NASA

Sunlight glints off the International Space Station with the blue limb of Earth providing a dramatic backdrop in this photo taken by an astronaut on the shuttle Endeavour just before it docked after midnight on Feb. 10, 2010 during the STS-130.

By Charles Q. Choi
Space.com

Advanced strategies to fight cancer are taking inspiration from experiments in the final frontier of outer space, researchers say.

The gravity experienced in low-Earth orbit, which is 10,000 to 1 million times less powerful than that felt on Earth's surface, allows researchers to study cell behavior that's normally masked by responses to gravity. Learning more about these processes is shedding light on how cells usually work, and how they can malfunction in the case of cancer.

"When you take away the force of gravity, you can unmask some things you can't readily see on Earth," said cell biologist Jeanne Becker of Nano3D Biosciences in Houston. "When gravitational force is reduced, cell shape changes, the way they grow changes, the genes they activate change, the proteins they make change." [6 Cool Space Shuttle Experiments]

Scientists have been taking note of such effects for decades. For instance, experiments in the 1970s on Skylab, the first U.S. space station, discovered that red blood cells develop bumpy surfaces in space, a change that disappeared within hours once astronauts returned to Earth.

More recently, research investigating 10,000 genes found that the behavior of 1,632 of them — including genes linked with cell death and tumor suppression — was altered in microgravity.

Although microgravity can distort normal biology, conventional procedures for studying cells on Earth can introduce their own problems. For instance, experiments on Earth often grow cells as flat layers in dishes, obscuring how they behave in real life when they can interact with each other in three dimensions in complex ways.

"When you grow cancers in three dimensions as opposed to flat layers, their response to drugs is vastly different — they become more resistant to drugs," Becker told Space.com.

These discoveries spurred the creation of devices that could mimic the effects of microgravity on Earth so researchers could see how cells behave in three dimensions. For example, so-called rotating wall vessel bioreactors constantly spin cells, keeping them as close to the free-fall seen in space as possible.

Other devices use magnetic fields to levitate cells and counteract the pull of gravity.

Such machines have supported analyses of a wide variety of cancers, such as those of the breast, cervix, kidney, colon, liver, skin, lung, bone, ovaries and prostate.

"The work we do can help address how cancer grows, reveal new ways of tackling drug resistance," Becker said.

Although devices that seek to mimic or induce microgravity are valuable to science, they cannot fully replace the effects seen in orbit. For instance, the crew of the final doomed flight of the space shuttle Columbia in 2003 found that prostate cancer cells grown in space developed into golf-ball-size structures, while clumps grown in rotating wall vessel bioreactors only reached 3 to 5 millimeters (0.1 to 0.2 inches) in size.

"With the International Space Station, we have a lab that doesn't exist anywhere else," Becker said. "It's an exciting platform for discovery."

Space-based science also has improved microencapsulation technology that envelops molecules in capsules, helping develop new delivery systems for cancer drugs. In addition, research exploring how plants respond to light has also shown new ways to reduce pain associated with cancer treatments.

Although NASA's space shuttle program retired in 2011, "we have commercial access to the space station coming up the pipeline, and we still have access to it through vehicles like the Russians' Progress spacecraft," Becker said. "So the opportunities are really limitless."

Becker and her colleague Glauco Souza detailed this research online Friday in the journal Nature Reviews Cancer.

Follow us @Spacedotcom, Facebook or Google+. Originally published on Space.com.

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Starry Night Software

The small, faint constellation Cancer is rich in open clusters and double stars.

By Joe Rao
Space.com

The dim constellation of Cancer, the Crab, high toward the south during the mid-to-late evening hours recently, is the least conspicuous of the 12 zodiacal constellations.

Aside from being in the Zodiac, Cancer is probably noteworthy only because it contains one of the brightest galactic star clusters in the sky. It appears to the eye as a fuzzy patch of light, but binoculars will reveal its stellar nature. 

But what to call it?
Some astronomy texts speak of "Praesepe, the Manger," while others simply call this cluster the "Beehive."

A manger is defined as "a trough in which feed for donkeys is placed." The cluster was apparently first called Praesepe 20 centuries ago. Perhaps the older designation Praesepe is preferable since in the middle of Cancer are two stars called the Aselli ("donkeys") known for over 2,000 years as Asellus Borealis and Asellus Australis — the northern and southern colts — feeding from a manger. [Night Sky Observing Guide: April 2013 (Sky Maps)]

Galileo first resolved Praesepe into individual stars (36 of them) in 1610. More than 100 stars can be seen in binoculars or a small telescope, and they seem to be spread out over an area about three times the apparent diameter of the moon. 

The cluster's relatively new moniker, Beehive, apparently evolved almost four centuries ago, when some anonymous person, upon seeing so many stars revealed in one of the first crude telescopes exclaimed,  "It looks just like a swarm of bees!" Hence, some astronomy books call the cluster Beehive, while others still call it Praesepe.  

Celestial weather forecaster
Interestingly, Praesepe was also used in medieval times to forecast the weather. It was one of the very few clusters that was mentioned in antiquity. 

Aratus (around 260 B.C.) and Hipparchus (about 130 B.C.) called it the "Little Mist" or "Little Cloud." But Aratus also noted that on those occasions when the sky was seemingly clear, but Praesepe was invisible, this meant a storm was approaching. 

Of course, we know today that prior to the arrival of any unsettled weather maker, high, thin cirrus clouds (composed of ice crystals) begin to appear in the sky. Such clouds are thin enough to dim the sun, moon and brighter stars only slightly, but apparently just opaque enough to hide a dim patch of light like Praesepe.

Crushed Crab
Because it contains no star brighter than 4th magnitude, the Crab is difficult, if not impossible, to see under a light-polluted sky. 

Cancer is essentially a Greek creation. This creeping creature was sent by Zeus' jealous wife Hera to fatally bite Hercules, Zeus's son from his liaison with Alcmene. The crab arrived just as Hercules was slaying the multiheaded Hydra, one of his assigned 12 "labors." 

Cancer's bite was no more than a mere annoyance to Hercules, who crushed the crab under his heel. Infuriated, Hera banished the hapless sea creature to the heavens as one of the most inconspicuous constellations. Furthermore, nearby, directly under the Crab we find the head (and only one head) of the Hydra.

To the Egyptians, Cancer was Scarabaeus, a sacred insect who was charged with rolling the sun across the sky. Roughly 3,000 years ago, the point in the sky marking the position of the June solstice lay very close to Praesepe. But thanks to precession — the "wobble" that the Earth's axis describes over an interval of 25,800 years — the solstice point has shifted out of constellation Cancer and is now located in the adjacent constellation of Gemini, having apparently slid backward toward the west over the last three millennia. 

The crab is a creature that can go in one direction as well as another, so it seems only fitting that this part of the sky where the sun has seemingly reversed its direction at the beginning of summer has since been dedicated to this animal.

Joe Rao serves as an instructor and guest lecturer at New York's Hayden Planetarium. He writes about astronomy for The New York Times and other publications, and he is also an on-camera meteorologist for News 12 Westchester, N.Y. Follow us @Spacedotcom, Facebook and Google+. Original article on Space.com.

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Courtesy of Rodrigue Hamende

A Tasmanian devil with devil facial tumor disease.

By Stephanie Pappas
LiveScience

A cancer that has wiped out 70 percent of wild Tasmanian devils became contagious by "switching off" certain genes that would otherwise enable the immune system to recognize it, a new study finds.

Devil facial tumor disease is one of only two contagious cancers in the world (the other affects dogs and is nonfatal). It spreads when the Australian marsupials bite or nip each other, transmitting cancerous cells that grow into enormous face tumors. The cancer either metastasizes to other organs or prevents Tasmanian devils from eating or drinking. Either way, death usually occurs within six months. Experts predict the species could vanish within 20 years if the tumor disease isn't stopped.

The immune system should catch these tumor cells, but the cancerous invasion causes no immune response in devils, said Hannah Siddle, a University of Cambridge immunology researcher. Siddle and her colleagues have now discovered why: The tumor cells lack surface molecules called major histocompatibility complex molecules. These MHC molecules allow the immune system to detect the invading cells. Without them, the cancer is essentially invisible.

"That explains why the immune system of the devils doesn't recognize those DFTD (devil facial tumor disease) cells as foreign, as it should, or as cancerous, for that matter," Siddle told LiveScience.

But there is good news. Typically, cancer cells that ditch their surface coating of MHCs do so via a permanent genetic mutation. That's not the case for DFTD cells, said study researcher Jim Kaufman, also of Cambridge.

"What we stumbled on was the fact that the MHC molecules disappeared by regulation," Kaufman told LiveScience.

Regulating genes
In other words, the genes that hold the instructions for making the MHC molecules still exist in the cancer cells' genome. Those instructions simply aren't transcribed, and the molecules never form. What that means, Kaufman said, is that the cancer cells' invisibility is reversible.

The researchers proved the concept by using a communication protein called gamma interferon to "switch on" the MHC-coding genes in a culture of devil tumor cells in a Petri dish. The once-MHC-free cells started making MHC molecules again. 

In addition, the researchers examined tumor biopsies from wild Tasmanian devils and found that in some rare portions of tumor, immune cells were invading. In these areas, the cancer cells were making MHC molecules, suggesting that the genes can sometimes be spontaneously switched back on. It's not enough to save Tasmanian devils from death, but it does suggest hope for a vaccine, Kaufman and Siddle said. [See Photos of the Infected Tasmanian Devils]

"What we hope to do is to figure out a way to tip the balance so that the immune system does a better job of recognizing and can get rid of the tumor," Kaufman said. The researchers published the findings Monday in the journal Proceedings of the National Academy of Sciences. 

Key to contagious cancers
Development is going to take some time, Siddle said, but the researchers suspect the MHC finding could be a key step to creating a vaccine for the disease in the wild. Currently, the only way to save Tasmanian devils from extinction is to keep non-infected captive populations in zoos.

The finding is also a useful weapon in the arsenal against human diseases, Kaufman said. The more known about a particular disease agent in animals, the better prepared scientists are to face it should it ever strike humans. When the human immunodeficiency virus (HIV), a lentivirus, appeared on the scene, lentiviruses were largely a mystery, Kaufman said. It took years to catch up on a basic understanding of how the disease worked as humans died. In contrast, health professionals were much better prepared for the emergence of mad cow disease, because similar disorders such as scrapie had been studied in sheep and goats.

"There aren't any contagious tumors in humans yet," Kaufman said. "But one never knows when one is going to arise, whether it's next year or 1,000 years from now."

Follow Stephanie Pappas @sipappas. Follow LiveScience on Twitter @livescience, Facebook or Google+. Original article on LiveScience.com.

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Jean-Paul Rodriguez

Image based on an X-ray crystal structure of a G-quadruplex formed from the DNA sequence found in human genomes.

By Jeanna Bryner, LiveScience

Sixty years after scientists described the chemical code of life — an interweaving double helix called DNA — researchers have found four-stranded DNA is also lurking in human cells.

The odd structures are called G-quadruplexes because they form in regions of deoxyribonucleic acid (DNA) that are full of guanine, one of the DNA molecule's four building blocks, with the others being adenine, cytosine, thymine. The structure comprises four guanines held together by a type of hydrogen bonding to form a sort of squarelike shape. (The DNA molecule is itself a double strand held together by these building blocks and wrapped together like a helix.)

The new visualization of the G-quadruplex is detailed this week in the journal Nature Chemistry.

"I think this paper is important in showing directly the existence of this structure in vivo in the human genome, but it is not completely unexpected," said Hans-Joachim Lipps, of the University of Witten in Germany, who was not involved in the study. [ See Images of the 4-Stranded DNA ]

Scientists had shown in the past that such quadruplex DNA could form in test tubes and had even been found in the cells of ciliated protozoa, or single-celled organisms with hairlike appendages. Also there were hints of its existence in human cells, though no direct proof, Lipps said.

But scientists still didn't have concrete evidence for its existence in the human genome. In the new study, researchers, including chemist Shankar Balasubramanian, of the University of Cambridge and Cambridge Research Institute, crafted antibody proteins specifically for this type of DNA. The proteins were marked with a fluorescent chemical, so when they hooked up to areas in the human genome packed with G-quadruplexes, they lit up.

Next, they incubated the antibodies with human cells in the lab, finding these structures tended to occur in genes of cells that were rapidly dividing, a telltale feature of cancer cells. They also found a spike in quadruplexes during the s-phase of the cell cycle, or the phase when DNA replicates just before the cell divides.

As such, the researchers think the four-stranded DNA could be a target for personalized medicine in the future. If they could block these odd ducks perhaps they could stop the rapid cell division of cancer cells.

"We are seeing links between trapping the quadruplexes with molecules and the ability to stop cells dividing, which is hugely exciting," Balasubramanian said in a statement.

The finding "is certainly a technical (not scientific) breakthrough in designing antibodies sensitive enough to demonstrate this structure in vivo in the human genome," Lipps wrote.

Lipps and his colleagues had suggested previously these structures regulate basic biological mechanisms, such as the replication of DNA.

"What makes me personally very happy about this work is that it again demonstrates that mechanisms first described in ciliated protozoa hold also true for other organisms up to human, demonstrating the strength of this model organism," wrote Lipps wrote.

The team still has several questions about quadruplexes, such as how the structures operate. "One thought is that these quadruplex structures might be a bit of a nuisance during DNA replication — like knots or tangles that form," Balasubramanian said.

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