5 ms·

Two things come to mind immediately: 1. Cancer cells are human cells and behave very similar to human cells compared to foreign bacteria or viruses which have

Two things come to mind immediately: 1. Cancer cells are human cells and behave very similar to human cells compared to foreign bacteria or viruses which have a vastly different metabolism. 2. Cancer is not a single disease but a gazillion different mutations which may have vastly different characteristics. Point 1 most of the time prevents cures such as "kill the human cells" from working effectively without killing the patient, too. Successufull cancer cells look so "human" that even the immune system doesn't see the difference. Point 2 means that the "cure for cancer" may be found for some kinds of cancer but there are thousands more. If we cure all cancers known today we will find new ones when the patients are just a few years older. Remember that the death rate increases exponentially with age and so will diseases like cancer.

agumonkey 11y ago
Recent articles about tumor growth heterogeneity : http://www.nature.com/nature/journal/v525/n7568/full/nature14971.html http://www.nature.com/nature/journal/v525/n7568/full/nature1... Videos below are pretty telling.
mehrzad 11y ago
Do you study biochemistry or medicine? Because it would seem that your first point is completely true but technically an oversimplification when it comes to treatment of common cancers. https://en.wikipedia.org/wiki/Asparaginase#As_a_drug https://en.wikipedia.org/wiki/Asparaginase#As_a_drug https://en.wikipedia.org/wiki/Bcr-Abl_tyrosine-kinase_inhibitor https://en.wikipedia.org/wiki/Bcr-Abl_tyrosine-kinase_inhibi...
- suchire 11y ago
  Those are classic success stories mainly because they were the low-hanging fruit for targeted cancer treatment. For blood-cell cancers like leukemia and lymphoma, treatment has come a long way due to advances like the ones you mentioned. For "solid" tumor cancers like breast, pancreatic, prostate, and skin cancer, we're still struggling to make a dent in the death rate.
  - frozenport 11y ago
    Lets distinguish between diagnosis and treatment. Many cancers can be identified by the over-expression of genes or other genetic material. This knowledge is immediately useful to clinical staff. Although its hard to use this information to target specific cells, it hints at mechanisms that are of interest to academic research.
  - bsder 11y ago
    > For "solid" tumor cancers like breast, pancreatic, prostate, and skin cancer, we're still struggling to make a dent in the death rate. Actually, we are not "struggling" on breast cancer. The death rate comes down a reasonable percentage each year. It's just that a small percentage compounds slower and slower once you take out the low hanging fruit. As you point out, the problem is that cancer isn't just one disease with one mechanism. Even "breast" cancer isn't just one disease with one mechanism. So, it's not terribly profitable to go after say "cancer X with mutations P, D, and Q". This really needs government funding. We'd have been far better off with a governmental "War on Cancer" than on any of the other "War on X" that they've done.
    - danieltillett 11y ago
      >So, it's not terribly profitable to go after say "cancer X with mutations P, D, and Q". This really needs government funding. This is one of the key problems. The effective size of most true cancers types is so small that pharmaceutical companies can’t make a profit developing a drug that targets these cancers. Imagine you identify a new drug that 100% cures people with a cancer that has three specific mutations. Now lets assume that out of the millions of people who get cancer each year only 500 have this particular combinations of mutations. This drug will cost the same as any other drug to develop (lets assume $1 billion), but you can only sell it to 500 people per year. Even if you set the price at $100,000 per person you don’t come close to earning enough money to pay back the development costs. Add in the fact that very few drugs make it through the whole development process you can see why we have a problem.
      - astazangasta 11y ago
hhjj 11y ago
Can't we just kill half the cells periodically until there is no more cancerous cells ?
- carterehsmith 11y ago
  We can, but that kills the patient.
  - ubernostrum 11y ago
    One of the approaches used in chemotherapy is drugs which disrupt cell division or associated processes. Which means the cells dividing most frequently (i.e., cancerous cells) are the ones hardest hit by the drug. Though this does affect other cell types which divide frequently, which is why chemotherapy patients lose their hair (hair follicles need rapid cell division) have digestive problems (digestive cells divide rapidly) and can suffer immune-related issues (bone marrow divides rapidly).
- ubernostrum 11y ago
  This is not far off from what much traditional chemotherapy actually does. The approach is to literally poison yourself, and hope that as a whole you can take more of it than the cancerous cells can.
tsotha 11y ago
3. Cancer cells can be hard to get to with drug therapy. Even if we have a drug that kills the cell in question we can't always get therapeutic concentrations into the core of solid tumors, and we can't get many drugs past the blood brain barrier. 4. Cancer cells can be highly unstable, genetically, depending on what part of the DNA got mangled. Unstable cells that mutate rapidly follow the same Darwinian logic you see in microbes. A single tumor can contain thousands of different mutations of the original cell type, and if your therapy kills 99% of them the 1% that come roaring back will be highly resistant to whatever strategy you used the first time around.

agumonkey 11y ago

Recent articles about tumor growth heterogeneity : http://www.nature.com/nature/journal/v525/n7568/full/nature14971.html http://www.nature.com/nature/journal/v525/n7568/full/nature1... Videos below are pretty telling.

mehrzad 11y ago

Do you study biochemistry or medicine? Because it would seem that your first point is completely true but technically an oversimplification when it comes to treatment of common cancers. https://en.wikipedia.org/wiki/Asparaginase#As_a_drug https://en.wikipedia.org/wiki/Asparaginase#As_a_drug https://en.wikipedia.org/wiki/Bcr-Abl_tyrosine-kinase_inhibitor https://en.wikipedia.org/wiki/Bcr-Abl_tyrosine-kinase_inhibi...

suchire 11y ago
Those are classic success stories mainly because they were the low-hanging fruit for targeted cancer treatment. For blood-cell cancers like leukemia and lymphoma, treatment has come a long way due to advances like the ones you mentioned. For "solid" tumor cancers like breast, pancreatic, prostate, and skin cancer, we're still struggling to make a dent in the death rate.
- frozenport 11y ago
  Lets distinguish between diagnosis and treatment. Many cancers can be identified by the over-expression of genes or other genetic material. This knowledge is immediately useful to clinical staff. Although its hard to use this information to target specific cells, it hints at mechanisms that are of interest to academic research.
- bsder 11y ago
  > For "solid" tumor cancers like breast, pancreatic, prostate, and skin cancer, we're still struggling to make a dent in the death rate. Actually, we are not "struggling" on breast cancer. The death rate comes down a reasonable percentage each year. It's just that a small percentage compounds slower and slower once you take out the low hanging fruit. As you point out, the problem is that cancer isn't just one disease with one mechanism. Even "breast" cancer isn't just one disease with one mechanism. So, it's not terribly profitable to go after say "cancer X with mutations P, D, and Q". This really needs government funding. We'd have been far better off with a governmental "War on Cancer" than on any of the other "War on X" that they've done.
  - danieltillett 11y ago
    >So, it's not terribly profitable to go after say "cancer X with mutations P, D, and Q". This really needs government funding. This is one of the key problems. The effective size of most true cancers types is so small that pharmaceutical companies can’t make a profit developing a drug that targets these cancers. Imagine you identify a new drug that 100% cures people with a cancer that has three specific mutations. Now lets assume that out of the millions of people who get cancer each year only 500 have this particular combinations of mutations. This drug will cost the same as any other drug to develop (lets assume $1 billion), but you can only sell it to 500 people per year. Even if you set the price at $100,000 per person you don’t come close to earning enough money to pay back the development costs. Add in the fact that very few drugs make it through the whole development process you can see why we have a problem.
    - astazangasta 11y ago

hhjj 11y ago

Can't we just kill half the cells periodically until there is no more cancerous cells ?

carterehsmith 11y ago
We can, but that kills the patient.
- ubernostrum 11y ago
  One of the approaches used in chemotherapy is drugs which disrupt cell division or associated processes. Which means the cells dividing most frequently (i.e., cancerous cells) are the ones hardest hit by the drug. Though this does affect other cell types which divide frequently, which is why chemotherapy patients lose their hair (hair follicles need rapid cell division) have digestive problems (digestive cells divide rapidly) and can suffer immune-related issues (bone marrow divides rapidly).
ubernostrum 11y ago
This is not far off from what much traditional chemotherapy actually does. The approach is to literally poison yourself, and hope that as a whole you can take more of it than the cancerous cells can.

tsotha 11y ago

3. Cancer cells can be hard to get to with drug therapy. Even if we have a drug that kills the cell in question we can't always get therapeutic concentrations into the core of solid tumors, and we can't get many drugs past the blood brain barrier. 4. Cancer cells can be highly unstable, genetically, depending on what part of the DNA got mangled. Unstable cells that mutate rapidly follow the same Darwinian logic you see in microbes. A single tumor can contain thousands of different mutations of the original cell type, and if your therapy kills 99% of them the 1% that come roaring back will be highly resistant to whatever strategy you used the first time around.