#22) Propose one or more reasons why it makes sense that faster-growing cells (either cancer cells or normal cells) should be harmed more (as compared with cells that grow more slowly) by chemicals that either damage DNA or inhibit formation of mitotic spindles. Honestly, I don't agree that it makes sense, and you don't have to believe it, either. After all, on what basis would we expect that slower-growing cells would be selectively killed by drugs that stimulate faster growth?

The point of this question is for you to make the best case for this widespread assumption, and analyze whatever point of view or sets of assumptions help make it more plausible that faster-growing cells are selectively killed by drugs that disrupt mitosis or DNA synthesis.

#23) Colchicine inhibits mitosis by binding to tubulin, and so do vinblasine, vincristine and taxol.

But colchicine harms normal cells just as much as it harms cancer cells, unlike vinblastine etc. which (for some unknown reason) are a little more harmful to cancer cells than to normal cells. The reason can't be permeability, since colchicine inhibits mitosis just as effectively as the others.

Please invent some possible explanations, and for each explanation, suggest experimental tests.

#24) The maximum amount of any chemotherapy drug (or other treatment, like X-radiation) that can be used on a patient is limited by how much damage the drug does to the patient's normal cells. To what extent does it therefore make sense that if you developed methods for selectively protecting non-cancerous cells from being harmed by chemotherapy, then any such protective methods would magnify the usefulness of all anti-cancer treatments, even to the extent of allowing those drugs to produce cures. Please explain your reasoning in some detail.

#25) Suggest how Burton and Taylor could have discovered more than they did about cytokinesis, using the same combinations of methods.

#26) Make a list of as many imaginable cures for Multiple Sclerosis as you can possibly think of: Be creative.

#27) Invent experiments or other methods by which you could discover what percentage of cancer cells' deaths during chemotherapy are by means of apoptosis, rather than necrosis. On the basis of what you already know, would you expect the percentage of cancer cells dying by apoptosis to be 0%, 25%,50%, 90%, 99%, or 100?

Next, suppose that the true answer turned out to be 50%, then would that be useful in designing better treatments for cancer? What would be the implications for each of the percentages listed above as possibilities (Or for as many of these alternative potentials as you can think of some conclusion to draw)

#28) What if it were discovered that the percentage of cancer cells dying by apoptosis as a result of chemotherapy..

    A) ...was very different for some chemotherapy drugs as compared with other chemotherapy drugs?

    B) ...was very different for some kinds of cancer than for other kinds of cancer (leukemias as compared with carcinoma, for example)?

    C) ...was very different depending on which oncogenes had caused a given cancer?

    D) ...was very different for non-cancerous cells (dying as a side-effect of chemotherapy) as compared with cancer cells dying in the same patient.

#29) Imagine that embryonic cells can (somehow) compare which Hox gene proteins are present in those other cells with which they are in direct contact, as compared with which hox gene proteins are present in their own cytoplasm.

In addition, imagine that cells tolerate having neighbors that contain either the same combination of hox gene proteins as themselves, or at most also contain proteins coded for by hox genes located (on the chromosome) immediately next door to a hox gene that they themselves are transcribing.

But also imagine (and this is the key point) that cells get upset if, for example, cells containing the D1, D2 and D3 protein are right next to cells containing the D10, D11 and D12 proteins (with neither adjacent cells having any D4, D5, D6, D7, D8 or D9 proteins) and that cells respond to this situation by beginning transcription of these (previously not transcribed) intermediate hox genes (i.e. D4, D9 etc.)

Figure out what phenomena this can explain, and how? (including co-linearity itself) and the mirror-image branching that occurs in limb buds, when their tips are cut off and grafted on backwards.

#30) Imagine that tissue culture cells derived from the head and neck contained only the low-numbered hox-gene proteins (1,2,3), but tissue culture cells derived from tail tissue contained all, or nearly all, the different hox gene proteins (1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13). Is this what you would expect?

Or would you expect the opposite? Or no particular pattern?

What if you took a piece of tail tissue, and put it in culture right next to a piece of neck tissue, and then observed that cells developed a continuous set of gradients (e.g. with cells between the neck-derived and tail-derived tissue culture cels then beginning to transcribe the hox genes numbered 4, 5, 6, etc. but NOT 1 or 2).

Alternatively, invent your own experiments with tissue cultures from different parts of the body, and which hox genes they might be expected to transcribe (notice how I am fighting the temptation to say "express" instead of transcribe, translate, or produce a phenotypic effect.). What patterns would you look for, from which you could learn the underlying function of co-linearity?

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