3 ms·

we won't be able to repair these various cancers until we can do whole cell emulation on the offending cell and contrast/compare it to a healthy equivalent. We

by maeon3 14y ago

we won't be able to repair these various cancers until we can do whole cell emulation on the offending cell and contrast/compare it to a healthy equivalent. We need to understand the mechanics of cells down to the molecular level. Then maybe we can think of a fix. At this stage in society, we know just enough about cancers to do more harm than good in the remaining years of life for the worst forms of cancer.

deleted 14y ago
[deleted]
reasonattlm 14y ago
There are plausible ways to fix cancer, outlined in some detail, but they are so different from the present status quo of cancer research that the community does not pursue them. If it doesn't look a lot like a drug, good luck in obtaining funding for your research. For example, WILT / OncoSENS. Which is to say turn off all mechanisms for telomere lengthening and work around the issues that will cause by replacing stem cell populations: http://www.fightaging.org/archives/2011/10/accumulating-the-groundwork-for-the-ultimate-cure-for-cancer.php http://www.fightaging.org/archives/2011/10/accumulating-the-... http://sens.org/research/introduction-to-sens-research/onco http://sens.org/research/introduction-to-sens-research/onco --- Further, even a robust cure for a specific cancer based on targeted cell killing (by surface chemistry or other markers) doesn't require a complete understanding of the cancer cell - you just need to identify a reliable marker, no need to understand why it's a reliable marker.
crygin 14y ago
We won't* fully correctly emulate a single human cell using deterministic computers in any reasonable timeframe. Even if we had a fully characterized model of a healthy cell, what mechanism would we then use to prevent/eliminate cancers? You still have to get something in there in order to kill the cancerous tissue, whether it's drug-based, mechanical, or radioactive. Claiming that attempting prevention/treatment is futile until a probably-not-in-our-lifetime goal is achieved is defeatist at the highest level. *: Before responding, read the still-highly-relevant: http://www.andersonlocalization.com/pdf/more_is_different.pdf http://www.andersonlocalization.com/pdf/more_is_different.pd...
robbiep 14y ago
Respectfully I disagree. This level of understanding is not necessary. Metaphor: if you are fighting a fire, you don't kneed to understand the full composition of th various fuels and the exact molecular characteristics of the fire at every point, it is enough to know that water will quench it. - I realise that many on HN have an aversion to metaphors so please forgive me and let me continue to elaborate. Wole cell emulation is certainly not necessary, although it would no doubt be interesting to be able to do this at some long-distant point. We don't need to do this because it really does seem as though it is enough to understand the mechanisms of unconstrained cellular proliferation through genetic analysis and surface protein characterisation. This will allow targeted therapies through: 1) Find the genes that are Broken, or allow the final common pathway of cell proliferation to be stuck in the 'on' position, and work out how to block them. -Initially this will be done by designed drugs following the model of glivec but one day soon (i hope) it seems likely that siRNA technologies will make it a lot easier and faster 2) characterise the surface molecules that are different in the cancerous cells and design targeted therapies for them, - as with Trastuzamab for HER2 in receptor positive breast cancers; in the future it seems more likely that we will be able to achieve good efficacy with musing camel antibodies (smaller, high affinity), and by combining the antibodies to substances to deliver targeted radiation, chemotherapy and upregulate the immune response against the cells 3) immune system-boosting therapies which prime the immune system against specific cancers - already shown in proof of concept for various leukemias, see New England Journal of Medicine 'Chimeric Antigen Receptor–Modified T Cells in Chronic Lymphoid Leukemias' , doi://10.1056/NEJMoa1103849 You say we need to understand the mechanics of cells down to a molecular level; in a very many cases we do:'we understand huge areas of cellular biology down to the atomic and molecular level. There are of course many things we don't understand or know yet, but emulation is not necessary for knowing them and it seems quite clear that proliferation pathways are very well characterised indeed, and have been for around 20-25 years; since all cancerous cells must proliferate by this pathway it is simply (I know, it is very difficult, but still, I say again, simply) a matter of determining which pathway is being used and blocking it, whilst also destroying the cell. Not easy work, but I believe something that we are making good progress on. - my 2c given a background in molecular biology and as a final year med student

by maeon3 14y ago

deleted 14y ago

[deleted]

reasonattlm 14y ago

There are plausible ways to fix cancer, outlined in some detail, but they are so different from the present status quo of cancer research that the community does not pursue them. If it doesn't look a lot like a drug, good luck in obtaining funding for your research. For example, WILT / OncoSENS. Which is to say turn off all mechanisms for telomere lengthening and work around the issues that will cause by replacing stem cell populations: http://www.fightaging.org/archives/2011/10/accumulating-the-groundwork-for-the-ultimate-cure-for-cancer.php http://www.fightaging.org/archives/2011/10/accumulating-the-... http://sens.org/research/introduction-to-sens-research/onco http://sens.org/research/introduction-to-sens-research/onco --- Further, even a robust cure for a specific cancer based on targeted cell killing (by surface chemistry or other markers) doesn't require a complete understanding of the cancer cell - you just need to identify a reliable marker, no need to understand why it's a reliable marker.

crygin 14y ago

We won't* fully correctly emulate a single human cell using deterministic computers in any reasonable timeframe. Even if we had a fully characterized model of a healthy cell, what mechanism would we then use to prevent/eliminate cancers? You still have to get something in there in order to kill the cancerous tissue, whether it's drug-based, mechanical, or radioactive. Claiming that attempting prevention/treatment is futile until a probably-not-in-our-lifetime goal is achieved is defeatist at the highest level. *: Before responding, read the still-highly-relevant: http://www.andersonlocalization.com/pdf/more_is_different.pdf http://www.andersonlocalization.com/pdf/more_is_different.pd...

robbiep 14y ago

Respectfully I disagree. This level of understanding is not necessary. Metaphor: if you are fighting a fire, you don't kneed to understand the full composition of th various fuels and the exact molecular characteristics of the fire at every point, it is enough to know that water will quench it. - I realise that many on HN have an aversion to metaphors so please forgive me and let me continue to elaborate. Wole cell emulation is certainly not necessary, although it would no doubt be interesting to be able to do this at some long-distant point. We don't need to do this because it really does seem as though it is enough to understand the mechanisms of unconstrained cellular proliferation through genetic analysis and surface protein characterisation. This will allow targeted therapies through: 1) Find the genes that are Broken, or allow the final common pathway of cell proliferation to be stuck in the 'on' position, and work out how to block them. -Initially this will be done by designed drugs following the model of glivec but one day soon (i hope) it seems likely that siRNA technologies will make it a lot easier and faster 2) characterise the surface molecules that are different in the cancerous cells and design targeted therapies for them, - as with Trastuzamab for HER2 in receptor positive breast cancers; in the future it seems more likely that we will be able to achieve good efficacy with musing camel antibodies (smaller, high affinity), and by combining the antibodies to substances to deliver targeted radiation, chemotherapy and upregulate the immune response against the cells 3) immune system-boosting therapies which prime the immune system against specific cancers - already shown in proof of concept for various leukemias, see New England Journal of Medicine 'Chimeric Antigen Receptor–Modified T Cells in Chronic Lymphoid Leukemias' , doi://10.1056/NEJMoa1103849 You say we need to understand the mechanics of cells down to a molecular level; in a very many cases we do:'we understand huge areas of cellular biology down to the atomic and molecular level. There are of course many things we don't understand or know yet, but emulation is not necessary for knowing them and it seems quite clear that proliferation pathways are very well characterised indeed, and have been for around 20-25 years; since all cancerous cells must proliferate by this pathway it is simply (I know, it is very difficult, but still, I say again, simply) a matter of determining which pathway is being used and blocking it, whilst also destroying the cell. Not easy work, but I believe something that we are making good progress on. - my 2c given a background in molecular biology and as a final year med student