|12-29-2012, 04:53 PM||Topic Starter|
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Two pretty awesome things science could bestow upon us in 2013.
2012 gave us the god particle.
2013 will give us an alien Earth, and may give us a cure for cancer.
The world is going to be very, very different, scientifically, much sooner than we think.
First 'Alien Earth' Will Be Found in 2013, Experts Say
by Mike Wall, SPACE.com Senior Writer
Date: 27 December 2012 Time: 05:00 AM ET
The first truly Earth-like alien planet is likely to be spotted next year, an epic discovery that would cause humanity to reassess its place in the universe.
While astronomers have found a number of exoplanets over the last few years that share one or two key traits with our own world — such as size or inferred surface temperature — they have yet to bag a bona fide "alien Earth." But that should change in 2013, scientists say.
"I'm very positive that the first Earth twin will be discovered next year," said Abel Mendez, who runs the Planetary Habitability Laboratory at the University of Puerto Rico at Arecibo.
Astronomers discovered the first exoplanet orbiting a sunlike star in 1995. Since they, they've spotted more than 800 worlds beyond our own solar system, and many more candidates await confirmation by follow-up observations.
NASA's prolific Kepler Space Telescope, for example, has flagged more than 2,300 potential planets since its March 2009 launch. Only 100 or so have been confirmed to date, but mission scientists estimate that at least 80 percent will end up being the real deal.
The first exoplanet finds were scorching-hot Jupiter-like worlds that orbit close to their parent stars, because they were the easiest to detect. But over time, new instruments came online and planet hunters honed their techniques, enabling the discovery of smaller and more distantly orbiting planets — places more like Earth.
Last December, for instance, Kepler found a planet 2.4 times larger than Earth orbiting in its star's habitable zone — that just-right range of distances where liquid water, and perhaps life as we know it, can exist.
The Kepler team and other research groups have detected several other worlds like that one (which is known as Kepler-22b), bringing the current tally of potentially habitable exoplanets to nine by Mendez' reckoning.
Zeroing in on Earth's twin
None of the worlds in Mendez' Habitable Exoplanets Catalog are small enough to be true Earth twins. The handful of Earth-size planets spotted to date all orbit too close to their stars to be suitable for life.
But it's only a matter of time before a small, rocky planet is spotted in the habitable zone — and Mendez isn't the only researcher who thinks that time is coming soon.
"The first planet with a measured size, orbit and incident stellar flux that is suitable for life is likely to be announced in 2013," said Geoff Marcy, a veteran planet hunter at the University of California, Berkeley, and a member of the Kepler team.
Mendez and Marcy both think this watershed find will be made by Kepler, which spots planets by flagging the telltale brightness dips caused when they pass in front of their parent stars from the instrument's perspective.
Kepler needs to witness three of these"transits" to detect a planet, so its early discoveries were tilted toward close-orbiting worlds (which transit more frequently). But over time, the telescope has been spotting more and more distantly orbiting planets — including some in the habitable zone.
An instrument called HARPS (short for High Accuracy Radial velocity Planet Searcher) is also a top contender, having already spotted a number of potentially habitable worlds. HARPS, which sits on the European Southern Observatory's 3.6-meter telescope in Chile, allows researchers to detect the tiny gravitational wobbles that orbiting planets induce in their parent stars.
"HARPS should be able to find the most interesting and closer Earth twins," Mendez told SPACE.com via email, noting that many Kepler planets are too far away to characterize in detail. "A combination of its sensitivity and long-term observations is now paying off."
And there are probably many alien Earths out there to be found in our Milky Way galaxy, researchers say.
"Estimating carefully, there are 200 billion stars that host at least 50 billion planets, if not more," Mikko Tuomi, of the University of Hertfordshire in England, told SPACE.com via email.
"Assuming that 1:10,000 are similar to the Earth would give us 5,000,000 such planets," added Tuomi, who led teams reporting the discovery of several potentially habitable planet candidates this year, including an exoplanet orbiting the star Tau Ceti just 11.9 light-years from Earth. "So I would say we are talking about at least thousands of such planets."
What it would mean
Whenever the first Earth twin is confirmed, the discovery will likely have a profound effect on humanity.
"We humans will look up into the night sky, much as we gaze across a large ocean," Marcy told SPACE.com via email. "We will know that the cosmic ocean contains islands and continents by the billions, able to support both primitive life and entire civilizations."
Marcy hopes such a find will prod our species to take its first real steps beyond its native solar system.
"Humanity will close its collective eyes, and set sail for Alpha Centauri," Marcy said, referring to the closest star system to our own, where an Earth-size planet was discovered earlier this year.
"The small steps for humanity will be a giant leap for our species. Sending robotic probes to the nearest stars will constitute the greatest adventure we Homo sapiens have ever attempted," Marcy added. "This massive undertaking will require the cooperation and contribution from all major nations around world. In so doing, we will take our first tentative steps into the cosmic ocean and enhance our shared sense of purpose on this terrestrial shore."
In Girl’s Last Hope, Altered Immune Cells Beat Leukemia
By DENISE GRADY
Published: December 9, 2012
PHILIPSBURG, Pa. — Emma Whitehead has been bounding around the house lately, practicing somersaults and rugby-style tumbles that make her parents wince.
It is hard to believe, but last spring Emma, then 6, was near death from leukemia. She had relapsed twice after chemotherapy, and doctors had run out of options.
Desperate to save her, her parents sought an experimental treatment at the Children’s Hospital of Philadelphia, one that had never before been tried in a child, or in anyone with the type of leukemia Emma had. The experiment, in April, used a disabled form of the virus that causes AIDS to reprogram Emma’s immune system genetically to kill cancer cells.
The treatment very nearly killed her. But she emerged from it cancer-free, and about seven months later is still in complete remission. She is the first child and one of the first humans ever in whom new techniques have achieved a long-sought goal — giving a patient’s own immune system the lasting ability to fight cancer.
Emma had been ill with acute lymphoblastic leukemia since 2010, when she was 5, said her parents, Kari and Tom. She is their only child.
She is among just a dozen patients with advanced leukemia to have received the experimental treatment, which was developed at the University of Pennsylvania. Similar approaches are also being tried at other centers, including the National Cancer Institute and Memorial Sloan-Kettering Cancer Center in New York.
“Our goal is to have a cure, but we can’t say that word,” said Dr. Carl June, who leads the research team at the University of Pennsylvania. He hopes the new treatment will eventually replace bone-marrow transplantation, an even more arduous, risky and expensive procedure that is now the last hope when other treatments fail in leukemia and related diseases.
Three adults with chronic leukemia treated at the University of Pennsylvania have also had complete remissions, with no signs of disease; two of them have been well for more than two years, said Dr. David Porter. Four adults improved but did not have full remissions, and one was treated too recently to evaluate. A child improved and then relapsed. In two adults, the treatment did not work at all. The Pennsylvania researchers were presenting their results on Sunday and Monday in Atlanta at a meeting of the American Society of Hematology.
Despite the mixed results, cancer experts not involved with the research say it has tremendous promise, because even in this early phase of testing it has worked in seemingly hopeless cases. “I think this is a major breakthrough,” said Dr. Ivan Borrello, a cancer expert and associate professor of medicine at the Johns Hopkins University School of Medicine.
Dr. John Wagner, the director of pediatric blood and marrow transplantation at the University of Minnesota, called the Pennsylvania results “phenomenal” and said they were “what we’ve all been working and hoping for but not seeing to this extent.”
A major drug company, Novartis, is betting on the Pennsylvania team and has committed $20 million to building a research center on the university’s campus to bring the treatment to market.
Hervé Hoppenot, the president of Novartis Oncology, called the research “fantastic” and said it had the potential — if the early results held up — to revolutionize the treatment of leukemia and related blood cancers. Researchers say the same approach, reprogramming the patient’s immune system, may also eventually be used against tumors like breast and prostate cancer.
To perform the treatment, doctors remove millions of the patient’s T-cells — a type of white blood cell — and insert new genes that enable the T-cells to kill cancer cells. The technique employs a disabled form of H.I.V. because it is very good at carrying genetic material into T-cells. The new genes program the T-cells to attack B-cells, a normal part of the immune system that turn malignant in leukemia.
The altered T-cells — called chimeric antigen receptor cells — are then dripped back into the patient’s veins, and if all goes well they multiply and start destroying the cancer.
The T-cells home in on a protein called CD-19 that is found on the surface of most B-cells, whether they are healthy or malignant.
A sign that the treatment is working is that the patient becomes terribly ill, with raging fevers and chills — a reaction that oncologists call “shake and bake,” Dr. June said. Its medical name is cytokine-release syndrome, or cytokine storm, referring to the natural chemicals that pour out of cells in the immune system as they are being activated, causing fevers and other symptoms. The storm can also flood the lungs and cause perilous drops in blood pressure — effects that nearly killed Emma.
Steroids sometimes ease the reaction, but they did not help Emma. Her temperature hit 105. She wound up on a ventilator, unconscious and swollen almost beyond recognition, surrounded by friends and family who had come to say goodbye.
But at the 11th hour, a battery of blood tests gave the researchers a clue as to what might help save Emma: her level of one of the cytokines, interleukin-6 or IL-6, had shot up a thousandfold. Doctors had never seen such a spike before and thought it might be what was making her so sick.
Dr. June knew that a drug could lower IL-6 — his daughter takes it for rheumatoid arthritis. It had never been used for a crisis like Emma’s, but there was little to lose. Her oncologist, Dr. Stephan A. Grupp, ordered the drug. The response, he said, was “amazing.”
Within hours, Emma began to stabilize. She woke up a week later, on May 2, the day she turned 7; the intensive-care staff sang “Happy Birthday.”
Since then, the research team has used the same drug, tocilizumab, in several other patients.
In patients with lasting remissions after the treatment, the altered T-cells persist in the bloodstream, though in smaller numbers than when they were fighting the disease. Some patients have had the cells for years.
Dr. Michel Sadelain, who conducts similar studies at the Sloan-Kettering Institute, said: “These T-cells are living drugs. With a pill, you take it, it’s eliminated from your body and you have to take it again.” But T-cells, he said, “could potentially be given only once, maybe only once or twice or three times.”
The Pennsylvania researchers said they were surprised to find any big drug company interested in their work, because a new batch of T-cells must be created for each patient — a far cry from the familiar commercial strategy of developing products like Viagra or cholesterol medicines, in which millions of people take the same drug.
But Mr. Hoppenot said Novartis was taking a different path with cancer drugs, looking for treatments that would have a big, unmistakable impact on a small number of patients. Such home-run drugs can be approved more quickly and efficiently, he said, with smaller studies than are needed for drugs with less obvious benefits.
“The economic model is totally acceptable,” Mr. Hoppenot said.
But such drugs tend to be extremely expensive. A prime example is the Novartis drug Gleevec, which won rapid approval in 2001 for use against certain types of leukemia and gastrointestinal tumors. It can cost more than $5,000 a month, depending on the dosage.
Dr. June said that producing engineered T-cells costs about $20,000 per patient — far less than the cost of a bone-marrow transplant. Scaling up the procedure should make it even less expensive, he said, but he added, “Our costs do not include any profit margin, facility depreciation costs or other clinical care costs, and other research costs.”
The research is still in its early stages, and many questions remain. The researchers are not entirely sure why the treatment works, or why it sometimes fails. One patient had a remission after being treated only twice, and even then the reaction was so delayed that it took the researchers by surprise. For the patients who had no response whatsoever, the team suspects a flawed batch of T-cells. The child who had a temporary remission apparently relapsed because not all of her leukemic cells had the marker that was targeted by the altered T-cells.
It is not clear whether a patient’s body needs the altered T-cells forever. The cells do have a drawback: they destroy healthy B-cells as well as cancerous ones, leaving patients vulnerable to certain types of infections, so Emma and the other patients need regular treatments with immune globulins to prevent illness.
So far, her parents say, Emma seems to have taken it all in stride. She went back to school this year with her second-grade classmates, and though her grades are high and she reads about 50 books a month, she insists impishly that her favorite subjects are lunch and recess.
“It’s time for her to be a kid again and get her childhood back,” Mr. Whitehead said.