Tuesday, April 23, 2013

A different view of cancer cells

New study measures physical changes in tumor cells as they become metastatic.

Most cancer deaths are caused by metastatic tumors, which break free from the original cancer site and spread throughout the body. For that to happen, cancer cells must undergo many genetic and physical changes. Now, MIT researchers have developed a way to study three key physical properties of cancer cells — their mass, stiffness and friction — on a large scale. 

Using this system, the researchers have analyzed how changes in those traits may allow cancer cells to migrate to new sites: Scientists have previously observed that cell lines with higher metastatic potential are generally more deformable, but the MIT team found that decreased friction also appears to help cancer cells traverse narrow channels, suggesting that friction may play a role in the ability of cancer cells to travel in blood vessels and reach new tumor sites. 

“Our measurements provide an additional perspective on cell properties that may complement genomic and proteomic approaches,” says Sangwon Byun, an MIT postdoc and lead author of a paper describing the findings in the Proceedings of the National Academy of Sciences the week of April 22.

The system that Byun and colleagues used to study the cancer cells is based on a device previously developed by Scott Manalis, a member of MIT's Koch Institute for Integrative Cancer Research and an MIT professor of biological engineering. Manalis, the senior author of the PNAS paper, has previously demonstrated that this system, known as a suspended microchannel resonator (SMR), can very accurately measure the mass and density of individual cells. 

The new MIT system is “probably the world’s most sensitive instrument for measuring a number of different biophysical properties of individual cells,” says Mehmet Toner, a professor of biomedical engineering at Massachusetts General Hospital and Harvard Medical School who was not part of the research team. “It’s very important to know whether metastatic cells have biophysical properties different than normal or nonmetastatic cancer cells, allowing them to go through narrow spaces.”

“When you use a specific marker to look for these cells, you find the cells that you’re looking for, but you may be missing a whole population of cells,” says Josephine Shaw, an MIT graduate student and a co-author of the paper. “It’s possible that by using a more holistic and physical approach, we may be able to find certain cells that we wouldn’t be able to find molecularly, because we wouldn’t be able to guess ahead of time what these cells would be expressing.”

Other authors of the paper are MIT postdoc Sungmin Son; Stanford University postdoc Dario Amodei; MIT grad students Nathan Cermak, Joon Ho Kang and Vivian Hecht; former MIT postdoc Monte Winslow; Tyler Jacks, the David H. Koch Professor of Biology at MIT and director of the Koch Institute; and Parag Mallick, an assistant professor of radiology at Stanford.

The research was funded by the National Cancer Institute, through MIT’s Physical Sciences Oncology Center and Stanford’s Center for Cancer Nanotechnology Excellence and Translation, and Stand Up to Cancer.

Friday, April 19, 2013

Major boost in solar-cell efficiency


Throughout decades of research on solar cells, one formula has been considered an absolute limit to the efficiency of such devices in converting sunlight into electricity: Called the Shockley-Queisser efficiency limit, it posits that the ultimate conversion efficiency can never exceed 34 percent for a single optimized semiconductor junction.

Now, researchers at MIT have shown that there is a way to blow past that limit as easily as today’s jet fighters zoom through the sound barrier — which was also once seen as an ultimate limit.

Their work appears this week in a report in the journal Science, co-authored by graduate students including Daniel Congreve, Nicholas Thompson, Eric Hontz and Shane Yost, alumna Jiye Lee ’12, and professors Marc Baldo and Troy Van Voorhis.

Since this was just a first proof of principle, the team has not yet optimized the energy-conversion efficiency of the system, which remains less than 2 percent. But ratcheting up that efficiency through further optimization should be a straightforward process, the researchers say. “There appears to be no fundamental barrier,” Thompson says.

While today’s commercial solar panels typically have an efficiency of at most 25 percent, a silicon solar cell harnessing singlet fission should make it feasible to achieve efficiency of more than 30 percent, Baldo says — a huge leap in a field typically marked by slow, incremental progress. In solar cell research, he notes, people are striving “for an increase of a tenth of a percent.”

Solar panel efficiencies can also be improved by stacking different solar cells together, but combining solar cells is expensive with conventional solar-cell materials. The new technology instead promises to work as an inexpensive coating on solar cells.

Friday, April 12, 2013

Robot truck platoons roll forward

Will this be the first step toward autonomous cars?

Convoys of wireless-linked semi-autonomous vehicles could soon be hitting our roads, giving drivers a chance to put their feet up on the morning commute.

In February this year, a similar line-up of four large trucks circled an oval test track in Tsukuba City, Japan to help get so-called “truck platooning” technology ready for real-world use. This technology aims to create semi-autonomous road trains, where convoys of vehicles enter a snaking train of vehicles under the command of the lead vehicle.

“We think that this new technology can also lead to a reduction in the amount of road space used by vehicles, which would help to reduce traffic congestion,” says Nobuo Iwai, senior researcher on the project. In fact, some estimates suggest it could double the capacity of existing highways.

Platoon prototype

The Japanese demonstration was the latest of a couple of projects set up to trial and develop the technology. A couple of years ago a project at RWTH Aachen University in Germany operated a platoon of four trucks spaced at 10m (33ft) intervals. In the US, research at the University of California, Berkeley put three-truck caravans on the road with spacing from 3 to 6m. And last year, the Scania Transport Laboratory in Swedentested aspects of truck platooning on a 520km (325 miles) shipping route between the cities of Sodertalje and Helsingborg.

In addition, a recently completed European project led by Volvo calledSafe Road Trains for the Environment (Sartre) has explored using cars and lorries simultaneously. Its platoons cruised at 85 km/h (50mph) with a gap between each vehicle of 6m. The study vehicles put in some 10,000 km (6,200 miles) of road, and – like the Japanese study – indicated that platooning could offer substantial benefits.

Engineers and planners working on the technology that road trains could be cruising highways sometime in the next decade. Perhaps in the not-too-distant future, you yourself will commute to work on a robotic conga line, along with a line up of other drivers not paying attention to driving.

Source: http://www.bbc.com/future/story/20130409-robot-truck-platoons-roll-forward/2

Wednesday, April 10, 2013

'Aggressive' prostate cancer gene find

The BRCA2 gene is linked to hereditary breast cancer, as well as prostate and ovarian cancer.

Now scientists say that as well as being more likely to get prostate cancer, men with BRCA2 are also more likely to develop aggressive tumours and have the poorest survival rates.

They say these men should be treated quickly to save lives.

Prof Ros Eeles and colleagues at The Institute of Cancer Research in London and The Royal Marsden NHS Foundation Trust found prostate cancers spread more quickly and were more often fatal in men who had inherited a faulty BRCA2 gene than in men without the faulty gene.

Prof Eeles said: "It is clear from our study that prostate cancers linked to inheritance of the BRCA2 cancer gene are more deadly than other types.

"It must make sense to start offering affected men immediate surgery or radiotherapy, even for early-stage cases that would otherwise be classified as low-risk.

Men with a significant family history of breast and/or ovarian cancer in addition to prostate cancer can be offered BRCA1/2 testing at diagnosis, but it is not routinely offered to all patients diagnosed with prostate cancer in the UK.

Dr Julie Sharp of Cancer Research UK, said: "This study shows that doctors need to consider treating men with prostate cancer and a faulty BRCA2 gene much sooner than they currently do, rather than waiting to see how the disease develops.

Source: http://www.bbc.co.uk/news/health-22065289

Scientists track leukaemia's origins 'back to the womb'

Scientists say they have traced the root genetic cause of leukaemia back to early life in the womb. "It told us for the first time that this is the key mutation that starts the whole process of leukaemia” said Researcher Prof Mel Greaves.

The Institute of Cancer Research experts analysed the entire three billion letter sequence of DNA-coding in identical twins to reveal what sets off the disease.

They hope the findings, published in PNAS journal, could lead to new drugs to fight the condition at source.

It is already known that multiple faulty genes are linked to the condition and that environmental factors probably act as triggers along the way. But the precise sequence of events leading up to a diagnosis of ALL is unclear.

By comparing blood and bone marrow samples of the twins in later childhood, the researchers found one genetic mutation identical in both twins - a common leukaemia-causing gene called ETV6-RUNX1.

Study co-author Prof Greaves said: "We were able to sequence the entire human genome. It told us for the first time that this is the key mutation that starts the whole process of leukaemia. The other mutations must have happened after birth."

Dr Julie Sharp of Cancer Research UK said: "This interesting research shows how studying the DNA of twins can shed light on the genetic mistakes that first initiate cancer in children and the subsequent faults that occur as the cancer evolves.

"Studies like this could reveal new ways to target the very roots of cancer and help us better understand how the disease develops over time. Survival rates have increased significantly over the past decades thanks to research, but there is still more to do to make treatments better with fewer side-effects."

Source: http://www.bbc.co.uk/news/health-22062616

Monday, April 08, 2013

Radical roads drive robot cars

A lot is written about the rise of autonomous cars, such as those developed by Google, but these vehicles will also change our highways forever.

Los Angeles in California has just finished installing $400m of technology to synchronise its traffic lights. The Automated Traffic Surveillance and Control system uses an array of cameras and sensors in the road to measure traffic flow, and a centralised computer system to make constant tweaks and changes to the city’s 4,400 lights to keep traffic running as smoothly as possible. In theory, it is now possible to cross the city without ever stopping.

“By schronising our traffic signals we will spend less time waiting, and less time polluting,” says Mayor Antonio Villaraigosa. It is estimated to increase travel speeds by 16% and cutting journey times by 12%.

The figures are impressive, but other congested cities looking on in envy may do well to wait a few more years before rethinking their own traffic systems. While the LA system may seem cutting edge now, it could seem as outdated as a traffic officer guiding traffic with white gloves in a few years time. That is because engineers are planning a radical rethink of our streets that will change just about every aspect of how we drive – including who is in control of the vehicle.

Autonomous cars

In this new world, cars are packed nose to tail travelling at speeds in excess of current limits. They weave their way through unmarked junctions, with no traffic lights. Lane markings are non-existent, and stretches of road switch from being one-way in one direction, to the opposite, with no warning. Perhaps most alarming of all, very few of the “drivers” have even passed a driving test.

It may sound like an impossibly chaotic scene, where accidents are inevitable. But this is one future based on predictions about the uptake of autonomous cars.

In the United States the Instititute of Electrical and Electronics Engineers (IEEE) predicts that driverless cars will account for 75% of all vehicles on the roads by 2040. Vehicles, such as Google’s self driving car,  are already leading the way.  And small-scale trials of linked-up roads are being conducted in some cities.

 “In the future smart intersections may not need lights,” says Azim Eskandarian, director of the IEEE’s Center for Intelligent Systems Research.  “These intersections will very efficiently harmonise and synchronise speeds in one direction, and then the other.” The groundwork for this is already being laid in the US by the Vehicle Infrastructure Integration Consortium, a group of car manufacturers trying to develop specific applications and protocols for a system.

The hub of the future will take this to an extreme - accumulating all the data across a metropolis and plan traffic loads and optimise routes accordingly. It will also send commands back to the vehicles about when to safely enter an intersection, and what speed to hold to minimize stop-start driving.

Meanwhile the cars will also talk to each other, using vehicle-to-vehicle communication, constantly checking their environments and positions relative to other cars around them.

Vehicle-to-vehicle communication is already in development.  In 1999, the United States Congress set aside a region of the 5.9 GHz radio frequency band – already used for wireless – specifically for the purpose. And a host of manufacturers are already developing applications.

Cars that talk to each other can also match their speeds, and drive more closely together without risk of the car in front suddenly braking. As a result, many envisage the idea of “car platooning” that will link together cars on high-speed highways to travel faster, more safely, and using less space. Various trails of this technology are already taking place, with one of the most advanced run by an EU consortium called Satre, which demonstrated trains of vehicles travelling at speeds of up to 90km/h sometimes travelling just 4m apart.

Source: http://www.bbc.com/future/story/20130405-radical-roads-drive-robot-cars

Study reveals how melanoma evades chemotherapy

Nitric oxide (NO), a gas with many biological functions in healthy cells, can also help some cancer cells survive chemotherapy. A new study from MIT reveals one way in which this resistance may arise, and raises the possibility of weakening cancer cells by cutting off their supply of NO.

The findings, presented today at the annual meeting of the American Association for Cancer Research, focus on melanoma — a cancer that is difficult to treat, especially in its later stages. The prognosis is generally worse for patients whose tumors have high levels of NO, says Luiz Godoy, an MIT research associate and lead author of the study. Godoy and his colleagues have unraveled the mechanism behind melanoma’s resistance to cisplatin, a commonly used chemotherapy drug, and, in ongoing studies, have found that cisplatin treatment also increases NO levels in breast and colon cancers.

“Now we have a mechanistic link between nitric oxide and the increased aggressiveness of melanoma,” says Douglas Thomas, an assistant professor of medicinal chemistry and pharmacognosy at the University of Illinois at Chicago, who was not part of the research team. “It certainly would be worth exploring whether this mechanism is also present in different tumor types as well.”

The MIT researchers also found in some cancer cells, NO levels were five times higher than normal following cisplatin treatment. Godoy is now investigating how cisplatin stimulates that NO boost, and is also looking for other proteins that NO may be targeting.

Researchers in Wogan’s lab also plan to start testing cisplatin in combination with drugs that block NO production in animals.

The research was funded by the National Cancer Institute and the National Institute of Environmental Health Sciences. The research team also published its findings in a November 2012 article in the Proceedings of the National Academy of Sciences. Other authors of that paper were graduate student Chase Anderson, postdoc Rajdeep Chowdhury and technical associate Laura Trudel.

Friday, April 05, 2013

How to minimize the side effects of cancer treatment

Measuring enzyme levels in patients may reveal healthy cells’ ability to survive chemotherapy.

New research from MIT may allow scientists to develop a test that can predict the severity of side effects of some common chemotherapy agents in individual patients, allowing doctors to tailor treatments to minimize the damage.

The study focused on powerful cancer drugs known as alkylating agents, which damage DNA by attaching molecules containing carbon atoms to it. Found in tobacco smoke and in byproducts of fuel combustion, these compounds can actually cause cancer. However, because they can kill tumor cells, very reactive alkylating agents are also used to treat cancer. 

The new paper, which appears in the April 4 issue of the journal PLoS Genetics, reveals that the amount of cellular damage that alkylating agents produce in healthy tissues can depend on how much of a certain DNA-repair enzyme is present in those cells. Levels of this enzyme, known as Aag, vary widely among different tissues within an individual, and among different individuals.

Leona Samson, a member of MIT’s Center for Environmental Health Sciences and the David H. Koch Institute for Integrative Cancer Research, is the senior author of the paper. She has previously shown that when alkylating agents damage DNA, the Aag enzyme is called into action as part of a DNA-repair process known as base excision repair. Aag cuts out the DNA base that is damaged, and other enzymes cleave the DNA sugar-phosphate backbone, trim the DNA ends and then fill in the empty spot with new DNA.