Musings: a question about cancer

OK. BTW, I am sorry, I am probably going to butcher some of the terminology due to being completely ignorant on the subject. So here is the way I undertand cancer:

– random mutations in cells lead to a considerate increase in cell longevity and/or high growth rate
– since these are random mutations, every instance of cancer is unique

So, if cancer is indeed found, it is necessary to identify the mutated cells and destroy them/mark them for destruction by antibodies or destroy the entire region (chemo, amputation, etc.)

And so the question: how are cells recognized by the antibodies?

Given a cell, is it possible to create its model and identify the culprit elements in the DNA? What is the temporal and computational cost of the procedure?

What are the main methods for destruction of cells (artificial antibodies, marking cells, nanotech robots)?

Once the mutation is isolated, do present methods allow for cleansing of the system?

Basically, it seems like a fairly simple-to-understand problem. What are the bottlenecks?

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One response to “Musings: a question about cancer

  1. Anonymous

    Ok. Interesting format, but ok.

    So I’m going to try to answer your questions somewhat chronologically for simplicity.

    Yes, it’s thought that mutations giving rise to cancer occur randomly; however mutations giving rise to cancer must occur in specific genes. These cancer related genes(oncogenes) are typically involved in cell cycle control and “programmed” cell death(apoptosis). These mutations allow the cancerous cell to bypass the normal control mechanisms that prevent the given cell from dividing uncontrollably. So, although the exact location of mutations in a given cancerous cell can be unique, typically the mutated set of genes which are involved are the same–of course different kinds of cancers typically involve different sets of mutated genes.

    The method of using antibodies to promote the destruction of tumors works because dividing cells, ie. cancerous cells, display higher levels of certain molecules on their cell surface than their non-dividing counterparts–note that these molecules are natural mammilian cell molecules. Since most cells in the mammilian body are not actively dividing, using these molecules as a target for mediating specific cell death is relatively specific for cancerous cells.

    Regarding the model question, I’m not quite sure what your exactly asking. However, let me say that if you can identify a given cancerous cell, then isolate it, and then extract DNA from it, there are test, PCR for instance, that allow for the sequencing of oncogenic genes and identify whether they are mutated in the given cancerous cell. This identification test, once the cancerous cell is obtained, is relatively inexpensive.

    Monoclonal antibodies are one of the leading biotechnologies being developed against cancers in general, but there are several other developing drugs with anti-angiogenic drugs and gene therapies using viral vectors being some of the most promising in the near future.

    So, as you suggest, cancers are at this time fairly simple to understand in one sense. However the critical problems are in trying to battle cancers that have spread and are no longer localized in one location and which may migrate to “hard- to-reach” places. Anyway, that’s all I have for the moment. Let me know if you have any follow up questions. Later.

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