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Paul Davies PhD (1946 to present)

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Paul Davies is a physicist, writer, professor, broadcaster, and founder/director of the Beyond Center for Fundamental Concepts in Science at Arizona State University. His latest book is The Goldilocks Enigma: Why Is the Universe Just Right for Life? His research interests are in the fields of cosmology, quantum field theory, and astrobiology. He has proposed that a one-way trip to Mars could be a viable option. In 2005, he took up the chair of the SETI: Post-Detection Science and Technology Task group of the International Academy of Astronautics. He is also an adviser to the Microbes Mind Forum.

 

Davies was brought up in Finchley, London, and attended Woodhouse Grammar School on Woodhouse Road. In 1970, he completed his PhD under the supervision of Michael J. Seaton and Sigurd Zienau at University College London. He then carried out postdoctoral research under Fred Hoyle at the University of Cambridge.

 

Davies’ inquiries have included theoretical physics, cosmology, and astrobiology and his research has been mainly in the area of quantum field theory in curved spacetime. His notable contributions are the so-called Fulling-Davies-Unruh effect, according to which an observer accelerating through empty space will perceive a bath of thermal radiation, and the Bunch-Davies vacuum state, often used as the basis for explaining the fluctuations in the cosmic background radiation left over from the big bang. A paper co-authored with Stephen Fulling and William Unruh was the first to suggest that black holes evaporating via the Hawking effect lose mass as a result of a flux of negative energy streaming into the hole from the surrounding space.

 

Davies has had a longstanding association with the problem of time’s arrow, and was also an early proponent of the theory that life on Earth may have come from Mars cocooned in rocks ejected by asteroid and comet impacts. During his time in Australia he helped establish the Australian Centre for Astrobiology. Davies was a co-author of Felisa Wolfe-Simon on the Science article “A Bacterium That Can Grow by Using Arsenic Instead of Phosphorus.“

 

Davies is now Principal Investigator at Arizona State University’s Center for Convergence of Physical Science and Cancer Biology. This is part of a program set up by the National Institutes of Health’s National Cancer Institute to involve physicists in cancer research which has set up a network of 12 Physical Sciences-Oncology Centers.

 

Davies’ talent as a communicator of science has been recognized in Australia by an Advance Australia Award and two Eureka Prizes, and in the UK by the 2001 Kelvin Medal and Prize by the Institute of Physics, and the 2002 Faraday Prize by The Royal Society. Davies received the Templeton Prize in 1995.

 

Davies wrote an article in the Wall Street Journal where he stated that he supported the ?arsenic can replace phosphorus’ idea of Felisa Wolfe-Simon because “I had the advantage of being unencumbered by knowledge. I dropped chemistry at the age of 16, and all I knew about arsenic came from Agatha Christie novels.“ He also made the statement, “Well, I would be astonished if this was the only arsenic-based organism on Earth and Felisa just happened to scrape it up from the bottom of Mono Lake on the first try, It’s quite clear that it is the tip of an iceberg. I think it’s a window into a whole new world of microbiology.“ In the same vein, in an article in The Guardian, Davies suggests that the origin of life will be uncovered through information theory rather than chemistry. Concerns have been raised about his responsibility as one of Wolfe-Simon’s co-authors.

 

The basis of a new theory of cancer is developed by Paul Davies and Charles Lineweaver in the following paper published in the journal of Physical Biology:

 

Abstract

 

The genes of cellular cooperation that evolved with multicellularity about a billion years ago are the same genes that malfunction to cause cancer. We hypothesize that cancer is an atavistic condition that occurs when genetic or epigenetic malfunction unlocks an ancient ?toolkit’ of pre-existing adaptations, re-establishing the dominance of an earlier layer of genes that controlled loose-knit colonies of only partially differentiated cells, similar to tumors. The existence of such a toolkit implies that the progress of the neoplasm in the host organism differs distinctively from normal Darwinian evolution. Comparative genomics and the phylogeny of basal metazoans, opisthokonta and basal multicellular eukaryotes should help identify the relevant genes and yield the order in which they evolved. This order will be a rough guide to the reverse order in which cancer develops, as mutations disrupt the genes of cellular cooperation. Our proposal is consistent with current understanding of cancer and explains the paradoxical rapidity with which cancer acquires a suite of mutually-supportive complex abilities. Finally we make several predictions and suggest ways to test this model.

 

To read more, click on this link for the entire paper:

http://cancer-insights.asu.edu/wp-content/uploads/2012/01/Cancer-tumors-as-Metazoa-1-0-tapping-genes-of-ancient-ancestors1.pdf

 

From the (UK) Telegraph, By Paul Davies

 

When President Nixon declared war on cancer 40 years ago, he also sanctioned one of the biggest research programs in history. The budget of America’s National Cancer Institute (NCI) is now $5 billion a year, more than NASA spends on space exploration. Cancer accounts for a large slice of research funds in most other developed countries, too: Cancer Research UK, for example, has a budget of 500 million British pounds a year. But despite this vast investment, the long-awaited “breakthrough“ remains elusive. Although certain drugs (often very expensive) can prolong life, the brutal truth is that most patients diagnosed with metastatic cancer today fare little better than their counterparts did decades ago. And as life expectancy rises, more people will die of cancer. Given the escalating costs of treatment, the economic impact is unsustainable.

 

I became embroiled in this depressing story four years ago when I was called out of the blue by the deputy director of the NCI, Anna Barker. Dr Barker talked about the glacial pace of clinical progress and her frustration that, even with some of the world’s finest minds involved, no light could be discerned at the end of the tunnel. Her question to me was: “Can physicists help?“

 

I explained that my career was focused on quantum mechanics, cosmology, black holes. “I know nothing about cancer,“ I said. “It doesn’t matter!“ was her response. Physicists, she pointed out, think about the world in a distinctive way. They have elucidated the secrets of the atom and probed the farthest reaches of the cosmos, and have a good track record at cracking tough, complex problems. It was not so much new technology that she was after, but insights from our problem-solving approach.

 

Two years later, in a bold attempt to exploit this untapped expertise, the NCI created 12 centers of physical science and oncology, and I found myself directing the one at Arizona State University. So, how are we getting on?

 

Well, one of the virtues of being unencumbered by much knowledge of a subject is the ability to come at it afresh, to see it through different eyes. The basic story of cancer is very simple. Somewhere in the body, cells start to proliferate uncontrollably. If unchecked, they spread to other organs and colonize them. At that stage, the patient’s prospects are grim. Yet nobody has a convincing explanation for why this happens. The individual steps can be partially explained in terms of changes in the cells. But precisely why a cell from, say, a breast duct or the prostate gland starts roaming the body to make a home in the liver or the lung – a process called metastasis – remains a mystery.

 

Most research has focused on cancer as a human disease. But tumors are also widespread among animals and plants, suggesting that they have deep evolutionary roots. Cancer is such a formidable adversary because it is a fundamental part of the story of life itself, and I believe it can be properly understood only by seeing the grand evolutionary picture. The earliest traces of life on Earth date back 3.5 billion years, but only about a billion years ago did complex, multi-celled organisms begin to evolve. This was a profound transition. Single cells have but one imperative – to replicate. They are, in effect, immortal. But when cells first formed co-operative assemblages, a new deal was struck. Most organisms outsourced their immortality to specialized germ cells (e.g. sperm and ova), and in return accepted death for themselves. Thus a typical tissue cell might reproduce a handful of times and then die.

 

Organisms police this contract with a variety of regulatory systems, including specialized genes that suppress runaway growth. I believe that cancer is a breakdown in this contract, initiated when a common-or-garden cell refuses to die on cue and embarks on its own agenda. It would be a mistake, however, to suppose that cancer merely represents a cell that has “gone wrong“, and started running amok in the body. In fact, cancers possess a surprising degree of organization. As they become more malignant, they deploy sophisticated tricks designed to evade the body’s defenses and enhance their own prospects. This pre-programmed box of tricks is what makes combating them such a challenge.

 

Together with Charles Lineweaver at the Australian National University, I have been developing a theory of cancer based on the concept that it is an evolutionary throwback to our earliest ancestors. About 600 million years ago, there appeared a riot of modern-looking metazoa (the multi-celled creatures that make up the bulk of the animal kingdom), with many specialized cell types and organs. But this explosion didn’t happen in a vacuum. Hundreds of millions of years before, they – we – had precursors: clumps of semi-organized cells forming robust, tumor-like forms. Our bodies are replete with ancestral genes that evolution has built on. These genes are retained because they are active in the early stages of embryo development, when the basic body plan is being laid down. Curiously, human embryos temporarily develop gills and tails, representing long-lost features of our evolutionary history. Normally these ancient genes are silenced thereafter. But Lineweaver and I have proposed that cancer results from an accidental reawakening of the earliest metazoan genes, the ones programmed to build the sort of structures that inhabited Earth millions of years ago. Rather like a computer starting up in safe mode after an error of some sort, cancer may be a reversion to a tried-and-tested ancestral lifestyle in response to a physical stress such as a carcinogen. By connecting the dots of evolutionary, developmental and cancer biology, we have come to view cancer not so much as a disease to be cured as a condition to be controlled. Like ageing, cancer must be accepted as part of life. But by careful management, its effects can be mitigated. For example, 90 per cent of cancer deaths result from metastasis. Slowing or arresting this spread would make a big difference.

 

Even when cancer cells make a home in a remote organ, the micro-tumors often fail to progress, or may lie dormant. Many people who appear to have survived unscathed eventually succumb when the cancer returns years or even decades later, with enhanced malignancy. If we can understand how these micro-tumors remain in equilibrium with their environment, we could work to extend that quiescent phase. After all, a cancer that reappears after 50 years instead of five is not too serious a health risk. The great advantage here is that such improvements could come without requiring us to unravel fully the stupendously complex innards of cancer cells, with their myriad genetic and chemical pathways and survival mechanisms. If Lineweaver and I are right, and a special cassette of ancient genes drives the basic behavior of cancer, then we will have a well-defined target for therapy. The challenge is to find a way to seize control of the cassette’s operating system and tweak it to do our bidding, by reducing the cancer cells’ wanderlust or keeping the micro-tumors stable.

 

Cancer touches all of us. Public health programmers, such as the campaign against smoking, have had a big impact. And a handful of cancers are, in effect, curable. But headway against this scourge has stalled, and requires some radical new thinking, including concepts that cross subject boundaries and emphasize control over cure. The NCI’s bold initiative of inviting perspectives from physical science needs to become an integral part of the next phase of cancer research.

 

Paul Davies is founder/director of the Beyond Center for Fundamental Concepts in Science at Arizona State University. For more details, see http://cancer-insights.asu.edu/

 


Paul Davies address: Breast Cancer Deadline 2020

 


Paul Davies: New Scientist, “Cancer from a physicist’s perspective: a new theory of cancer“

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