This has been covered in a few places like the BBC and ScienceDaily. It seems that some researchers at Queen Mary College in London have recently come with a non animal 3D human breast cancer model.
This is interesting at more than one level. Their research was funded by a research charity (Dr Hadwen Trust) that supports the development of methods that avoid animal experiments. Working with rats is not that satisfactory for ethical reasons and also because there are many cases in which the results of rat experiments cannot be extrapolated to humans (seems we are not so similar in some respects after all). It is also much more realistic than just taking some human cancer cells and studying them on a petri dish.
Being capable of performing experiments using realistic 3D models quickly and efficiently is one of the holy grails of theoreticians since it would make experimental validation of our models much easier (confusingly enough what theoreticians call model, eg, equations or computer rules, is not what experimentalists understand as a model, eg. rat, arabidopsis or drosophila). This validation is quite complicated as I have already mentioned in another post. Making this validation easier and more convenient will go a long way in terms of making our work more reliable and quantitative.
Studying cancer as an evolutionary disease. News and reviews about research on cancer and evolution.
Showing posts with label Press. Show all posts
Showing posts with label Press. Show all posts
Wednesday, May 16, 2007
Monday, February 12, 2007
Cancer and biofuels
I have recently commented how (in my particular view, especially at the theoretical level) research in some area can be used in a different one but I guess I did not expect this: Cancer research may help biofuels.
It seems that, inspired by research done at the Fred Hutchinson Cancer Research Center in Seattle, a company called Targeted Growth is doing to corn the opposite of what oncologists do to human cancer cells taking advantage of the fact that some pathways in these two different cells are similar. The idea is to promote plant growth by overriding the genetic clock that tells the cell when to stop growing. The advantage is that plants thus modified are not transgenic (whith the load that this label carries to many consumers) and that it can lower the price of growing them as biofuels and thus promoting them as a good value alternative to oil.
It seems that, inspired by research done at the Fred Hutchinson Cancer Research Center in Seattle, a company called Targeted Growth is doing to corn the opposite of what oncologists do to human cancer cells taking advantage of the fact that some pathways in these two different cells are similar. The idea is to promote plant growth by overriding the genetic clock that tells the cell when to stop growing. The advantage is that plants thus modified are not transgenic (whith the load that this label carries to many consumers) and that it can lower the price of growing them as biofuels and thus promoting them as a good value alternative to oil.
Thursday, October 19, 2006
Darwin online

Heard it on the radio this morning while listening to the BBC: the University of Cambridge has digitised the text and images of thousands of pages from the publications of Charles Darwin. The website can be found here: http://darwin-online.org.uk/.
Included in the collection are works on other members of the Darwin family (such as the almost-as-famous-as-his-grandson Erasmus Darwin) as well as mp3 audio books for those who would like something more intellectual to entertain their daily jog or gym workout.
Wednesday, October 18, 2006
Evolution and cancer news
Every morning I check a couple of sites in order to get an overview of what is going on in the world. Today I found a couple of curious things:
On the more serious (and cancer related) front, A group of researchers at the University of Missouri-Columbia have found a way to find out the spread of skin cancer cells through the blood. The technique relies on the fact that the vibrations produced by a laser into a melanoma cell is different from that of other cells like red blood cells and plasma.
More information can be obtained here (for those with a subscription to the journal of optics letters).
A different kind of research has been noticed by the bigger media (BBC, Telegraph) and it seems to illustrate how not to use the theory of evolution. Researchers at the Darwin centre at the London School of Economics have seen the future and came back to tell us: Mankind will split into two separate species: the clever and beautiful and the dim-witted goblin-like. I have already heard people labelling these groups as the Macs and the PCs.
On the more serious (and cancer related) front, A group of researchers at the University of Missouri-Columbia have found a way to find out the spread of skin cancer cells through the blood. The technique relies on the fact that the vibrations produced by a laser into a melanoma cell is different from that of other cells like red blood cells and plasma.
More information can be obtained here (for those with a subscription to the journal of optics letters).
A different kind of research has been noticed by the bigger media (BBC, Telegraph) and it seems to illustrate how not to use the theory of evolution. Researchers at the Darwin centre at the London School of Economics have seen the future and came back to tell us: Mankind will split into two separate species: the clever and beautiful and the dim-witted goblin-like. I have already heard people labelling these groups as the Macs and the PCs.
Friday, September 08, 2006
Genes and cancer
I start the week with a post about something really exciting that I read in Science. Unfortunately my institution does not have access to articles in Science published online before they have been printed on paper so I had to be satisfied for the time being with the reports pusblished by conventional media like the Washington Post.
It seems that researchers have screened for and found 189 genes that are altered in colon and breast cancers. Although we are talking about only two types of cancer, breast and colon cancer are two of the most diagnosed cancers in the western hemisphere. It is remarkable that both types of cancer share very few cancer-related genes and that most of the genes discovered to have a role in these cancers have not been known to be so before.
It seems that researchers have screened for and found 189 genes that are altered in colon and breast cancers. Although we are talking about only two types of cancer, breast and colon cancer are two of the most diagnosed cancers in the western hemisphere. It is remarkable that both types of cancer share very few cancer-related genes and that most of the genes discovered to have a role in these cancers have not been known to be so before.
Tumour supressor gene and aging
Read at the NYT: Researchers at the universities of North Carolina, Michigan and Harvard have found that p16 gradually inhibits the proliferation capabilities of stem cells when they reach certain age. The mechanism is useful to prevent the proliferation of cells that, due to their age, have a significantly increased probability of creating tumours.
The paper reporting the research will be published in Nature. One interesting comment by one of the authors is that in his opinion aging is not random but an anticancer mechanism. I find this observation plausible but having an interest in evolution I cannot help thinking that the reason for aging could also be that once an organism has fulfilled its replication duties, its evolutionary-shaped genetic program does not care much for the long term survival of the individual. In other words, evolution does not favour individuals who are good at surviving for ever but that are good at surviving for long enough as to have lots of equally successful offspring.
The paper reporting the research will be published in Nature. One interesting comment by one of the authors is that in his opinion aging is not random but an anticancer mechanism. I find this observation plausible but having an interest in evolution I cannot help thinking that the reason for aging could also be that once an organism has fulfilled its replication duties, its evolutionary-shaped genetic program does not care much for the long term survival of the individual. In other words, evolution does not favour individuals who are good at surviving for ever but that are good at surviving for long enough as to have lots of equally successful offspring.
Thursday, September 07, 2006
Article in high-performance computing magazine
It seems that the research at our group has been noticed by a news site specialised on high performance computing. Oh well, I guess it helps that our group (BIOS) is hosted in a department of high performance computing and that TU Dresden has just hosted a major conference on parallel computing.
For those interested, here is the link: http://www.hoise.com/primeur/06/articles/live/LV-PL-06-06-21.html
For those interested, here is the link: http://www.hoise.com/primeur/06/articles/live/LV-PL-06-06-21.html
Tuesday, September 05, 2006
Scientists find molecule that tricks cancer cells into dying
Taken from The Guardian, 28th August. It's molecular biology but still interesting: Scientists at the University of Illinois at Urbana-Champaign have found the way to restore apoptotic capabilities to tumour cells. It is known that tumour cells tend to have a defective apoptotic mechanism so they do not die when they should (eg. when the DNA repair mechanism is rendered useless).
One way to give back apoptotic capabilities to tumour cells is to provide the cell with a synthetic molecule that reactivates the production of enzymes involved in apoptosis. This is what Paul Hergenrother and fellow researchers seem to have acomplished.
One way to give back apoptotic capabilities to tumour cells is to provide the cell with a synthetic molecule that reactivates the production of enzymes involved in apoptosis. This is what Paul Hergenrother and fellow researchers seem to have acomplished.
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