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Daniel Weber M health Sci.

 

Daniel Weber began his study of Oriental Medicine in 1969 in Boston. He studied with J. R. Worsley and J. D. van Buren in the UK from 1974 before receiving his B.Ac. Daniel went to Japan in 1976 and studied with Dr. Masahiro Oki and Dr. Okada. He has been in practice in Sydney Australia since 1977 and created the first English language data base for Chinese herbal medicine in 1992. This data base was awarded 'Innovations in Australian Design' and put on exhibit in the Powerhouse Museum.

Daniel has studied in China from 1988, visiting more than a dozen times with numerous awards and two honorary Ph.Ds as well as being an advisor to Hangzhou TCM Institute in Hangzhou. Daniel has a Master of Health Science (Aust) and is completing his research Doctorate. Daniel is not just an academic but a committed clinician, and continues a clinic as well as his ongoing studies. His research into complimentary cancer treatments and his seminars to practitioners in Australia, South Africa and the US have attracted positive comment from leaders in the field. He is committed to creating a dialogue between all types of health care professionals.

Cancer Cells don't grow up

 

Article from nature.com Published online: 21 September 2007; | doi:10.1038/news070917-11

It's not easy making a human. Getting from a fertilized egg to a full-grown adult involves a near-miracle of orchestration, with replicating cells acquiring specialized functions in just the right places at the right times. So you'd think that, having done the job once, our bodies would replace cells when required by the simplest means possible.

Oddly, they don't. Our tissues don't renew themselves by mere copying, with old skin cells dividing into new skin cells and so forth. Instead, they keep repeating the laborious process of starting each cell from scratch. Now scientists think they know why: it could be nature's way of making sure that we don't evolve as we grow older

Evolution is usually thought of as something that happens to whole organisms. But there's no fundamental reason why, for multicelled organisms, it shouldn't happen within a single organism too.

In a colony of single-celled bacteria, researchers can watch evolution in action. As the cells divide, mutants appear; and under stress, there is a selective pressure that favours some mutants over others, spreading advantageous genetic changes through the population.

In principle, precisely the same thing could occur throughout our bodies. Our cells are constantly being replaced in vast numbers: the human body typically contains about a hundred trillion cells, and many billions are shed and replaced every day.

If this happened simply by replication of the various specialized cells in each tissue, our tissues would evolve: mutations would arise, and some would spread. In particular, mutant cells that don't do their specialized job so well tend to replicate more quickly than non-mutants, and so gain a competitive advantage, freeloading off the others. In such a case, our wonderfully wrought bodies could grind to a halt.

Avoiding fate

While working at the Santa Fe Institute in New Mexico , evolutionary biologist John Pepper of the University of Arizona in Tucson and his co-workers came up with a theory for how multicelled organisms avoid this fate. They say it explains why the epithelial tissue cells that line all parts of the body take such an apparently long-winded route to replication, rather than just copying themselves in their mature form.

To renew themselves, epithelial tissues retain a population of undifferentiated stem cells, like the unformed cells present in embryos, that have the ability to grow into different types of cells. When replacements are needed, some of these stem cells divide to make transient amplifying cells (TACs). The TACs then divide several times, and Pepper and his co-workers think that each division produces cells that are a little more developed into mature tissue cells.

All this costs a lot of metabolic energy, so it is not very efficient. But, the researchers say, it means that the functions of self-replication and proliferation are divided between separate groups of cells. The stem cells replicate, but only a little, and so there's not much chance for mutations to arise or for selective pressure to fix them in place. The proliferating TACS may mutate, but they aren't simply copying themselves, so there isn't any direct competition between the cells to create an evolutionary pressure. As a result, evolution can't get started.

Pepper and his colleagues have used computer modelling to show that this proposed mechanism can suppress evolution in a long-lived, multicelled organism.

Inside job

One case in which this scheme might not operate, they say, is in the immune system. Here evolution is beneficial, as it introduces adaptations that fight previously encountered invaders.

 

One drawback of this, however, is that it would be expected to make the immune system more prone to cancers. And that seems to be so: leukaemia and lymphoma are cancers associated with the immune system, and they seem to be more common in younger people than many other cancers, suggesting that the failure to suppress evolution allows its problems to show up rather quickly.

 

The researchers think that their hypothesis could provide new insights into cancers more generally. Whereas conventional wisdom has it that cancer is caused by some genetic mutation that leads cells to proliferate uncontrollably, this new picture implies that the problem would lie with TAC mutations that interfere with differentiation — so that a TAC cell ends up just copying itself instead of producing cells on the next rung up on the way to mature tissue cells.

 

Carlo Maley, Pepper's colleague at the Wistar Institute, a biomedical research centre in Philadelphia , Pennsylvania , says that if their picture is right, incipient cancer formation might be detected very early by looking for biomolecules in body fluids that signal disruption of cell differentiation, even before there are any physical signs of tumour growth.

References

Pepper, J. W., et al. PLoS Comput. Biol. (in the press).