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How chemical castration makes tumours drug resistant
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CORBIS
THE heart of Venus may belong to Earth. Our planet could be tugging on the core of Venus, exerting control over its spin. Whenever Venus and Earth arrive at the closest point in their orbits, Venus always presents the same face to us. This could mean that Earth’s gravity is tugging subtly on Venus, affecting its rotation rate. That idea, raised decades ago, was disregarded when it turned out that Venus is spinning too fast to be in such a gravitational “resonance”. But Earth could still be pulling on Venus by controlling its core, according to calculations by Gérard Caudal of the University of Versailles-Saint Quentin (Journal of Geophysical Research, in press). Caudal made large assumptions about Venus’s interior, which we know little about. For his hypothesis to be correct, the planet would, like Earth, need a solid core surrounded by a liquid layer. This could allow the solid core to rotate slower than the rest of the planet. The core would also have to be heterogeneous, so that Earth can exert a variable tug as Venus spins. “There should be something that the gravity of the Earth could grasp,” Caudal says. David Stevenson of the California Institute of Technology in Pasadena thinks the resonance theory is worth revisiting, even though persistent imperfections in the core are unlikely.
Turning the tables on prostate cancer’s drug resistance DRUGS that keep prostate cancer at bay often stop working after a few years. That now appears to be because they prompt the growth of the very tumour cells they are meant to kill. It’s not all bad news, though: blocking this growth pathway could buy time for men with drug-resistant tumours. Most early prostate cancers require male sex hormones, known as androgens, to grow. Anti-androgen drugs can cause these tumours to regress, but eventually they become resistant to them and start to grow again.
Yet unlike other drug-resistant cancers, these tumours have no telltale mutations. To learn how prostate tumours become drug resistant, researchers led by Michael Karin at the University of California, San Diego, implanted prostate tumours into mice and gave them anti-androgens. They found that the resulting death of the tumour cells led to an inflammatory response in which white blood cells converged on the tumour and secreted a signalling molecule called lymphotoxin.
This in turn triggered an androgen-independent cellgrowth pathway in the remaining tumour cells (Nature, DOI: 10.1038/nature08782). The researchers have yet to show the same pathway is active in human prostate cancers. If it is, it offers a promising way to delay tumour resistance. Blocking the lymphotoxin pathway in mice caused tumours to remain dormant for three to four additional weeks, equivalent to two to three years of remission in humans, Karin says. ANOEK DE GROOT/AFP/GETTY
Venus and Earth, strange attractors
High-carbon ice age mystery solved HOW come a big ice age happened when carbon dioxide levels were high? It’s a question that climate sceptics often ask. But sometimes the right answer is the simplest: it turns out CO2 levels were not that high after all. The Ordovician ice age happened 444 million years ago, and until now records have suggested that CO2 levels were relatively high then. But when Seth Young of Indiana University in Bloomington did a detailed analysis of carbon-13 levels in rocks from Canada and Estonia that were formed at the time, the picture that emerged was very different. Young found that CO2 concentrations were in fact relatively low when the ice age began (Palaeogeography, Palaeoclimatology, Palaeoecology, DOI: 10.1016/j.palaeo.2010.02.033). Lee Kump of Pennsylvania State University in University Park says earlier studies missed the dip because they calculated levels at 10-million-year intervals and the ice age lasted only half a million years. The dip, he says, was triggered by a burst of volcanic activity that deposited new silicate rocks. These draw CO2 out of the air as they erode.
The luck of the devils is in their genes A CARNIVOROUS marsupial on the verge of being wiped out by a transmissible cancer could be saved – by the discovery of animals resistant to the disease. Since 1996 Tasmanian devils have lost 90 per cent of some populations to the deadly and highly infectious devil facial tumour disease, which is spread by biting. But widespread pockets of Australia’s island state, such as the north-west and Bronte Park, remain unscathed. Biologists were unsure if this was luck – perhaps the disease hadn’t reached the areas yet – or resilience.
It turns out to be the latter. Kathy Belov’s team at the University of Sydney has found that the immune system of infected and unharmed devils works differently. Belov already knew that devils in eastern Tasmania are vulnerable because their immune system mistakes foreign cancer cells for “self” cells. Now her team has analysed the immune system’s key controller genes for the first time and found that resistant devils have genes that equip them to attack the disease (Proceedings of the Royal Society B, DOI: 10.1098/rspb.2009.2362).
13 March 2010 | NewScientist | 17
CORBIS
THE heart of Venus may belong to Earth. Our planet could be tugging on the core of Venus, exerting control over its spin. Whenever Venus and Earth arrive at the closest point in their orbits, Venus always presents the same face to us. This could mean that Earth’s gravity is tugging subtly on Venus, affecting its rotation rate. That idea, raised decades ago, was disregarded when it turned out that Venus is spinning too fast to be in such a gravitational “resonance”. But Earth could still be pulling on Venus by controlling its core, according to calculations by Gérard Caudal of the University of Versailles-Saint Quentin (Journal of Geophysical Research, in press). Caudal made large assumptions about Venus’s interior, which we know little about. For his hypothesis to be correct, the planet would, like Earth, need a solid core surrounded by a liquid layer. This could allow the solid core to rotate slower than the rest of the planet. The core would also have to be heterogeneous, so that Earth can exert a variable tug as Venus spins. “There should be something that the gravity of the Earth could grasp,” Caudal says. David Stevenson of the California Institute of Technology in Pasadena thinks the resonance theory is worth revisiting, even though persistent imperfections in the core are unlikely.
Turning the tables on prostate cancer’s drug resistance DRUGS that keep prostate cancer at bay often stop working after a few years. That now appears to be because they prompt the growth of the very tumour cells they are meant to kill. It’s not all bad news, though: blocking this growth pathway could buy time for men with drug-resistant tumours. Most early prostate cancers require male sex hormones, known as androgens, to grow. Anti-androgen drugs can cause these tumours to regress, but eventually they become resistant to them and start to grow again.
Yet unlike other drug-resistant cancers, these tumours have no telltale mutations. To learn how prostate tumours become drug resistant, researchers led by Michael Karin at the University of California, San Diego, implanted prostate tumours into mice and gave them anti-androgens. They found that the resulting death of the tumour cells led to an inflammatory response in which white blood cells converged on the tumour and secreted a signalling molecule called lymphotoxin.
This in turn triggered an androgen-independent cellgrowth pathway in the remaining tumour cells (Nature, DOI: 10.1038/nature08782). The researchers have yet to show the same pathway is active in human prostate cancers. If it is, it offers a promising way to delay tumour resistance. Blocking the lymphotoxin pathway in mice caused tumours to remain dormant for three to four additional weeks, equivalent to two to three years of remission in humans, Karin says. ANOEK DE GROOT/AFP/GETTY
Venus and Earth, strange attractors
High-carbon ice age mystery solved HOW come a big ice age happened when carbon dioxide levels were high? It’s a question that climate sceptics often ask. But sometimes the right answer is the simplest: it turns out CO2 levels were not that high after all. The Ordovician ice age happened 444 million years ago, and until now records have suggested that CO2 levels were relatively high then. But when Seth Young of Indiana University in Bloomington did a detailed analysis of carbon-13 levels in rocks from Canada and Estonia that were formed at the time, the picture that emerged was very different. Young found that CO2 concentrations were in fact relatively low when the ice age began (Palaeogeography, Palaeoclimatology, Palaeoecology, DOI: 10.1016/j.palaeo.2010.02.033). Lee Kump of Pennsylvania State University in University Park says earlier studies missed the dip because they calculated levels at 10-million-year intervals and the ice age lasted only half a million years. The dip, he says, was triggered by a burst of volcanic activity that deposited new silicate rocks. These draw CO2 out of the air as they erode.
The luck of the devils is in their genes A CARNIVOROUS marsupial on the verge of being wiped out by a transmissible cancer could be saved – by the discovery of animals resistant to the disease. Since 1996 Tasmanian devils have lost 90 per cent of some populations to the deadly and highly infectious devil facial tumour disease, which is spread by biting. But widespread pockets of Australia’s island state, such as the north-west and Bronte Park, remain unscathed. Biologists were unsure if this was luck – perhaps the disease hadn’t reached the areas yet – or resilience.
It turns out to be the latter. Kathy Belov’s team at the University of Sydney has found that the immune system of infected and unharmed devils works differently. Belov already knew that devils in eastern Tasmania are vulnerable because their immune system mistakes foreign cancer cells for “self” cells. Now her team has analysed the immune system’s key controller genes for the first time and found that resistant devils have genes that equip them to attack the disease (Proceedings of the Royal Society B, DOI: 10.1098/rspb.2009.2362).
13 March 2010 | NewScientist | 17