Loophole for Cancer Cells Found

Many cancers only become a mortal danger if they form metastases elsewhere in the body. Such secondary tumours are formed when individual cells break away from the main tumour and travel through the bloodstream to distant areas of the body. To do so, they have to pass through the walls of small blood vessels. Scientists from the Max Planck Institute for Heart and Lung Research in Bad Nauheim and Goethe University Frankfurt have now shown that tumour cells kill specific cells in the vascular wall. This enables them to leave the vessels and establish metastases, a process facilitated by a molecule called DR6.

The most common cause of cancer deaths is not the primary tumour itself but metastases that subsequently form. Most tumour cells spread via the bloodstream. To do so, individual tumour cells have to enter blood vessels and leave the bloodstream again at remote locations.

Together with scientists at the universities of Cologne and Heidelberg, the Research Group led by Stefan Offermanns, Director of the Department of Pharmacology at the Max Planck Institute for Heart and Lung Research and professor at Goethe University Frankfurt, has now succeeded in clarifying the underlying mechanism. The researchers, working with cell cultures, first observed how individual tumour cells kill specific cells in the vascular wall, called endothelial cells. This process, known as necroptosis, enabled cancer cells to overcome an endothelial cell layer in the laboratory. "We were then able to show in studies on mice that the same process occurs in living organisms," says Boris Strilic, first author of the study.

The scientists also found that endothelial cells themselves give the signal for their own death: To do this, the vascular wall cells have a receptor molecule called Death Receptor 6 (DR6) on their surface. "When a cancer cell comes into contact with it, a protein on the cell's surface, known as APP, activates DR6. This marks the start of the cancer cells' attack on the vascular wall, which culminates in the necroptosis of wall cells," Strilic explains.

Death Receptor in the cell membrane

The Max Planck researchers then showed that less necroptosis of endothelial cells and less metastasis occur in genetically modified animals in which Death Receptor 6 is disabled. "This effect was also found after a blockade of DR6 or the cancer-cell protein APP, thus confirming our previous observations," Strilic says.

It is still not entirely clear whether the cancer cells migrate directly through the resulting gap in the vascular wall or whether there is an indirect effect: "We have evidence that many more molecules are released when the vascular wall cell dies and that they render the surrounding area more permeable to cancer cells," says Offermanns.

"This mechanism could be a promising starting point for treatments to prevent the formation of metastases," says Offermanns. First, however, it must be determined whether a blockade of DR6 triggers unwanted side effects. It must also be determined to what extent the observations can be transferred to humans.

Scientists Find Brain's Generosity Center

Scientists from Oxford University and UCL have identified part of our brain that helps us learn to be good to other people. The discovery could help understanding of conditions like psychopathy where people's behaviour is extremely antisocial.

The researchers were led by Dr Patricia Lockwood, who explained: 'Prosocial behaviours are social behaviours that benefit other people. They are a fundamental aspect of human interactions, essential for social bonding and cohesion, but very little is currently known about how and why people do things to help others.

'Although people have a remarkable inclination to engage in prosocial behaviours there are substantial differences between individuals. Empathy, the capacity to vicariously experience and understand another person's feelings has been put forward as a critical motivator of prosocial behaviours, but we wanted to test why and how they might be linked.'

The scientists used a well-understood model of how people learn to maximise good outcomes for themselves and applied this model to understand how people learn to help others. While being scanned in a MRI machine, volunteers had to work out which symbols were more likely to give them, or someone else, a reward.

They found that while people readily learn to make choices that benefit other people, they do not learn it quite as fast as they learn to benefit themselves. However, they also identified a particular brain area involved in learning to get the best result for other people.

Dr Lockwood said: 'A specific part of the brain called the subgenual anterior cingulate cortex was the only part of the brain that was activated when learning to help other people. Put another way, the subgenual anterior cingulate seems to be especially tuned to benefiting other people.

'However, this region of the brain was not equally active in every person. People who rated themselves as having higher levels of empathy learnt to benefit others faster than those who reported having lower levels of empathy. They also showed increased signalling in their subgenual anterior cingulate cortex when benefitting others.'

'This the first time anyone has shown a particular brain process for learning prosocial behaviours -- and a possible link from empathy to learning to help others. By understanding what the brain does when we do things for other people, and individual differences in this ability, we are better placed to understand what is going wrong in those whose psychological conditions are characterised by antisocial disregard for others.'

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Cancer on a Paleo-diet?

An international team of researchers led by scientists from the University of the Witwatersrand's Evolutionary Studies Institute and the South African Centre for Excellence in PalaeoSciences today announced in two papers, published in the South African Journal of Science, the discovery of the most ancient evidence for cancer and bony tumors yet described in the human fossil record.

The discovery of a foot bone dated to approximately 1.7 million years ago from the site of Swartkrans with definitive evidence of malignant cancer, pushes the oldest date for this disease back from recent times into deep prehistory. Although the exact species to which the foot bone belongs is unknown, it is clearly that of a hominin, or bipedal human relative.

In an accompanying paper appearing in the same journal, a collaborating team of scientists identify the oldest tumor ever found in the human fossil record, a benign neoplasm found in the vertebrae of the well-known Australopithecus sediba child, Karabo from the site of Malapa, and dated to almost two million years in age. The oldest previously demonstrated possible hominin tumor was found in the rib of a Neanderthal and dated to around 120,000 years old.

Edward Odes, a Wits doctoral candidate and lead author of the cancer paper, and co-author on the tumor paper, notes "Modern medicine tends to assume that cancers and tumors in humans are diseases caused by modern lifestyles and environments. Our studies show the origins of these diseases occurred in our ancient relatives millions of years before modern industrial societies existed."

The cancer in a foot bone, a metatarsal, was identified as an osteosarcoma, an aggressive form of cancer which usually affects younger individuals in modern humans, and, if untreated typically results in early death. "Due to its preservation, we don't know whether the single cancerous foot bone belongs to an adult or child, nor whether the cancer caused the death of this individual, but we can tell this would have affected the individuals' ability to walk or run," says Dr Bernhard Zipfel, a Wits scientist and an expert on the foot and locomotion of early human relatives. "In short, it would have been painful."

Lead author of the tumor paper and co-author of the cancer paper, Dr Patrick Randolph-Quinney of Wits University and the University of Central Lancashire in the UK, suggests "The presence of a benign tumor inAustralopithecus sediba is fascinating not only because it is found in the back, an extremely rare place for such a disease to manifest in modern humans, but also because it is found in a child. This, in fact, is the first evidence of such a disease in a young individual in the whole of the fossil human record."

Prof. Lee Berger, an author on both papers and leader of the Malapa project where the fossil vertebra was found adds "not only has there been an assumption that these sorts of cancers and tumors are diseases of modernity, which these fossils clearly demonstrate they are not, but that we as modern humans exhibit them as a consequence of living longer, yet this rare tumor is found in a young child. The history of these types of tumors and cancers is clearly more complex than previously thought."

Both incidents of disease were diagnosed using state of the art imaging technologies including those at the European Synchrotron Research Facility in Grenoble, France, medical CT at the Charlotte Maxeke Hospital in Johannesburg, and the micro-CT facility at the Nuclear Energy Corporation of South Africa at Pelindaba.

"Researchers in South Africa are at the forefront of using various X-Ray modalities to discover new and interesting facts about ancient human relatives," notes Dr Jacqueline Smilg, a radiologist based at Charlotte Maxeke Hospital, who is an author on both papers and was involved in the clinical diagnoses. "This is another good example of how the modern clinical sciences and the science of palaeoanthropology are working together in South Africa and with international collaborators to advance our understanding of diseases in both the past and the present."

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