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.

Source: http://web.mit.edu/newsoffice/2013/a-different-view-of-cancer-cells-0422.html

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.

Source: http://web.mit.edu/newsoffice/2013/photon-to-electron-conversion-0418.html?utm_source=feedly

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

'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

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.

Source: http://web.mit.edu/newsoffice/2013/how-melanoma-evades-chemotherapy-0407.html

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. 

Source: http://web.mit.edu/newsoffice/2013/chemotherapy-side-effects-cancer-0404.html

Skin patches 'tackle prostate cancer'

Skin patches which deliver oestrogen into the blood may be a cheaper and safer treatment for prostate cancer than current therapies, a study says.

The main treatment is injections of a chemical to cut levels of testosterone - the driving force of many prostate cancers - but it causes side effects.

The Imperial College London study in the Lancet Oncology compared patches and injections in 254 patients.

It found patches were safe and should avoid menopause-like side effects.

Prof Paul Abel, from Imperial College London, said: "We're not claiming this is equivalent to current therapies yet, but it does look like we are getting castration levels of testosterone."

Kate Law, from the charity Cancer Research UK which part funded the study, said: "More men than ever are surviving prostate cancer thanks to advances in research, but we still urgently need to find more effective treatments and reduce side effects.

"This trial is an important step towards better and kinder treatments that could bring big benefits to men with prostate cancer in the future."

Dr Iain Frame, director of research at Prostate Cancer UK, said: "It is unclear as yet if hormone patches could be an effective alternative to hormone injections, but we await with anticipation the results of the further trials planned which could in time offer men hope for the future."

Source: http://www.bbc.co.uk/news/health-21628911#sa-ns_mchannel=rss&ns_source=PublicRSS20-sa

Chemists find help from nature in fighting cancer

Inspired by a chemical that fungi secrete to defend their territory, MIT chemists have synthesized and tested several dozen compounds that may hold promise as potential cancer drugs.

A few years ago, MIT researchers led by associate professor of chemistry Mohammad Movassaghi became the first to chemically synthesize 11,11’-dideoxyverticillin, a highly complex fungal compound that has shown anti-cancer activity in previous studies.

In the new study, recently published online in the journal Chemical Science, Movassaghi and colleagues at MIT and the University of Illinois at Urbana-Champaign (UIUC) designed and tested 60 compounds for their ability to kill human cancer cells.

“What was particularly exciting to us was to see, across various cancer cell lines, that some of them are quite potent,” Movassaghi says.

Lead author of the paper is MIT postdoc Nicolas Boyer. Other authors are MIT graduate student Justin Kim, UIUC chemistry professor Paul Hergenrother and UIUC graduate student Karen Morrison.

Many of the compounds tested in this study, known as epipolythiodiketopiperazine (ETP) alkaloids, are naturally produced by fungi. Scientists believe these compounds help fungi prevent other organisms from encroaching on their territory.

The compounds that kill cancer cells appear to be very selective, destroying them 1,000 times more effectively than they kill healthy blood cells.

The researchers also identified sections of the compounds that can be altered without discernably changing their activity. This is useful because it could allow chemists to use those points to attach the compounds to a delivery agent such as an antibody that would target them to cancer cells, without impairing their cancer-killing ability.

Larry Overman, a professor of chemistry at the University of California at Irvine, says the new study is an impressive advance.The research was funded by the National Institute of General Medical Sciences.

Source: http://web.mit.edu/newsoffice/2013/chemists-find-help-from-nature-in-fighting-cancer-0227.html

Indian Plant Compound Could Play Role In Cancer Cell Death

Gedunin, an extract of the Indian neem tree that has been used for centuries in Asia as a natural remedy to treat inflammation, fever, and malaria, may also be used to help kill cancer cells.

 Cancer cells typically avoid death by hijacking molecular chaperones that guide and protect the proteins that ensure normal cellular function and then tricking them into helping mutated versions of those proteins stay alive, says Dr. Ahmed Chadli, a researcher at the GRU Cancer Center and senior author of the study.

Drug development has focused on the chaperone Hsp90 (heat shock protein 90) because it plays a key role in assisting mutated proteins, making it an attractive cancer drug target. But small molecules targeting Hsp90 have inadvertently resulted in the expression of proteins that protect cancer cells from programmed cell death, compromising the Hsp90 inhibitors in the clinic.

Chadli and his team found that gedunin attacks a co-chaperone, or helper protein, of Hsp90 called p23. Hence, gedunin leads to the inactivation of the Hsp90 machine and the killing of cancer cells without the production of anti-apoptotic proteins.

Source:
http://www.asianscientist.com/in-the-lab/gedunin-indian-plant-compound-cancer-cell-death-2013/
http://www.jbc.org/content/early/2013/01/25/jbc.M112.427328

Nanoscale capsule kills cancer cells without harming healthy cells

A degradable nanoscale shell to carry proteins to cancer cells and stunt the growth of tumors without damaging healthy cells has been developed by a team led by researchers from the UCLA Henry Samueli School of Engineering and Applied Science.

The process does not present the risk of genetic mutation posed by gene therapies for cancer, or the risk to healthy cells caused by chemotherapy, which does not effectively discriminate between healthy and cancerous cells, said Yi Tang, a professor of chemical and biomolecular engineering and a member of the California NanoSystems Institute at UCLA.

The research was funded by the David and Lucille Packard Foundation and a breast cancer research grant from the Congressionally Directed Medical Research Program.

Source: http://www.kurzweilai.net/nanoscale-capsule-kills-cancer-cells-without-harming-healthy-cells

New world-record efficiency for thin-film silicon solar cells

EPFL’s Institute of Microengineering has reached a remarkable 10.7% efficiency for a single-junction microcrystalline silicon solar cell, surpassing the previous world record of 10.1% held by the Japanese company Kaneka Corporation since 1998.

The efficiency increase was also achieved with with only 1.8 microns of photovoltaic active material — 100 times less material than with standard wafer-based crystalline silicon PV technology.

Thin-film silicon technology indeed offers the advantages of saving up on raw material and offering low energy payback time, thus allowing module production prices as low as 35 €/m2 (47 $/m2), reaching the price level of standard roof tiles.

Work leading to this result was supported by the Swiss Federal Office of Energy (SFOE), the EU-FP7 program, the Swiss National Science Foundation (SNSF), and the Commission for Technology and Innovation (CTI).

Source: http://www.kurzweilai.net/new-world-record-efficiency-for-thin-film-silicon-solar-cells

Cancer battle: Scientists engineer new tumor-killing virus

A new genetically-engineered virus has been developed to kill cancer tumors and prevent the growth of new ones, according to a study. It was tested in 30 terminally-ill liver cancer patients and proved to significantly prolong their lives.
The study, which was recently published in the journal Nature Medicine, describes a four-week trial of the vaccine Pexa-Vec or JX-594 marking a step forward towards a successful treatment of solid tumors, AFP reports.

Sixteen out of 30 patients who were given a high dosage of therapy lived for 14.1 months on average, while the other 14 patients were given a low dosage and survived for 6.7 months.
"For the first time in medical history we have shown that a genetically-engineered virus can improve survival of cancer patients," study co-author David Kirn from California-based biotherapy company Jennerex told AFP.
The results of the study indicate that "Pexa-Vec treatment at both doses resulted in a reduction of tumor size and decreased blood flow to tumors," Jennerex said in a statement. “This is the first randomized clinical trial of an oncolytic immunotherapy demonstrating significantly prolonged overall survival.”

The new treatment uses oncolytic immunotherapy, which is a genetically modified type of virus that attacks tumors to induce a systemic immune response to cancer. It selectively replicates in tumor cells to achieve an antitumor effect.
The new virus "is designed to multiply in and subsequently destroy cancer cells, while at the same time making the patients' own immune defense system attack cancer cells also," added Kirn.

This trial shows concrete progress and proves that “Pexa-Vec treatment induces an immune response against the tumor."

Source: http://rt.com/news/new-virus-battles-cancer-888/

Some cancer mutations slow tumor growth

A typical cancer cell has thousands of mutations scattered throughout its genome and hundreds of mutated genes. However, only a handful of those genes, known as drivers, are responsible for cancerous traits such as uncontrolled growth. Cancer biologists have largely ignored the other mutations, believing they had little or no impact on cancer progression.

But a new study from MIT, Harvard University, the Broad Institute and Brigham and Women’s Hospital reveals, for the first time, that these so-called passenger mutations are not just along for the ride. When enough of them accumulate, they can slow or even halt tumor growth.

The findings, reported in this week’s Proceedings of the National Academy of Sciences, suggest that cancer should be viewed as an evolutionary process whose course is determined by a delicate balance between driver-propelled growth and the gradual buildup of passenger mutations that are damaging to cancer, says Leonid Mirny, an associate professor of physics and health sciences and technology at MIT and senior author of the paper.

In computer simulations, the researchers tested the possibility of treating tumors by boosting the impact of deleterious mutations. In their original simulation, each deleterious passenger mutation reduced the cell’s fitness by about 0.1 percent. When that was increased to 0.3 percent, tumors shrank under the load of their own mutations.

The same effect could be achieved in real tumors with drugs that interfere with proteins known as chaperones, Mirny suggests. After proteins are synthesized, they need to be folded into the correct shape, and chaperones help with that process. In cancerous cells, chaperones help proteins fold into the correct shape even when they are mutated, helping to suppress the effects of deleterious mutations.

Several potential drugs that inhibit chaperone proteins are now in clinical trials to treat cancer, although researchers had believed that they acted by suppressing the effects of driver mutations, not by enhancing the effects of passengers.

In current studies, the researchers are comparing cancer cell lines that have identical driver mutations but a different load of passenger mutations, to see which grow faster. They are also injecting the cancer cell lines into mice to see which are likeliest to metastasize.

The research was funded by the National Institutes of Health/National Cancer Institute Physical Sciences Oncology Center at MIT.

Source: http://web.mit.edu/newsoffice/2013/some-cancer-mutations-slow-tumor-growth-0204.html

Mercedes engineers expect autonomous cars by 2020

German ingenieurs from Mercedes expect that by 2020 series models can at least partially drive themselves.

Source: http://www.zeit.de/auto/2013-01/auto-autonom

Will we ever... grow synthetic organs in the lab?

Grow synthetic organs in the lab

Growing synthetic windpipes, artificial skin and replacement blood vessels is now a reality, but scientists are now turning their attention to their ultimate goal: growing new human kidneys or hearts.

In June 2011, an Eritrean man entered an operating theatre with a cancer-ridden windpipe, but left with a brand new one. People had received windpipe transplants before, but Andemariam Teklesenbet Beyene’s was different. His was the first organ of its kind to be completely grown in a lab using the patient's own cells.

The practicalities are, as you can imagine, less straightforward. Take the example I have already described. The process began with researchers taking 3D scans of Beyene’s windpipe, and from these scans Alexander Seifalian at University College London built an exact replica from a special polymer and a glass mould. This was flown to Sweden, where surgeon Paolo Macchiarini seeded this scaffold with stem cells taken from Beyene’s bone marrow. These stem cells, which can develop into every type of cell in the body, soaked into the structure and slowly recreated the man’s own tissues. The team at Stockholm’s Karolinska University Hospital incubated the growing windpipe in a bioreactor – a vat designed to mimic the conditions inside the human body.

Two days later, Macchiarini transplanted the windpipe during a 12-hour operation, and after a month, Beyene was discharged from the hospital, cancer-free. A few months later, the team repeated the trick with another cancer patient, an American man called Christopher Lyles.

“A good way to think about it is that there are four levels of complexity,” says Anthony Atala from the Wake Forest Institute for Regenerative Medicine, one of the leaders of the field. The first level includes flat organs like skin, which comprise just a few types of cells. Next up are tubes, like windpipes or blood vessels, with slightly more complex shapes and more varied collections of cells. The third level includes hollow sac-like organs, like the bladder or stomach. Unlike the tubes, which just act as pipes for fluid, these organs have to perform on demand – secreting, expanding or filtering as the situation arises.

Even after scientists successfully devise ways of growing organs, there are many logistical challenges to overcome before these isolated success stories can become everyday medical reality. “Can you manufacture them and grow them on large scales?” asks Robert Langer, a pioneer in the field. “Can you create them reproducibly? Can you preserve them [in the cold] so they have a reasonable shelf-life? There are a lot of very important engineering challenges to overcome.”

Source: http://www.bbc.com/future/story/20120223-will-we-ever-create-organs

Printing a human kidney

Surgeon Anthony Atala demonstrates an early-stage experiment that could someday solve the organ-donor problem: a 3D printer that uses living cells to output a transplantable kidney. Using similar technology, Dr. Atala's young patient Luke Massella received an engineered bladder 10 years ago.

Anthony Atala asks, "Can we grow organs instead of transplanting them?" His lab at the Wake Forest Institute for Regenerative Medicine is doing just that - engineering over 30 tissues and whole organs. Anthony Atala is the director of the Wake Forest Institute for Regenerative Medicine, where his work focuses on growing and regenerating tissues and organs. His team engineered the first lab-grown organ to be implanted into a human - a bladder - and is developing experimental fabrication technology that can "print" human tissue on demand.

In 2007, Atala and a team of Harvard University researchers showed that stem cells can be harvested from the amniotic fluid of pregnant women. This and other breakthroughs in the development of smart bio-materials and tissue fabrication technology promises to revolutionize the practice of medicine.

Source: http://www.bbc.com/future/story/20120621-printing-a-human-kidney

Epigenetic reveal clues to ageing

Why do we develop wrinkles and why do our muscles waste away? Why do our brains and immune systems become less effective with time?

Epigenetics is all about changing the way our genes function by turning them off or making them more active.

Genes are the blueprint for building the human body. There's a copy of the whole blueprint in nearly every cell in the body, but clearly you don't need to use all of it all of the time. Bone cells will use different bits of the blueprint to nerve cells or light sensing cells in the eye.

Manel Esteller's team, at the Bellvitge Biomedical Research Institute, has shown that this control over the blueprint decays over time.

Adding small chemicals, methyl groups, to specific points of DNA is one of the main ways of turning a gene off.

Longer or healthier life?

It is possible to change a person's epigenome. Studies have already shown how a pregnant mother's diet can affect her child's risk of obesity epigenetically.

Prof Tim Spector, the author of a book on epigenetics, Identically Different, said: "There are epigenetic drugs in development, four for cancer. In terms of lifestyle, we know that exercise can switch off the main obesity genes epigenetically.

"Apart from stem cells, this is the hot area of ageing at the moment, finding ways of encouraging our genes to remain healthy is going to be a top priority in the next few years."

Source: http://www.bbc.co.uk/news/health-18400219

Mass cancer mapping centre opens

The devastating changes that turn healthy tissue into cancer are to be investigated in the biggest centre of its kind in the NHS.

The laboratories at the Institute of Cancer Research (ICR) will use information in tumour DNA to help find the best "personalised" treatments.

Its director said this was not science fiction and would be day-to-day practice in the NHS within a decade.

Rapid advances in being able to sequence the genetic code of patients are allowing breakthroughs in understanding which mutations transform a healthy cell into a cancerous one.

Identifying the mutations can then be used to choose the best treatment. The most famous example of this is the drug Herceptin, which is used in breast cancers with a certain genetic abnormality.

The new centre will test samples from patients at the Royal Marsden Hospital in London.

The ICR's director, Prof Alan Ashworth, said: "None of this is science fiction. This is now happening. We think we're pioneering the clinical application of this by setting up the Tumour Profiling Unit, but one would think this would be absolutely routine practice for every cancer patient - and that's what we're aiming to bring about."

Other challenges for the field include storing the data. The genetic codes of one million cancer patients would take up the same amount of space as YouTube.

Source: http://www.bbc.co.uk/news/health-21235103

Leprosy bacteria use 'biological alchemy'

Infectious bacteria have for the first time been caught performing "biological alchemy" to transform parts of a host body into those more suited to their purposes, by a team in Edinburgh.

The study, in the journal Cell, showed leprosy-causing bacteria turning nerves into stem cells and muscle.

The authors said the "clever and sophisticated" technique could further therapies and stem-cell research.

Prof Rambukkana also believes it is "probable" that other species of bacteria would have evolved the same ability to reprogramme their host.

Prof Chris Mason, a specialist in stem cell research at University College London, said: "The ability of bacteria to convert one mammalian cell type to another is 'alchemy' by nature on a grand scale.

"The next essential step is to translate this valuable piece of knowledge into tangible benefits for patients - a process that may take a decade before its relevance to clinical medicine is fully understood."

Prof Diana Lockwood, from the London School of Hygiene and Tropical Medicine, said: "Their finding that bacteria can reprogramme cells is very interesting and exciting."

Dr Rob Buckle, head of regenerative medicine at the Medical Research Council, said: "This discovery is important not just for our understanding and treatment of bacterial disease, but for the rapidly progressing field of regenerative medicine."

Source: http://www.bbc.co.uk/news/health-21056644