers.

Scott Newman’s office is in the Brooks Brothers Computational Biology Center, where a team of researchers is applying computer science and mathematics to the question of why cancer happens to children. Like many computer people, Newman is very smart and a little quiet and doesn’t always exactly meet your eyes when he speaks to you. He works on St. Jude’s Genomes for Kids project, which invites newly diagnosed patients to have both their healthy and tumor cells genetically sequenced so researchers can poke around.

“Have you seen a circle plot before?” Newman asks, pulling out a diagram of the genes in a child’s cancer. “If I got a tattoo, it would be one of these.” Around the outside of the circle plot is something that looks like a colorful bar code. Inside, a series of city skylines. Through the center are colored arcs like those nail-and-string art projects students make in high school geometry class. The diagram represents everything that has gone wrong within a child’s cells to cause cancer. It’s beautiful.

A Genetic Disaster: This circular visualization shows real gene mutations found in 3,000 pediatric cancers at St. Jude Children’s Research Hospital. Genes with sequence mutations are labeled in blue; those with structural variations are in red; and those

“These are the genes in this particular tumor that have been hit,” Newman says in a Yorkshire accent that emphasizes the t at the end of the word hit in a quietly violent way. “And that’s just one type of thing that’s going on. Chromosomes get gained or lost in cancer. This one has gained that one, that one, that one, that one,” he taps the page over and over. “And then there are structural rearrangements where little bits of genome get switched around.” He points to the arcs sweeping across the page. “There are no clearly defined rules.”

It’s not like you don’t have cancer and then one day you just do. Cancer—or, really, cancers, because cancer is not a single disease—happens when glitches in genes cause cells to grow out of control until they overtake the body, like a kudzu plant. Genes develop glitches all the time: There are roughly twenty thousand genes in the human body, any of which can get misspelled or chopped up. Bits can be inserted or deleted. Whole copies of genes can appear and disappear, or combine to form mutants. The circle plot Newman has shown me is not even the worst the body can do. He whips out another one, a snarl of lines and blocks and colors. This one would not make a good tattoo.

“As a tumor becomes cancerous and grows, it can accumulate many thousands of genetic mutations. When we do whole genome sequencing, we see all of them,” Newman says. To whittle down the complexity, he applies algorithms that pop out gene mutations most likely to be cancer-related, based on a database of all the mutations researchers have already found. Then, a genome analyst manually determines whether each specific change the algorithm found seems likely to cause problems. Finally, the department brings its list of potentially important changes to a committee of St. Jude’s top scientists to discuss and assign a triage score. The mutations that seem most likely to be important get investigated first.

It took thirteen years and cost $2.7 billion to sequence the first genome, which was completed in 2003. Today, it costs $1,000 and takes less than a week. Over the last two decades, as researchers like Newman have uncovered more and more of the individual genetic malfunctions that cause cancer, teams of researchers have begun to tinker with those mutations, trying to reverse the chaos they cause. (The first big success in precision medicine was Gleevec, a drug that treats leukemias that are positive for a common structural rearrangement called the Philadelphia chromosome. Its launch in 2001 was revolutionary.) Today, there are eleven genes that can be targeted with hyperspecific cancer therapies, and at least thirty more being studied. At Memorial Sloan Kettering Cancer Center in New York City, 30 to 40 percent of incoming patients now qualify for precision medicine studies.

Charles Mullighan,a tall, serious Australian who also works at St. Jude, is perhaps the ideal person to illustrate how difficult it will be to cure cancer using precision medicine. After patients’ cancer cells are sequenced, and the wonky mutations identified, Mullighan’s lab replicates those mutations in mice, then calls St. Jude’s chemical library to track down molecules—some of them approved medicines from all over the world, others compounds that can illuminate the biology of tumors—to see if any might help.

New York: Britta Weigelt and Jorge Reis-Filho use police forensics techniques to repair old tumor samples at Memorial Sloan Kettering so the samples can be genetically profiled.

If Mullighan is lucky, one of the compounds he finds will benefit the mice, and he’ll have the opportunity to test it in humans. Then he’ll hope there are no unexpected side effects, and that the cancer won’t develop resistance, which it often does when you futz with genetics. There are about twenty subtypes of the leukemia Mullighan studies, and that leukemia is one of a hundred different subtypes of cancer. This is the kind of precision required in precision cancer treatment—even if Mullighan succeeds in identifying a treatment that works as well as Gleevec, with the help of an entire, well-funded hospital, it still will work for only a tiny proportion of patients.

Cancer is not an ordinary disease. Cancer is the disease—a phenomenon that contains the whole of genetics and biology and human life in a single cell. It will take an army of researchers to defeat it.

Luckily, we’ve got one.

Interlude

“I used to do this job out in L.A.,” says the attendant at the Hertz counter at Houston’s George Bush Intercontinental Airport. “There, everyone is going on vacation. They’re going to the beaach or Disneyland or Hollywood or wherever.

“Because of MD Anderson, I see more cancer patients here. They’re so skinny. When they come through this counter, they’re leaning on someone’s arm. They can’t drive themselves. You think, there is no way this person will survive. And then they’re back in three weeks, and in six months, and a year. I’m sure I miss some, who don’t come through anymore because they’ve died. But the rest? They come back.”

II. Checkpoint Inhibitor Therapy: You Have the Power Within You!

On a bookshelf in Jim Allison’s office at MD Anderson Cancer Center in Houston (and on the floor surrounding it) are so many awards that some still sit in the boxes they came in. The Lasker-DeBakey Clinical Medical Research Award looks like the Winged Victory statue in the Louvre. The Breakthrough Prize in Life Sciences, whose benefactors include Sergey Brin, Anne Wojcicki, and Mark Zuckerberg, came with $3 million.

“I gotta tidy that up sometime,” Allison says.

Allison has just returned to the office from back surgery that fused his L3, L4, and L5 vertebrae, which has slightly diminished his Texas rambunctiousness. Even on painkillers, though, he can explain the work that many of his contemporaries believe will earn him the Nobel Prize: He figured out how to turn the immune system against tumors.

“One day, the miracles won’t be miracles at all. They’ll just be what happens.”

Allison is a basic scientist. He has a Ph.D., rather than an M.D., and works primarily with cells and molecules rather than patients. When T-cells, the most powerful “killer cells” in the immune system, became better understood in the late 1960s, Allison became fascinated with them. He wanted to know how it was possible that a cell roaming around your body knew to kill infected cells but not healthy ones. In the mid-1990s, both Allison’s lab and the lab of Jeffrey Bluestone at the University of Chicago noticed that a molecule called CTLA-4 acted as a brake on T-cells, preventing them from wildly attacking the body’s own cells, as they do in autoimmune diseases.

Allison’s mother died of lymphoma when he was a child and he has since lost two uncles and a brother to the disease. “Every time I found something new about how the immune system works, I would think, I wonder how this works on cancer?” he says. When the scientific world discovered that CTLA-4 was a brake, Allison alone wondered if it might be important in cancer treatment. He launched an experiment to see if blocking CTLA-4 would allow the immune system to attack cancer tumors in mice. Not only did the mice’s tumors disappear, the mice were thereafter immune to cancer of the same type.

Ipilimumab (“ipi” for short) was the name a small drug company called Medarex gave the compound it created to shut off CTLA-4 in humans. Early trials of the drug, designed just to show whether ipi was safe, succeeded so wildly that Bristol Myers Squibb bought Medarex for $2.4 billion. Ipilimumab (now marketed as Yervoy) became the first “checkpoint inhibitor”: It blocks one of the brakes, or checkpoints, the immune system has in place to prevent it from attacking healthy cells. Without the brakes the immune system can suddenly, incredibly, recognize cancer as the enemy.

“You see the picture of that woman over there?” Allison points over at his desk. Past his lumbar-support chair, the desk is covered in papers and awards and knickknacks and frames, including one containing a black card with the words “Never never never give up” printed on it. Finally, the photo reveals itself, on a little piece of blue card stock.

That’s the first patient I met,” Allison says. “She was about twenty-four years old. She had metastatic melanoma. It was in her brain, her lungs, her liver. She had failed everything. She had just graduated from college, just gotten married. They gave her a month.”

The woman, Sharon Belvin, enrolled in a phase-two trial of ipilimumab at Memorial Sloan Kettering, where Allison worked at the time. Today, Belvin is thirty-five, cancer- free, and the mother of two children. When Allison won the Lasker prize, in 2015, the committee flew Belvin to New York City with her husband and her parents to see him receive it. “She picked me up and started squeezing me,” Allison says. “I walked back to my lab and thought, Wow, I cure mice of tumors and all they do is bite me.” He adds, dryly, “Of course, we gave them the tumors in the first place.”

After ipi, Allison could have taken a break and waited for his Nobel, driving his Porsche Boxster with the license plate CTLA-4 around Houston and playing the occasional harmonica gig. (Allison, who grew up in rural Texas, has played since he was a teenager and once performed “Blue Eyes Crying in the Rain” onstage with Willie Nelson.) Instead, his focus has become one of two serious problems with immunotherapy: It only works for some people.

So far, the beneficiaries of immune checkpoint therapy appear to be those with cancer that develops after repeated genetic mutations—metastatic melanoma, non-small-cell lung cancer, and bladder cancer, for example. These are cancers that often result from bad habits like smoking and sun exposure. But even within these types of cancer, immune checkpoint therapies improve long-term survival in only about 20 to 25 percent of patients. In the rest the treatment fails, and researchers have no idea why.

Lately, Allison considers immune checkpoint therapy a “platform”—a menu of treatments that can be amended and combined to increase the percentage of people for whom it works. A newer drug called Keytruda that acts on a different immune checkpoint, PD-1, knocked former president Jimmy Carter’s metastatic melanoma into remission in 2015. Recent trials that blocked both PD-1 and CTLA-4 in combination improved long-term survival in 60 percent of melanoma patients. Now, doctors are combining checkpoint therapies with precision cancer drugs, or with radiation, or with chemotherapy. Allison refers to this as “one from column A, and one from column B.”

The thing about checkpoint inhibitor therapy that is so exciting—despite the circumscribed group of patients for whom it works, and despite sometimes mortal side effects from the immune system going buck-wild once the brakes come off—is the length of time it can potentially give people. Before therapies that exploited the immune system, response rates were measured in a few extra months of life. Checkpoint inhibitor therapy helps extremely sick people live for years. So what if it doesn’t work for everyone? Every cancer patient you can add to the success pile is essentially cured.

Jennifer Wargo and team remove lymph nodes from a melanoma patient.

Diabetes cured in mice. What next? Human Trials

May 9th, 2017

The new technique cures diabetes in mice by bypassing the immune system that attacks beta cells

According to the Center for Disease Control, 1.25 million people suffer from type 1 diabetes in the US alone. So far, it can only be managed with diet and regular doses of insulin, but scientists at UT Health San Antonio have invented a way of curing the disease in mice that may one day do the same for humans even with type 2 diabetes.

Type 1 diabetes is a particularly unpleasant condition. It occurs when the pancreas ceases to produce the insulin needed by the body to metabolize sugar and, until the invention of artificial insulin injections, it was as deadly as cancer. Type 2 is the less severe form of the disease, where the body produces insufficient insulin; it can often be managed through diet alone.

Surprisingly, diabetes is an autoimmune disease. Insulin is made by specialized cells in the pancreas, called beta cells, and sometimes the body’s immune system turns against itself and attacks these beta cells, destroying them. Diabetes results when this destruction is over 80 percent.

Invented by Bruno Doiron and Ralph DeFronzo, the UT Health technique uses gene transfer to alter cells in the pancreases of mice to make them think they’re beta cells and start making insulin. This involves taking selected genes from external beta cells and using viruses as carriers to move them into the new host cells, in the diabetic pancreas.

Bruno Doiron (left), and Ralph DeFronzo co-invented a technique that has cured diabetes in mice for one year without side effects (Credit: UT Health)

According to DeFronzo, the altered cells then produce insulin, but only in the presence of sugar, which is how a functioning beta cell is supposed to work. Otherwise, the cells would just keep cranking out the hormone, metabolizing all the sugar in the bloodstream and causing hypoglycemia.

Only about 20 percent of the lost cells need to be replaced, but if new beta cells are simply introduced, it’s likely that the body would attack and destroy them as well. One big advantage of this technique is that it works around the autoimmune system, which ignores the altered cells.

“If a type 1 diabetic has been living with these cells for 30, 40 or 50 years, and all we’re getting them to do is secrete insulin, we expect there to be no adverse immune response,” says DeFronzo.

The team emphasizes that there is a large gap between curing diabetic mice and achieving the same in human beings. They say that they’d like to start clinical trials in three years, but more animal testing is needed first at a cost of about US$5 million, as well as making an application to the US Food and Drug Administration for investigational new drug approval.

“It worked perfectly,” says Doiron. “We cured mice for one year without any side effects. That’s never been seen. But it’s a mouse model, so caution is needed. We want to bring this to large animals that are closer to humans in physiology of the endocrine system.”

Source: UT Health

Henry Sapiecha

Potent Plant powder power prevents malaria victims from dying

May 8th, 2017

So what is this plant?

Weathers has made several high-producing versions of the plant using tissue cultures  (Credit: Worcester Polytechnic Institute)

When 18 malaria patients in the Congo failed to respond to conventional treatments and instead continued to head toward terminal status, doctors knew they had to act fast – and try something different. So instead of turning to more synthetic drugs, they turned instead to nature and found a solution that delivered remarkable results.

The patients were first treated with the regimen described by the World Health Organization (WHO): artemisinin-based combination therapy (ACT). This drug combines an extract from a plant known as Artemisia annua, with other drugs that launch a multi-pronged attack on the malaria parasite. But just as is the case with antibiotic-resistant bacteria, the malaria parasite is evolving to resist the drugs designed to kill it. In fact, according to the WHO, three of the five malarial parasites that infect humans have shown drug resistance.

As the patients continued to decline, with one five-year-old even entering into a coma, the doctors administered a drug called artesunate intravenously, which is the preferred course of action when treating severe malaria. The treatment didn’t work.

Finally, doctors turned to the Artemisia annua plant itself. Also called sweet wormwood or sweet Annie, the plant is the source of the chemical artemisinin, which is used in ACT therapy. The plant has been used since ancient times in Chinese medicine to treat fevers, although this bit of knowledge was lost until 1970 when the Chinese Handbook of Prescriptions for Emergency Treatments (340 AD) was rediscovered. In 1971 it was found that extracts from the plant could fight malaria in primates.

Pamela Weathers, professor of biology and biotechnology at Worcester Polytechnic Institute began researching Artemisia annua over 25 years ago. Along with postdoctoral fellow Melissa Towler, Weathers created a pill made from nothing more than the dried and powdered leaves of the plant. When the pills were given to the 18 dying patients over the course of five days, all of them completely recovered, with no trace of the malaria parasite remaining in their blood.

“These 18 patients were dying,” Weathers said. “So to see 100 percent recover, even the child who had lapsed into a coma, was just amazing. It’s a small study, but the results are powerful.”

Weathers had previously shown that the dried leaves of the Artemisia annua plant (DLA) could deliver 40 times more Artemisia annua to the blood than extracts of the plant alone. In a later experiment, she showed that not only could the leaves beat drug-resistant bacteria in mice, but that after passing the malaria parasite through 49 generations of mice, the parasite still showed no resistance to the plant.

While the exact mechanism through which DLA operates is unclear, Weathers says it’s likely due to the intricate chemical dance that occurs between the phytochemicals in the leaves.

Weathers with the Artemisia plant (Credit: Worcester Polytechnic Institute)

Because the drug is inexpensive and relatively simply to produce, Weathers also says that it could be a source of industry for people living in the areas where malaria is a problem, such as Ghana, Kenya and Malawi where it was recently announced that the first malaria vaccines will be deployed. “This simple technology can be owned, operated, and distributed by Africans for Africans,” said Weathers, who has already established a supply chain on the continent for the leaves using local producers.

Weathers also said that further research into DLA could lead to effective ways to combat other maladies.

“We have done a lot of work to understand the biochemistry of these compounds, which include a number of flavonoids and terpenes, so we can better understand the role they play in the pharmacological activity of the dried leaves,” Weathers said. “The more we learn, the more excited we become about the potential for DLA to be the medication of choice for combatting malaria worldwide. Artemisia annua is known to be efficacious against a range of other diseases, including other tropical maladies and certain cancers, so in our lab we are already at work investigating the effectiveness of DLA with other diseases.”

The results of the case in the Congo have been described in the journal Phytomedicine. You can hear more from Weathers in the video below.

Source: Worcester Polytechnic Institute

www.pythonjungle.com

Henry Sapiecha

 

Mayne pharma company shares plunge on revised sales

May 1st, 2017

Mayne Pharma buried its bad news a long way back in its presentation to investors on Monday, but when shareholders caught on their reaction was sharp.

Mayne Pharma’s shares plunged more than 10 per cent after it revealed sales for a flagship suite of US generic drugs would not meet guidance.

The news was buried on on page 107 of a 110-page update released to coincide with an investor day the company was holding on Monday.

The company said in the investor update that tougher generic drug pricing was behind the revised guidance for the suite of drugs called the Teva portfolio.

“The US generics market is facing a tough price deflation cycle, there’s no doubt about that, and Mayne Pharma is not immune,” chief executive Scott Richards told investors.

“This is probably as tough as it’s been.”

Mayne bought the portfolio of drugs from pharmaceutical giant Teva Pharmaceuticals last year for $845 million. The aquisition saw Mayne’s first-half profit soar 278 per cent to $72.7 million in February.

Shares were trading at $1.20 on Monday afternoon and was down almost 11 per cent for the day wiping about $200 million off the market capitalisation of the company.

Shares closed at $1.20.

Mayne, which is worth more than $1.8 billion, re-affirmed its full-year profit guidance during its first half results in February.

Chief executive Scott Richards said at the time that the outlook for the group “continues to be positive” with significant growth opportunities from recent acquisitions and new product launches.

He said the generic product division would benefit in the second half from a full six months’ contribution from the Teva product acquisition.

But on Monday Mayne raised several threats to its pharma pricing including the fact that US President Donald Trump had accused the industry of “getting away with murder”.

The company has been under fire on multiple fronts in the US. Its shares dived in December on the back of news of a US price fixing lawsuit.

The civil complaint – originally filed by 20 US states, now 40 – accuses six companies including Teva and Mayne of conspiring to artificially inflate prices on an antibiotic and a diabetes drug.

It is also facing three civil class actions over the matter.

Mr Richards said on Monday the lawsuits would not have a material impact on the business.

“We still don’t believe that under any reasonable case we can see based on our knowledge that it’s going to be a material event in any fiscal year,” Mr Richards said.

A spokesperson for the company said nothing material had changed in terms of its full year earnings guidance for Teva.

“Teva sales are expected to be down due to increasing price deflation in the US generics market,” the spokesperson said.

“However, notwithstanding that, the FY17 Teva earnings before interest, tax, depreciation and amortization (EBITDA) is broadly in line with the guidance we gave at the time of the Teva acquisition.”

www.druglinks.info

Henry Sapiecha

 

Italian neuroscientist intends bringing frozen brains back to life

April 28th, 2017

London: A neuroscientist claims he will be able to “wake up” people who have been cryogenically frozen within three years, by transferring their brains to donor bodies.

Sergio Canavero, director of the Turin Advanced Neuromodulation Group, has already announced plans to carry out the first human head transplant, an operation which he claims is just 10 months away.

But he is now thinking further ahead, and wants to begin brain transplants within three years.

If the procedures are successful, he believes that frozen brains could be thawed and inserted into a donor, effectively bringing “dead” people back to life.

Hundreds of people who were dying or paralysed have had their bodies or brains cryogenically preserved in the hope that medical science will one day be able to cure their conditions.

Although many experts are sceptical that the brain can be thawed without damage, Professor Canavero said he planned to awaken patients frozen by the Alcor Life Extension Foundation, which is based in Arizona.

“As soon as the first human head transplant has taken place, no later than 2018, we will be able to attempt to reawaken the first frozen head,” he said.

“We are currently planning the world’s first brain transplant, and I consider it realistic that we will be ready in three years at the latest.”

British scientists are sceptical about whether the brain could be fully restored from frozen.

Clive Coen, professor of neuroscience at King’s College London, said the chances of bringing a brain back was “infinitesimal”.

Dr Channa Jayasena, clinical senior lecturer at Imperial College London added: “It is currently not possible to freeze and thaw human tissue without killing many cells contained within it.”

Professor Canavero is working with a Chinese team of doctors led by Dr Ren Xiaoping, of Harbin Medical Centre, who helped perform the first successful hand transplant in the US.

Although Russian computer scientist Valery Spiridonov, who has spinal muscular atrophy, had volunteered to become the first head transplant patient, the team expects the first operation to be with a Chinese donor and patient.

Last year, the team announced a successful head transplant performed on a monkey.

Telegraph, London

DEADLY BRAIN CANCER & STILL ALIVE AFTER 6 YEARS-DOCTORS SAID ONLY WEEKS..!!

April 16th, 2017

Grant Sanderson was diagnosed with brain cancer image www.newcures.info

WHEN Grant Sanderson was diagnosed with brain cancer six years ago, he was told that without immediate treatment, he had less than a week to live.

Today the Yengarie man and his fiancee, Sheridan Mosk, are eagerly awaiting the arrival of their miracle baby, which was conceived naturally despite fears that the treatment Grant had undergone would mean he would be unable to have children.

Grant was diagnosed with stage 4 glioblastoma multiforme brain cancer in 2011.

He underwent surgery, followed by chemotherapy and radiation and was told the treatment would extend his life by about 18 months.

But six years on, Grant is proving the doctors wrong.

“No one has ever survived past two years of this cancer at that size in Australia,” Sheridan said.

“He is the first person in Australia to beat brain cancer of this severity.”

Last year Sheridan and Grant met and “instantly fell in love”.

“It was like our souls saw each other and kind of went, ‘oh, there you are, I’ve been waiting for you’.

“Grant is the kindest person I have ever met and also the biggest dork I have ever met. He has such a contagious smile.”

The two are now happily expecting the arrival of their child in October.

“Our beautiful baby which is baking away was conceived 100% naturally, which again is a beautiful miracle considering what Daddy has been through with his chemo and radiation.

“If anyone deserves to be a father, it’s this man.”

Sheridan said they wanted to share Grant’s story to inspire others who were undergoing cancer treatment and their families going through it with them.

“If anything we hope someone can draw some strength from our story.

“Cancer does not discriminate, it attacks little children, it attacks mums and dads, nannies and poppies and it doesn’t care how much you need them either. But no matter – even if given the heart-wrenching diagnosis of terminal cancer, that cannot take away your ability to have faith.

“You can fight and win. Grant is walking, talking proof of that.”

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Henry Sapiecha

Cure for blindness: Tooth sewn into man’s eyeball restores his full sight

April 16th, 2017

A BLIND man has had his eyesight completely restored by Sydney surgeons — who sewed his tooth into his eyeball.

The risky but remarkable procedure involved planting a tiny lens inside the tooth, which now reflects light onto the back of the eye.

By using the patient’s own tooth, it ensures the body doesn’t reject it.

The operation, known as osteo-odonto-keratoprosthesis, was recently performed twice at Sydney Eye Hospital, with one of the procedures being carried out on 72-year-old Goulburn man John Ings.

Mr Ings, whose procedure will feature on Channel 9’s 60 Minutes tonight, had progressively lost his sight as a result of the herpes virus. His vision has now been restored by the breakthrough operation.

Goulburn man John Ings’ vision has been restored. image www.newcures.info

The second patient, 50-year-old Cairns woman Leonie Garrett, has also had her sight improved, from barely being able to see the difference between light and dark to now having 20/20 vision.

The operation, which treats corneal blindness, is the only one of its kind being performed in the southern hemisphere.

It was carried out by two former classmates of the University of NSW, oral and maxillofacial specialist Dr Shannon Webber and oculoplastic surgeon Dr Greg Moloney.

How the tooth eyeball procedure works.image www.newcures.info

How the procedure works.

The pair trained extensively in Germany to learn the procedure, which has been performed there on a handful of occasions since it was first tried in 2004. A German specialist came to Australia to supervise the two operations.

The procedure is broken down into two stages. First the patient’s tooth is extracted, a hole is drilled through it and a small plastic lens is placed inside.

It is then sewn into the patient’s cheek, where it grows tissue over a period of several months.

“We rely on the tooth to gain its own blood and tissue supply so when it is removed from the mouth, what you have essentially is a living complex,” Dr Webber said.

The groundbreaking eye tooth operation is performed by Sydney surgeons image www.newcures.info

The groundbreaking operation is performed by Sydney surgeons.

Picture: 60 Minutes

John Ings after the successful eye operation image www.newcures.info

John Ings after the successful operation. Picture: 60 Minutes

A flap of skin and mucus membrane from inside the mouth is then sewn over the eyeball.

Three months later, the tooth lens is removed from the cheek and sewn over the patient’s blind eyeball, then covered with the flap of skin. An opening is made to allow the new lens to see out.

It projects light onto the patient’s macular, in the back of the eye, much as happens with the lens of a healthy cornea.

The tooth which helped restore Mr Ings’ sight.image www.newcures.info

The tooth which helped restore Mr Ings’ sight. Picture: 60 Minutes

Both Dr Maloney and Dr Webber now expect to operate two or three times a year in Australia through the public health system at Sydney Eye Hospital.

“It’s pretty incredible and something we have been building towards for several years,” Dr Webber said.

“So to have done it successfully on two occasions is extremely satisfying. Both patients are doing really well and Leonie, in particular, is an amazing case because she had virtually no ability to see at all.

“We anticipate doing two to three of these surgeries a year and it will really come down to a supply and demand thing.”

Each patient would be assessed by Sydney Eye Hospital.

For Mr Ings, the successful surgery now means he is able to watch his own procedure on television tonight — something that would not have been possible six months ago.

“Before the operation I wouldn’t have been able to watch anything,” he said yesterday.

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Henry Sapiecha

 

Best and Worst Foods for Your Liver

April 9th, 2017

internal-liver-sketch image www.newcures.info

1…Oatmeal

berry_nut_oatmeal-bowl image www.foodpassions.net

Food with lots of fibre can help your liver work at its best. Want one that’s a great way to start your day? Try oatmeal. Research shows it can help you shed some extra pounds and belly fat, which is a good way to keep away liver disease.

2…Stay Away From Fatty Foods

neon-drive_thru_sign image www.foddpassions.net

French fries and burgers are a poor choice to keep your liver healthy. Eat too many foods that are high in saturated fat and it can make it harder for your liver to do its job. Over time it may lead to inflammation, which in turn could cause scarring of the liver that’s known as cirrhosis. So next time you’re in the drive-thru line, think about ordering a healthier option.

3…Broccoli

broccoli_greens_mix image www.foodpassions.net

Add lots of veggies to your diet if you want to keep your liver healthy. Broccoli can be part of this strategy. Some studies suggest this crunchy food can help protect you from non-alcoholic fatty liver disease. If steamed broccoli sounds a little too blah, shred it into a slaw and toss it with sliced almonds, dried cranberries, and a tangy vinaigrette. It’s also delicious roasted with garlic and a splash of balsamic vinegar.

4…Coffee

couple_having_coffee image www.foodpassions.net

If you can’t make it through the day without it, you’ll be glad to hear that it may have some benefits for your liver. Studies show that drinking two to three cups a day can protect your liver from damage caused by too much alcohol or an unhealthy diet. Some research suggests it may lower your risk of liver cancer.

5…Ease Up on Sugar

white-sugar_dunes image www.foodpassions.net

Too much of the sweet stuff can take a toll on your liver. That’s because part of its job is to convert sugar into fat. If you overdo it, your liver makes too much fat, which ends up hanging around where it doesn’t belong. In the long run, you could get a condition like fatty liver disease. So do your liver a favor and make sweets an occasional treat.

6…Green Tea

pouring_cup_hot_green_tea image www.foodpassions.net

It’s brimming with a type of antioxidant called catechins. Research suggests it may protect against some forms of cancer, including liver. You’ll get more catechins if you brew tea yourself and drink it hot. Iced tea and ready-to-drink green teas have much lower levels.

7…Water

woman_drinking_glass_of_water image www.foodpassions.net

One of the best things you can do for your liver is to keep a healthy weight. Get in the habit of drinking water instead of sweetened drinks like sodas or sports drinks. You’d be amazed at how many calories it will save you each day.

8…Almonds

bowl_of_almonds image www.foodpassions.net

Nuts — especially these — are good sources of vitamin E, a nutrient that research suggests may help protect against fatty liver disease. Almonds are good for your heart, too, so grab a handful the next time you feel like snacking. Or try them in salads, where they add a nice crunch.

9…Put a Cap on Salt

hand_holding_salt_shaker image www.foodpassions.net

Your body needs some salt — just not nearly as much as you probably get. Early research suggests a diet high in sodium may lead to fibrosis, which is the first stage of liver scarring. There are some easy things you can do to cut back. Avoid processed foods like bacon or deli meats. Choose fresh instead of canned veggies. And keep temptation at arm’s length by taking your salt shaker off the table.

10..Spinach

spinach_salad_with_fruit_walnuts image www.foodpassions.net

Leafy greens have a powerful antioxidant called glutathione, which can help keep your liver working right. And spinach couldn’t be easier to prepare. It makes a great base for a dinner salad, and it’s also delicious sauteed with garlic and olive oil. When it’s wilted, top it with a dusting of fresh parmesan.

11..Blueberries

bowls_of_fresh_blueberries image www.foodpassions.net

They’ve got nutrients in them called polyphenols that may help protect you against nonalcoholic fatty liver disease, which often goes hand in hand with obesity and high cholesterol. If blueberries aren’t your thing, other foods rich in polyphenols include dark chocolate, olives, and plums

12…Be Moderate With Alcohol

woman_relaxing_with_glass_of_wine image www.dfoodpassions.net

Drinking too much can wreak havoc on your liver. Over time it can lead to cirrhosis. Even occasional binge drinking — four drinks in one sitting for women and five for men — can be harmful, too. Try to limit yourself to one drink a day if you’re a woman or two a day if you’re a man.

13..Herbs and Spices

variety_of_herbs_and_spices image www.foodpassions.net

Want to protect your liver and your heart at the same time? Sprinkle on some oregano, sage, or rosemary. They’re a good source of healthy polyphenols. An extra benefit: they help you cut back on salt in many recipes. Cinnamon, curry powder, and cumin are good ones to try, too.

14..Limit Packaged Snack Foods

cup_of_mixed_fruit_on_desk image www.foodpassions.net

Next time you feel the call of the vending machine, reach for a healthy snack instead. The problem with chips and baked goods is that they’re usually loaded with sugar, salt, and fat. Cutting back is a relatively easy diet tweak with a little planning. One good strategy: Bring a stash of healthy snacks with you to work. Try an apple with a single-serve packet of nut butter, or sugar snap peas with a mini-cup of hummus.

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Henry Sapiecha

Ethics of Organ Donation from Prisoners on death row

March 29th, 2017

Organ Procurement and Transplantation Network

Dr David van der Poorten performs the transplant image www.newcures.info

Rationale for Deliberation

prison pic-5

As the scarcity of suitable organs for transplantation continues to grow, alternative sources for organs have been reported and others suggested. One such suggestion is to recover organs that would otherwise seem to go to waste, such as those from condemned prisoners. Reportedly the People’s Republic of China recovers organs from executed prisoners, and recent U.S. news reports have alleged that organ brokers operate in this country who arrange transplantation of the foreign prisoner’s organs. This discussion is not restricted to third world countries. In the United States, proposals of this type have come from prominent figures and bodies. While one proposal suggested that prisoners be given the option of donating organs upon their death, another suggests that condemned prisoners be offered the option of trading a kidney or their bone marrow in exchange for a commuted sentence of life in prison without parole.

While it is beyond the scope of the UNOS Ethics Committee to examine the moral and ethical issues encompassing the death penalty, it is worth noting that this topic is both ethically and judicially controversial. Acknowledgment should at least be made that the death penalty is rarely available or applied in most industrialized western nations, except for the United States. All western European countries, Canada, Mexico, Central and South American, with the exception of Chile, have abolished the death penalty. Recent U. S. data show an inequitable application of the death penalty with a significant evidence of racial bias particularly in the south. The data indicate that blacks are five times more likely to be sentenced to death than whites convicted of similar crimes and that the economically disadvantaged as well are more likely than the wealthy to receive the death penalty.

Any law or proposal that allows a person to trade an organ for a reduction in sentence, particularly a sentence from death to life in prison, raises numerous issues. Application of the death penalty is spasmodic and seemingly discriminatorily applied, which would suggest that these types of proposals would be coercive to particular classes of individuals–minorities and the poor. Would the reduction in sentence apply to the offer to donate, or would it only be honored if the act of donation took place? If the act of donation would exclusively qualify for the reduction in sentence, then the law or policy would discriminate against individuals found to be medically unsuitable to donate organs. Examples include:

  • those with common prison infections such as tuberculosis, HIV or hepatitis B
  • the prisoners with a single functioning kidney, or on dialysis, or with diabetes or other renal diseases

Were prisoners allowed to trade a kidney to mitigate a death sentence, it may affect the actual imposition of the death penalty. With greater publicity surrounding these types of proposals/laws, potential jurors could be influenced and ultimately impose the death penalty more often with a potential societal benefit in mind. Jurors might hope that the convicted persons would choose to trade their kidney for their life. This would present a gross inequity for those unable or unwilling to donate a kidney and who might otherwise have not received a death sentence.

The proposals that concern organ recovery from executed prisoners unveil another host of problems. One method of execution suggested is the act of organ donation itself. From a utilitarian standpoint this would make sense; the anesthetizing of the condemned and the recovery of organs in the usual manner would produce optimum organs for transplantation. However, the cross-clamping the aorta and the ensuing cardiectomy, followed by the disconnection of the ventilator, create an unacceptable situation for the organ recovery team. It clearly places the organ recovery team in the role of executioner. Many physician groups, including the American Medical Association, have prohibited physician participation in state executions on ethical grounds.

Issues of informed consent of potential donors as well as recipients need to be addressed. Obviously a person condemned to death cannot consider organ or bone marrow donation as a coercion-free option. Even a death row inmate should have the option of refusing an invasive surgical procedure–although unlikely, given the alternative. Correspondingly a person to be executed, or their next of kin/surrogate, should be able to make an informed decision regarding any donation options, including informed refusal if they so chose. Ultimately the potential organ/bone marrow recipient(s) should be informed that the source of the donation was a condemned prisoner, while maintaining the prisoner’s confidentiality. Individuals in opposition to the death penalty might object to accepting an organ from either an executed prisoner or a prisoner who traded their organ for their life.

Consider the effect that such a policy/law could have on organ donation overall. The number of potential organs recovered from condemned prisoners would be small. The conceivable stigma that would be attached to organ donation from its coupling with execution could lead to decreases in donation rates. This may especially be true within certain minority groups. Any notion that particular groups of people were receiving increased numbers of death sentences to provide organs for the rest of society would clearly make it difficult to attempt to obtain consent for altruistic donation from these groups.

Conclusion

The UNOS Ethics Committee has raised a small number of the many issues regarding organ donation from condemned prisoners. The Committee opposes any strategy or proposed statute regarding organ donation from condemned prisoners until all of the potential ethical concerns have been satisfactorily addressed.

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Henry Sapiecha

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Most cancers are caused by DNA replication errors, landmark study reveals

March 24th, 2017

Halfway through her HSC, Rachel Woolley suffered exhaustion and a stiff neck.

“All my friends were tired, but it got to the point where I couldn’t get up the stairs,” Ms Woolley said.

Rachel Woolley at home in Sydney. She is a candidate for a bachelor of music at UNSW and is recovering from Hodgkin lymphoma image www.newcures.info

Rachel was diagnosed with Hodgkin lymphoma, a cancer of the lymphatic system.

“It was just completely random,” Ms Woolley said.

“You certainly go through a ‘why me?’ phase. What had I done?” she said.

Now 19, Ms Woolley is studying for her bachelor of music at the University of NSW. Despite the cancer then coming back last year, she was given the all-clear again in January.

What triggered Ms Woolley’s cancer is not known, but a landmark study published on Friday shows that about two-thirds of all cancers are caused by random errors made during normal cell division.

“Our research has broken the paradigm that most cancers are environmental or inherited,” said Assistant Professor Cristian Tomasetti of the Johns Hopkins University school of medicine.

His study with Bert Vogelstein, published in Science, evaluated cancer occurrence in 69 countries, including Australia, covering 4.8 billion people.

Professor Vogelstein said: “Most of the time random mutations during cell division don’t do any harm. That’s good luck.

“Occasionally they occur in a cancer-driver gene. That’s bad luck.”

The study reviewed 32 types of cancer and found that about 66 per cent of cancer mutations result from random DNA copying errors, 29 per cent can be attributed to lifestyle or environmental factors and the remaining 5 per cent are inherited.

Comparative rates of cancer by heredity, random and environmental causes. Most cancers are caused by random errors in DNA replication during cell division. ScienceTomasetti image www.newcures.info

Comparative rates of cancer by heredity, random and environmental causes. Most cancers are caused by random errors in DNA replication during cell division. Photo: Science/Tomasetti

“Detecting cancers earlier can save lives regardless of what caused the mutation,” Assistant Professor Tomasetti and Professor Vogelstein said in a statement. “More research to find better ways to detect cancers earlier is urgently needed.”

The researchers are at pains to say that a cancer is very rarely caused by a single error in cell division, but is often a cumulative process, which is why cancers are more common in older people.

Professor David Thomas is head of the Garvan Institute’s cancer division and director of the Kinghorn Cancer Centre.

“The first Vogelstein study in 2015 was important and heretical. Here they have got a much larger data set that expands to the entire globe.

“I’m not surprised at the ratios of random errors to environmentally-induced mutations and hereditary causes. They seem about right.”

However, Professor Thomas said that in his view some of the assumptions made in the modelling “are very rubbery”, and there will be strong debate about the paper.

Despite his reservations, Professor Thomas said the paper is important: “I do think the broad balance is accurate.”

The overall balance also matches the expectations of Professor Sanchia Aranda, chief executive of the Cancer Council.

“We already know that about one-third of cancers are preventable,” she said. “Very few cancers are truly inherited.”

Professor Thomas said just because most cancers are caused by random mutation, it doesn’t mean environmental factors don’t play a role.

“Even if the bulk of mutations are random, a cell needs to get to the final step to become malignant. Environment and heredity play a role here,” he said.

Assistant Professor Tomasetti said: “Cancer rates vary widely by organ. If you look at lung cancer the concentration is in the environmental component.

“However, with brain cancers, bone cancers or childhood cancers the concentration is in the random component.

“That means virtually all the cancerous mutations are caused by simple mistakes caused by every cell when it divides.”

Is this any comfort to Ms Woolley?

“One perspective is ‘At least I didn’t do anything wrong’,” she said. “But you still feel ‘Why me?'”

Professor Thomas said that while the study was important it won’t change clinical practice.

“The fundamental advice we give as clinicians about how to manage and look out for cancer are not affected by this study.

“People should still try to minimise and manage their exposure to environmental or inherited risk factors.”

While the study won’t immediately impact clinical practice it could assist in the management of the psychological impacts of cancer.

Dr Pandora Patterson is general manager of research at CanTeen, the charity that supports young people living with cancer.

“People digest information in different ways, so it could be helpful to know ‘This is not my fault, it’s just random’,” she said.

Ms Woolley is a member of CanTeen. “By talking to people who have been through all this you can learn stuff that the doctors don’t tell you,” she said.

“It’s such a relief not feeling you’re on your own. You can just sit around with people talking about life – people just get you.”

Her message is that while going through treatment is “very shitty”, things can get better. “It’s really important to stay positive and look forward to the future.”

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Henry Sapiecha