Since the guys at SETI came with the idea of using the CPU time of internet users when they are not using their computers, several other projects draw inspiration from this idea to obtain some sort of highly distributed high performance computing when the funding is not there.
One of these projects is called the world community grid which involves many research centres and universities and tries to tackle several problems that should be of general concern. One of the projects is about Cancer. One of the ways to go about cancer research is by using tissue microarrays in which samples of tumour cells are treated differently and the results of the different treatments can be obtained and compared in a comparatively efficient way. I am writing this from Columbus airport but when I get the chance of getting back to Dresden I should install this client on my Linux workstation. They do have versions for Linux, Mac and Windows.
Of course one thought is that if I know that I will not use the computer in a while the right thing to do (assuming one cares about the world) is to switch the computer off but I guess that those times in which the screen saver kicks in I would be happier thinking that my computer is doing something interesting instead of just displaying pointless and CPU intensive openGL pictures.
Studying cancer as an evolutionary disease. News and reviews about research on cancer and evolution.
Sunday, March 18, 2007
Tuesday, March 13, 2007
Columbus workshop and interactions with life scientists
Being a workshop on mathematical biology one of the issues we all face here is how to work with life scientists and thus one of the panel session yesterdays was precisely about that.
It seems that there are different kind of problems theoreticians might find when dealing with clinicians and experimentalists depending on a number of factors:
It seems that there are different kind of problems theoreticians might find when dealing with clinicians and experimentalists depending on a number of factors:
- What kind of people are they? Are they 'math-skeptic'? do they have affinity towards theory?
- Do you want them to share their expertise with you or do you want to influence the experiments they perform so they can be used in your theoretical model? The latter is significantly more difficult.
- Do you work with biologists or with physicians? There is a real difference between the average PhD and the average MD that does some research on the side when it comes to understand the usefulness of theory.
Friday, March 09, 2007
Workshop in Ohio
I will not probably have much time for posts next week since I plan to attend a workshop in Columbus, Ohio. The workshop is organised by the Mathematical Biosciences Institute of the Ohio State University and is entitled Workshop for young researchers in mathematical biology (remember what the meaning of young researcher is from my previous post from my visit to Barcelona :().
At any rate there will be some interesting people both in the category of keynote speakers and "young" researchers. Some of them doing bio mathematics of cancer so expect a report on that when I come back.
At any rate there will be some interesting people both in the category of keynote speakers and "young" researchers. Some of them doing bio mathematics of cancer so expect a report on that when I come back.
Thursday, March 08, 2007
cancer genes
The information can be found tailored for all types of users. For those who want an easy take here is the BBC version. Nature has a nice overview and the article proper.
Here is my take: a (fairly large) group of researchers mainly at the Sanger, in UK have studied hundreds of genes that are mutated in about 200 types of cancers. The trick here is to find what genes DO drive cancer as opposed to 'just happen to be mutated' in a cancer. At the end of the day your average tumour cell in an advanced stage tumour is likely to contain several mutations and many of them will probably be hitchhikers not necessarily contributing to the overall fitness of the cell. Unfortunately the result of the research is that the number of genes mutated in many cancers is higher than expected and telling apart driving genes from others will be a challenging task. One thing of working with so many types of cancers (200) is that genes that might not play any significant role in one type of cancer might turn to be important in the next.
Here is my take: a (fairly large) group of researchers mainly at the Sanger, in UK have studied hundreds of genes that are mutated in about 200 types of cancers. The trick here is to find what genes DO drive cancer as opposed to 'just happen to be mutated' in a cancer. At the end of the day your average tumour cell in an advanced stage tumour is likely to contain several mutations and many of them will probably be hitchhikers not necessarily contributing to the overall fitness of the cell. Unfortunately the result of the research is that the number of genes mutated in many cancers is higher than expected and telling apart driving genes from others will be a challenging task. One thing of working with so many types of cancers (200) is that genes that might not play any significant role in one type of cancer might turn to be important in the next.
Wednesday, March 07, 2007
Telomeres, cancer and aging
One quite fascinating thing in animal biology is the question of immortality or, to be more precise, the lack of it. While most unicellular organisms can divide for as long as they have the luck to find resources and space to do so, human cells can divide only a limited amount of times (approximately around 50 times, although this does not apply to stem cells that can divide an unlimited amount of times). In principle the limitation in divisions for most human cells is due to a mechanism that has been evolved and is not an intrinsic limitation. The cancer hypothesis is that the limitation makes the appearance of cancer more unlikely. If a cell is limited to just a few divisions, if it acquires a mutation that mutation is unlikely to spread to far.
The reason for this limitation are the telomeres, situated at the end of the chromosomes, that get shorter each time the cell divides. Once these telomores reach a critical size and become to small the cell will enter a state called senescence by which they will not divide again.
This is an interesting link in which they talk about this and how in the next few decades we might know enough about the effects of limited cell replication in human life expectancy, how to increase it (maybe for ever) and how to do that avoiding nasty side effects (like increased probability of dying from cancer). The website in which this is hosted is covering all sorts of news, many of them of dubious scientific interest, but the information in the link looks sound.
On the other hand in a more reliable source (PNAS) there is a nice study on how telomere dysfunction can cause genetic instability. They work on a disease known as Werner syndrome but it is quite useful stuff for cancer research. This Werner syndrome results in people aging prematurely and researchers at the Salk institute have found how extra short telomeres can be the source of the problem.
The reason for this limitation are the telomeres, situated at the end of the chromosomes, that get shorter each time the cell divides. Once these telomores reach a critical size and become to small the cell will enter a state called senescence by which they will not divide again.
This is an interesting link in which they talk about this and how in the next few decades we might know enough about the effects of limited cell replication in human life expectancy, how to increase it (maybe for ever) and how to do that avoiding nasty side effects (like increased probability of dying from cancer). The website in which this is hosted is covering all sorts of news, many of them of dubious scientific interest, but the information in the link looks sound.
On the other hand in a more reliable source (PNAS) there is a nice study on how telomere dysfunction can cause genetic instability. They work on a disease known as Werner syndrome but it is quite useful stuff for cancer research. This Werner syndrome results in people aging prematurely and researchers at the Salk institute have found how extra short telomeres can be the source of the problem.
Monday, March 05, 2007
Bioinformatics and google
First of all, I am not a bioinformatician. I even thought I had an idea of what is the aim of bioinformatics but after a visit to the group of Nuria Lopez Bigas at the Biomedical Research Parc in Barcelona I realised that the scope of what I thought the field is about was too narrow (they do some nice machine learning and statistical work on disease related genes).
I have seen this video on Google video (only one of these sites that allows the user to download the video for offline use) some time this weekend. It is just a talk by David Vise, the author of a book about Google, to staff at Google Inc. Google is one company that fascinates (and in a sense, worries) me tremendously. As a side note, this blog is posted in one of their servers.
The thing is that at the end of the talk, David mentions the interests of one of Google founders (I think it is Larry Page) on biology. Then I thought (and I am sure that I will be the last of a long list of people) that, wow, that is really a good match: google and bioinformatics. Biology until know was mostly a science in which practitioners collected facts. There is loads of data and little idea of how to make sense of it, asides from evolution and a few other very general ideas. One of the aims of google is precisely to find patterns in the zitabytes of information stored in their servers. I have the feeling that we will see more of Google in that field.
I have seen this video on Google video (only one of these sites that allows the user to download the video for offline use) some time this weekend. It is just a talk by David Vise, the author of a book about Google, to staff at Google Inc. Google is one company that fascinates (and in a sense, worries) me tremendously. As a side note, this blog is posted in one of their servers.
The thing is that at the end of the talk, David mentions the interests of one of Google founders (I think it is Larry Page) on biology. Then I thought (and I am sure that I will be the last of a long list of people) that, wow, that is really a good match: google and bioinformatics. Biology until know was mostly a science in which practitioners collected facts. There is loads of data and little idea of how to make sense of it, asides from evolution and a few other very general ideas. One of the aims of google is precisely to find patterns in the zitabytes of information stored in their servers. I have the feeling that we will see more of Google in that field.
Thursday, March 01, 2007
Old Dawkins video on cooperation
I have found this video on google video. It is an old Richard Dawkins BBC TV programme in which he goes through some topics of which I am quite fond and which I personally think have some yet-to-be-explored relevance to cancer research.
The documentary was produced a few years after Dawkins wrote The selfish gene and not long after Robert Axelrod had written The evolution of cooperation. It takes from Axelrod's research on cooperation (whose own take on how this can be observed in cancer has been mentioned in this blog before) to illustrate how cooperation might evolve in an place in which agents (say humans, bacteria or buffaloes) are selfish. The topics are the usual ones in game theory such as prisoners dilemma (how playing if for an undetermined number of times changes what is the best strategy), tragedy of the commons (if everybody is overusing a resource why shouldn't you, and if few people overuse, why shouldn't you since it will make no difference whatsoever?).
The tragedy of the commons seems to me a suitable game to model global warming (why should your country cut on carbon emissions if nobody else does or why should you if everybody does? this seems to apply to most countries but the likes of U.S. and China whose weight is to big to be considered just another player) or cancer (at the end, tumour cells do kill the host and thus themselves).
The documentary was produced a few years after Dawkins wrote The selfish gene and not long after Robert Axelrod had written The evolution of cooperation. It takes from Axelrod's research on cooperation (whose own take on how this can be observed in cancer has been mentioned in this blog before) to illustrate how cooperation might evolve in an place in which agents (say humans, bacteria or buffaloes) are selfish. The topics are the usual ones in game theory such as prisoners dilemma (how playing if for an undetermined number of times changes what is the best strategy), tragedy of the commons (if everybody is overusing a resource why shouldn't you, and if few people overuse, why shouldn't you since it will make no difference whatsoever?).
The tragedy of the commons seems to me a suitable game to model global warming (why should your country cut on carbon emissions if nobody else does or why should you if everybody does? this seems to apply to most countries but the likes of U.S. and China whose weight is to big to be considered just another player) or cancer (at the end, tumour cells do kill the host and thus themselves).
Friday, February 23, 2007
In Barcelona
I have finished my stay in Lyon and arrived to Barcelona to attend a round table for young researchers organised by the Universitat Autonoma de Barcelona. Interestingly enough the definition of young researcher seemed to include any researcher after the PhD but without a stable contract (that is, postdocs, non tenured group leaders and people in teaching positions).
I was a rather interesting discussion that dealt with things that I imagine are common worries for young researchers across Europe and elsewhere. Mainly the difficulty of living on short term research contracts, (for those of us postdocing somewhere else) the strain of keeping up with friends, relatives and former colleagues while living abroad, the gap between our real age (late twenties or early thirties) and how our status is perceived by the rest of the population (not like assistant professors or people with "real" jobs and more like students with a fancy "Dr." in front). Other issues that I found very relevant not only for young researchers are the link between research and teaching (in Spain, like many other countries, university lecturers are paid to teach but their progress on the career ladder depends exclusively on publications) and linked to that if the main duty of academic staff is to perform research or to teach (there seemed to be some consensus that universities should be free to chose wether to have a research profile or a teaching profile).
I was a rather interesting discussion that dealt with things that I imagine are common worries for young researchers across Europe and elsewhere. Mainly the difficulty of living on short term research contracts, (for those of us postdocing somewhere else) the strain of keeping up with friends, relatives and former colleagues while living abroad, the gap between our real age (late twenties or early thirties) and how our status is perceived by the rest of the population (not like assistant professors or people with "real" jobs and more like students with a fancy "Dr." in front). Other issues that I found very relevant not only for young researchers are the link between research and teaching (in Spain, like many other countries, university lecturers are paid to teach but their progress on the career ladder depends exclusively on publications) and linked to that if the main duty of academic staff is to perform research or to teach (there seemed to be some consensus that universities should be free to chose wether to have a research profile or a teaching profile).
Tuesday, February 13, 2007
Lenski et al: Balancing robustness and evolvability
R. Lensi, J. Barrick and C. Ofria. Balancing robustness and evolvability. PLoS Biology, Vol. 4, 12, pp 2190-2193
This paper has not much to do with cancer but I have been interested in evolvability issues for a while so I decided to take a look at it. Tumour evolution has many but not all the features of the evolution involving longer time scales but its evolvability is not a thoroughly investigated topic. That is a shame because it seems that, given enough time, one would expect that tumour cells will not evolve only towards phenotypes that can take better advantage of the environment but also to genotypes that allow evolution to adapt better to that changing environment.
This paper does not explore this but something also interesting: that robustness and evolvability might be desirable but incompatible aims. Robustness can be seen as he ability to counteract change while evolvability represents the capability to adapt. In general it is true that species must strike some sort of compromise between these two abilities since organisms need the robustness provided, for instance, by the DNA repair mechanism but species need mutations that actually allow these organisms to better adapt to the environment. This is not always true and there are cases in which robustness and evolvability can go happily hand by hand. One such case is genomic redundancy. Up to a point, genomic redundancy improves robustness since functionality is kept in more than one location making it less vulnerable but also it helps evolvability since it allows duplicated genes to evolve different functions.
The general rule though is that organisms cannot be entirely robust to change in the form of genetic mutations since such an organism would freeze from an evolutionary point of view and thus subject to become extinct when a fitter rival comes around. I guess that that is a good explanation to cancer, a perfect reproduction mechanism would have not led from simple organisms to humans.
This paper has not much to do with cancer but I have been interested in evolvability issues for a while so I decided to take a look at it. Tumour evolution has many but not all the features of the evolution involving longer time scales but its evolvability is not a thoroughly investigated topic. That is a shame because it seems that, given enough time, one would expect that tumour cells will not evolve only towards phenotypes that can take better advantage of the environment but also to genotypes that allow evolution to adapt better to that changing environment.
This paper does not explore this but something also interesting: that robustness and evolvability might be desirable but incompatible aims. Robustness can be seen as he ability to counteract change while evolvability represents the capability to adapt. In general it is true that species must strike some sort of compromise between these two abilities since organisms need the robustness provided, for instance, by the DNA repair mechanism but species need mutations that actually allow these organisms to better adapt to the environment. This is not always true and there are cases in which robustness and evolvability can go happily hand by hand. One such case is genomic redundancy. Up to a point, genomic redundancy improves robustness since functionality is kept in more than one location making it less vulnerable but also it helps evolvability since it allows duplicated genes to evolve different functions.
The general rule though is that organisms cannot be entirely robust to change in the form of genetic mutations since such an organism would freeze from an evolutionary point of view and thus subject to become extinct when a fitter rival comes around. I guess that that is a good explanation to cancer, a perfect reproduction mechanism would have not led from simple organisms to humans.
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.
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