Un caso impresionante que nos habla de nuevas tecnologías y esperanzas en cirugía plástica y reconstructiva. via NewScientist.

An 83-year-old Belgian woman is able to chew, speak and breathe normally again after a machine printed her a new jawbone. Made from a fine titanium powder sculpted by a precision laser beam, her replacement jaw has proven as functional as her own used to be before a potent infection, called osteomyelitis, all but destroyed it.

The medics behind the feat say it is a first. “This is a world premiere, the first time a patient‐specific implant has replaced the entire lower jaw,” says Jules Poukens, the researcher who led the operation at Biomed, the biomedical research department of the University of Hasselt, in Belgium. “It’s a cautious, but firm step.”

Until now, the largest 3D-printed implant is thought to have been half of a man’s upper jawbone, in a 2008 operation in Finland.

In this operation, a 3D printed titanium scaffold was steeped in stem cells and allowed to grow biocompatible tissue inside the abdomen of the recipient. Then, in 2009, researchers reportedsuccessfully printing copies of whole thumb bones – opening the way for the replacement of smashed digits using information from MRI scans.

Poukens’ team worked with researchers in Belgium and the Netherlands and a 3D printing firm called Layerwise in Leuven, Belgium, which specialises in printing with ultrastrong titanium to make dental implants (like bridges and crowns) and facial and spinal bone implants.

By using an MRI scan of their patient’s ailing jawbone to get the shape right, they fed it to a laser sintering 3D printer which fused tiny titanium particles layer by layer until the shape of her jawbone was recreated. It was then coated in a biocompatible ceramic layer. No detail was spared: it even had dimples and cavities that promoted muscle attachment, and sleeves that allowed mandibular nerves to pass through – plus support structures for dental implants the patient might need in future.

The team were astonished at the success of the four-hour jaw implant operation, which took place in June 2011 but which has only just been revealed.  “Shortly after waking up from the anaesthetic the patient spoke a few words, and the day was able to speak and swallow normally again,” says Poukens.

It’s only the start, predicts Layerwise managing director Peter Mercelis. “Patient‐specific implants can potentially be applied on a much wider scale than transplantation of human bone structures.”

Since 3D printers can create layers of material only micrometres thick, and from just about any material, researchers are investigating ways to print skin grafts for burns victims from them – and how to build up whole organs from depositing cells in the correct shape.



El Profesor Gerard Evan es el director del departamento de Bioquímica en la Universidad de Cambridge. En este artículo el profesor Evan explica por que el cáncer es un enemigo que se adapta y evoluciona.

Biology has undergone an unprecedented technical revolution in the past two decades. Despite its complexity, biological systems can now be mapped and catalogued in minute detail – we can monitor the activity of every one of our approximately 25,000 genes; identify almost every protein present in a cell; and even sequence the entire genomes of animals, plants, bacteria or cancer cells.

For cancer researchers, these technologies can appear a Godsend: cancers are extremely diverse diseases that arise through the build-up of mutations (errors) in the genes that regulate and restrain the growth, division, and movement of the cells that make up our bodies. The process is ‘Darwinian’ – in other words, the mutations occur at random over our lifetimes, and the faulty cells then either die out or survive and multiply as a result of the complex, changing and still largely mysterious selective pressures in the body.

The technical revolution of recent years has undoubtedly advanced our understanding of cancer, and is helping sustain impressive improvements in cancer survival rates, but why don’t we hear the word ‘cure’ very often when it comes to this disease? And what needs to be done so that we do?

Mapping complexity

Not surprisingly, given the haphazard and random way in which they evolve, every patient’s cancer is unique. Indeed, mapping and understanding the complexity within just one person’s cancer could occupy an entire research institute. In some ways, cancer research has reached an existential impasse – we can map and catalogue and annotate forever, but what is it about cancer that we really want to know?

For most of us, I suspect the answer is simple and pragmatic: we want to know how to cure patients.

Simple questions have the habit of exposing others that are more fundamental: in this case, “Why are cancers so difficult to cure?” Here, there are two general schools of thought.

Personalised medicine

Many would point to the disconcerting genetic diversity of cancers – an inevitable consequence of the haphazard way that they evolve. In the past, cancer therapies were applied fairly indiscriminately, but now many believe that effective therapies need to be specific and tailored to the particular genetic faults in each individual’s cancer – in other words cancer therapy needs to be ‘personalised’. With the advent of new targeted drugs (such as Herceptin for some breast cancers, Glivec for certain leukaemias, and brand new drugs like vemurafenib for some skin cancers), many hope that this may, at least one day soon, be feasible.

But simply personalising treatment so that it targets the genetic faults present in a tumour at the point of diagnosis, disregards the most fundamental reason for why cancers are difficult to eradicate forever: cancer cells adapt and evolve in response to treatment.

Because of this, even drugs that are initially very effective often have a progressively dwindling effect over time, as the biological systems that are blocked by the treatment spontaneously compensate by re-routing the cancer cells’ internal wiring, thereby restoring the cancer’s ability to grow and spread. To use an analogy, traffic hot spots in towns can cause major traffic jams, but cunning drivers will quickly find short cuts to get round the congestion.

Then, in those rare situations where cancer cells cannot take such ‘short cuts’, evolution takes over: in response to drug treatment, spontaneously arising mutant cancer cells that are resistant to the targeted drug rapidly outgrow their incapacitated siblings and the cancer comes back.

Although some patients can be successfully cured and their cancers don’t return – such as is often the case for testicular cancer and some childhood cancers – for other cancers the situation is different, as so many patients and their families are all too aware. It doesn’t matter how effective or specific a therapy is – if the system the treatment is targeting can be bypassed by compensation or evolution, that therapy will become less effective over time and eventually fail, and the cancer will return.

Evolutionary dead end

Against two such formidable adversaries as compensation and evolution what are we to do? A solution is to identify targets that are essential for the survival of cancer cells but whose inhibition cannot be bypassed by compensation or evolution. Rather than causing localized traffic jams within the city that can be circumvented by short cuts, we identify the bridge that is the only way out of town and then block that.

But do such fundamental targets exist? Can we make drugs that inhibit them? How bad might the side effects of such therapies be, given that such essential and non-redundant engines of biology are likely to serve important functions in ‘normal’ bodily processes? We don’t yet know.

A second idea is to chase each cancer down an evolutionary valley and into a dead end from which it cannot escape. We accept that localized traffic jams can be bypassed but, each time that happens, we identify the back route and then target that – and we keep doing it until there are no short cuts left. In practice, this would mean treating a patient with one targeted drug and, if their cancer returns with newly-developed resistance to this treatment, we then identify how that resistance evolved and hit the tumour with another drug directed at that resistance mechanism. The process is repeated until the cancer runs out of evolutionary headroom.

Both of these strategies will need a significant re-tooling and refocusing of our cancer research enterprise. We need to pay more attention to the inherent robustness and evolutionary ability of the targets against which our drugs are directed, and see if we can identify the essential engines of tumour maintenance.

One potential benefit of finding such fundamental engines is that they might be a common requirement of many, perhaps all, cancers: in which case a therapy targeted against them might usher in an exciting and far more affordable era of ‘impersonalised’ cancer treatment.

On the other hand, if we are going to chase tumours into extinction, we need to track the evolutionary trajectories of cancers in patients through sequential episodes of treatment and relapse. To do this, we must establish what information we need and how to get it without putting patients through repeated and onerous biopsies and procedures.

Common goal

All cancer researchers share the common goal of wanting cancer therapies that are effective and durable. But to do this we must never lose sight of the fact that cancers are just another example of evolution at work.

Cancers are blind. They are neither clever nor cunning – but humans are.

En los últimos 20 años la ciencia ha visto desfilar varios avances que han prometido ser un horizonte esperanzador en la cura del cáncer, sin embargo ninguno de ellos evoluciono, esto en gran parte debido a que ningún Hospital, laboratorio o Universidad apoyo de alguna manera el desarrollo de los mismos. En esta ocasión estamos hablando de una nanoparticula que ha sido desarrollada durante varios años, algo que parece prometedor y que en pocos años podremos saber de sus aplicaciones terapéuticas. Uno de los casos científicos mas sonados del 2011.

What were you doing when you were 17? Playing video games with your friends? Smoking outside the back door of your high school? Well, unless you answered “curing cancer,” prepare to feel like an underachiever compared to Angela Zhang. The impressive 17-year-old from Cupertino, California just won the $100,000 Grand Prize of the Siemens Competition in Math, Science & Technology for a project called, “Design of Image-guided, Photo-thermal Controlled Drug Releasing Multifunctional Nanosystem for the Treatment of Cancer Stem Cells.” Not too shabby, right?

It’s even more impressive once you can understand what that title of that project actually means. Basically she created a nanoparticle that kills cancer cells. Here’s what’s so special about it:

Zhang said the particle she designed improves on current cancer treatments because it delivers a drug directly to tumor cells and doesn’t affect healthy cells around it. The particle is also able to release a drug when activated by a laser.

A laser? Hot damn! Her creation is being heralded as a “swiss army knife of cancer treatments” because it has so many different potential uses. As is often the case with these types of innovations, it’s many years away from being used in actual patients, but it’s still quite an accomplishment—especially for a teenager.

Her research was spurred by the deaths of her grandfather and great-grandfather from cancer, she explained:

I asked, “Why does this happen. Why does cancer cause death? What are we doing to fix this and what can I do to help?”

And her win didn’t come without dedication. Zhang has been working on this nanoparticle since 2009 and has spent more than 1,000 hours on the project. Hmm, suddenly makes all of that time I spent wandering around the mall and listening to Nirvana seem like kind of a waste.


New Research: Getting Up From Your Desk Can Put the “Breaks” on Cancer

Experts Urge Americans to Rethink Outdated Notions of Physical Activity

WASHINGTON, DC — As many as 49,000 cases of breast cancer and 43,000 cases of colon cancer occurring in the U.S. every year are linked to a lack of physical activity, according to estimates presented today at the American Institute for Cancer Research annual conference. The estimate underscores the critical role that both activity and inactivity play in the development of specific cancers.

At the AICR Annual Research Conference on Food, Nutrition, and Physical Activity in Washington, experts presented data from a new paper on physical activity and breast cancer prevention and reviewed the mounting evidence that a brisk daily walk helps to reduce several key biological indicators of cancer risk, including sex hormone levels, insulin resistance, inflammation and body fatness.

The researchers also presented new findings from the emerging field of sedentary behavior research, which is finding that sitting for long periods of time can increase some of those same indicators of cancer risk, even among people who exercise daily.

“Taken together, this research suggests that every day, we’re each given numerous opportunities to be active and protect ourselves from cancer, not one,” said AICR spokesperson Alice Bender, MS RD. “We need to start thinking in terms of make time and break time.”

Based on these research findings, AICR is urging Americans to make time for physical activity and break every hour of sitting with 1 to 2 minutes of activity. These breaks can be as simple as walking to a colleague’s office instead of sending an email or going to the kitchen to get a glass of water.

“Making time to get at least half an hour of moderate to vigorous activity every day is great, and more Americans need to do it, but those 30 minutes represent only a sliver of our day,” Bender stated. “This new research on break time suggests there are small things we can do in the other 15 hours and 30 minutes we spend awake that also make a big difference.”

Make Time: Physical Activity Clearly Lowers Risk of Cancer

Providing the latest evidence of the protective link between physical activity and various cancers, Senior Research Epidemiologist Christine Friedenreich, PhD, of Alberta Health Services-Cancer Care in Canada, presented just-published findings from the Alberta Physical Activity and Breast Cancer Prevention (ALPHA) Trial. The latest results from this trial involve C-reactive protein, a marker of inflammation, which is linked to cancer risk. In a study appearing in the October issue of the journal Cancer Prevention Research, moderate to vigorous daily activity reduced C-reactive protein levels among post-menopausal women.

Although researchers have not yet identified how inflammation increases cancer risk, it is known that the inflammation process produces cytokines (immune-response chemicals that encourage cell proliferation and suppress cell death) that contribute to increased cancer risk. Previous studies have shown that the immune cells activated by the inflammatory response, such as macrophages and neutrophils, release reactive elements like oxygen and nitrogen, which can damage the DNA and produce mutations.

Dr. Friedenreich’s research demonstrates that even in previously sedentary postmenopausal women, a moderate- to vigorous-intensity exercise program results in changes in several biomarker levels that are consistent with a lower risk for postmenopausal breast cancer.

By extrapolating data from the ALPHA trial as well as previous epidemiological investigations involving adiposity, insulin resistance, mammographic density, sex hormone levels and other indicators of cancer risk, Dr. Friedenreich reported that engaging in moderate activity, like brisk walking, can significantly reduce the risk of certain cancers.

“In breast and colon cancers, for example, we’re seeing overall risk reductions of about 25 to 30 percent associated with higher levels of physical activity. With prostate cancer the evidence isn’t as strong but it’s still there – about 10 to 20 percent lower risk. For endometrial cancer, we are finding about 30 to 35 percent risk reduction with more physical activity.

“These numbers are powerful,” she said. “The bottom line: For many of the most common cancers, it seems like something as simple as a brisk walk for 30 minutes a day can help reduce cancer risk.”

via American Institute for Cancer Research (AICR): New Research: Getting Up From Your Desk Can Put the “Breaks” on Cancer.