Cancer 3

Continued from yesterday…

In many ways, the similarity between dividing cancer cells and my theoretical cells with their constant ratio of surface area to volume was rather difficult to escape. But I was totally foxed by this particular cancer cell:

Nasty piece of work, isn’t it? I think I may have known someone who had brain cancer like this. He said that he had spiders growing in his head. And this was probably what he meant. Fortunately, those aren’t real legs. This cancer cell doesn’t walk around.

But I couldn’t see how a cell could get to grow like this.

But then I thought that my investigation thus far had led me to believe that normal cells had a narrow growth strip around them which resulted in them developing a narrow notch, and producing perfect replicas of themselves. And that cancer cells (the kind I was looking at yesterday) had wide growth strips around them, which produced long double cones separating the two ends of the growing cell. What if some cells had growth regions dotted all over them where new internal volume and surface area were added in a constant ratio? What would these cells do?

Clearly they wouldn’t divide, because they weren’t growing in the right places that would result in division. These cells could only get bigger and bigger. But they couldn’t just swell up into spheres. But if they stuck out spikes, was it possible for them to maintain a constant ratio of surface area to volume?

And the answer, after I’d written another computer model, was Yes, they could. They could either grow long conical spikes, or they could grow shorter filamentary hairs. What might happen with these spiky ‘spider’ cells is that they’re surrounded by normal cells, and can’t grow and divide in the way most cancer cells do. So they grow in the only way that they are able to grow, which is by extending firstly small bumps, and then spikes and hairs, probably in between adjoining cells, but ultimately straight through them. Cells like this could kill everything around them as they slide daggers through them.

But if these are cells that don’t divide, how come they become very numerous? The chap I knew with brain cancer spoke of spiders in the plural. So maybe these cells can flip between two modes of growth. If they can, they develop a growth strip round their waists, and grow and divide normally. But if they can’t, they push out bumps and spikes and hairs.

Which brings me all the way back to the very first cancer cell that caught my eye.

When I first saw this cell, it was the double cone joining the two halves that caught my attention, because they were so like my dividing theoretical cells. I ignored the fluffy ends, which I didn’t understand. But now I think that the fluffy ends have grown lots of filamentary hairs (HeLa cells do this too). So most likely this cell has been unable to grow and divide, and has pushed out all these filaments instead. In fact, maybe it’s only growing and dividing now because it’s been transferred into a nice, spacious lab flask where it can grow and divide to its heart’s content (if it had a heart).

And that’s about as far as my cancer research has got. It all started with my new theory of cell growth and division, in which cells kept a constant ratio of surface area to volume. Cells like this, if they grew new surface and volume in particular places, and didn’t grow in other places, would grow and effortlessly divide.

But if I have one or two tentative answers, it seems that another 10 questions pop up for every answer I find. The biggest question now is: why do some cells have narrow growth strips, and others – cancer cells – have wide ones, and some seem to have growth regions scattered all over them?

My plan right now is to build some improved computer simulation models of growing cells. I spent much of yesterday and today constructing a 3D icosahedron of node masses and elastic ties. Tomorrow I’m going to multiply the number of triangular faces from 20 to 320. Then I’m going to figure out how to simulate an internal pressure acting from inside on all 320 triangular faces, and then inflate the icosahedron into a sphere. That’ll be my theoretical ‘stem cell’ from which all other cells grow and divide.

I’m hoping that, with judicious expansion of the surface triangles (and maybe the addition of more triangles) while keeping the cell volume and surface area in the same constant ratio (the A/V ratio of the stem cell), I’ll be able to get the stem cell to grow and divide. I’m hoping that I’ll be able to simulate normal cell growth and division, and also dual-cone cancer cell growth and division, and also spiky ‘spider’ cell growth.

And when (and if) I’ve got that working, I’ll investigate how much physical work is required to perform growth and division, and maybe estimate relative cell cycle durations. I’m supposing at the moment that it takes more work to make large cancer cells, and so they reproduce more slowly.

And maybe I’ll put the growing dual-cone cancer cells inside a matrix of cells, and see if they can muscle their way past like I think they can.

And maybe I’ll simulate heat flow too. And osmotic pressure (if I can figure out how that works).

That’s about 20 research programmes for a bunch of mathematicians and physicists and engineers and computer programmers (before the chemists and biologists and geneticists have showed up). So I’m thinking that if I get my cell growth simulation model working, I might make it available for other people to use, and do their own exploring. Maybe as a game. The Build Your Own Cancer Cell game.

Anyway, with luck, if I don’t encounter any major snags, I’ll have something working in a few weeks, and I think they’re going to be visually stunning. And everyone’s going to fall in love with cancer.


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11 Responses to Cancer 3

  1. Pingback: Cancer 2 | Frank Davis

  2. nisakiman says:

    Is it not possible, Frank, that those cells with the filamentary hairs use those hairs and spikes to destroy the cells around them, thus creating the space in which to divide?

    • Frank Davis says:

      Yes, exactly. Cells like this might kill the cells around them, and make space for themselves to divide. There might be an irregular cycle of getting stuck, pushing out spikes, clearing more space, and then dividing a few more times, before getting stuck again.

  3. Zaphod says:

    Your constant SA to V notion is inspired! Plus the notch mechanism to accommodate it.
    I know little about biology, but I do grasp the principle of emergent behaviour from simple rules.
    What makes you think anyone will listen?
    (As if that ever stopped pioneers!)

    • Frank Davis says:

      emergent behaviour from simple rules.

      That’s exactly what it is. The other view – the current orthodoxy – is that cell behaviour is highly complex and ‘beautifully orchestrated’. But where’s the score? And who’s conducting?

      What makes you think anyone will listen?

      They won’t, of course. But that won’t deter me.

  4. sadbutmadlad says:

    “But if I have one or two tentative answers, it seems that another 10 questions pop up for every answer I find.”

    That’s proper science. That’s why there can never be any consensus or settled science.

  5. Rose says:

    Anti-invasive activity of niacin and trigonelline against cancer cells.

    “The effects of niacin, namely, nicotinic acid and nicotinamide, and trigonelline on the proliferation and invasion of cancer cells were studied using a rat ascites hepatoma cell line of AH109A in culture. Niacin and trigonelline inhibited the invasion of hepatoma cells at concentrations of 2.5-40 microM without affecting proliferation. Hepatoma cells previously cultured with a reactive oxygen species (ROS)-generating system showed increased invasive activity. Niacin and trigonelline suppressed this ROS-potentiated invasive capacity through simultaneous treatment of AH109A cells with the ROS-generating system. The present study indicates for the first time the anti-invasive activities of niacin and trigonelline against cancer cells.”

    Role of Nicotinamide in DNA Damage, Mutagenesis, and DNA Repair

    “Studies in adult humans in the 1950s estimated that around 60 mg of tryptophan is hepatically converted to 1 mg of niacin, which is equal to 1 niacin equivalent (NE) [1]. Vitamins B2 (riboflavin) and B6 (pyridoxine) in addition to iron are needed as cofactors for conversion of tryptophan to niacin [1, 3]. The ability to convert tryptophan to niacin varies greatly between individuals and is enhanced by protein and tryptophan deficiency, and it is depressed by excessive dietary leucine [1]. The adult recommended daily intake expressed as niacin equivalent is 16 NE/day for men, 14 NE/day for women and 18 NE/day and 17 NE/day for pregnant and lactating women, respectively [4].

    But apparently none of this is important and you don’t need it anyway.

    Opinion of the Scientific Committee on Food on the Tolerable Upper Intake Level of Nicotinic Acid and Nicotinamide (Niacin)

    “Niacin is the term used to describe two related compounds, nicotinic acid and nicotinamide,both of which have biological activity.
    Niacin is not strictly speaking a vitamin because it is formed from the metabolism of tryptophan, and is not per se essential to the body, providing that there is an adequate supply of the essential amino acid tryptophan”

    Because of the metabolic formation of niacin from ryptophan, the dietary requirements for niacin are complex and related to the dietary content of both tryptophan and niacin (neglecting niacin in cereals, which is largely not bioavailable).

    By convention the total niacin equivalents in the diet is taken as the sum of preformed niacin plus 1/60 of the tryptophan content (Horwitt et al., 1981; SCF, 1993).

    There is no absolute requirement for preformed niacin in the diet, and the 1993 SCF evaluation recommended intakes of niacin equivalents between 9 and 18 mg/day.

    However, the SCF report stated “it is likely there is no requirement for any preformed niacin in the diet under normal conditions and that endogenous synthesis from tryptophan will meet requirements”.
    http: //

    10mg only, thou shalt not self-treat.

  6. Margo says:

    This is brilliant, and a game could really catch on, as the incidence of cancer continues to rise (33% of people a decade ago getting it at some point in their lives, 40% now, according to a Macmillan site I read). The game could be an educational tool or adapted as part of a Visualisation exercise – see – or just something to pass the time while you’re ill.

  7. Barbara says:

    Not sure if this is of any help but my daughter died of breast cancer and I was told that there is two kinds of Breast cancer. The most common one is hormone induced breast cancer, which is in the main if treated early is very treatable and is controlled by tamoxifen etc , The other type of breast cancer, the one my daughter had is called triple negative breast cancer which was in 2009 almost impossible to treat.
    During her illness I brought a book on line called Natural Therapies to conquer cancer by Robert Sopias . In it he explains his ideas and I found them quite interesting they could be helpful to you
    Kind regards Barbara

  8. Junican says:

    Not a long time ago, the Big C was not mentioned in newspapers or conversation. It was a fate worse than death (!!!). Suddenly, a few years ago, cancer became all the rage in the newspapers. I wonder how that hapened?
    But that is not really my point. My point is that, in the same way that the Big C was not mentioned at all, the new Big C is that no one describes precisely why and how cancer kills people. I think that the exact way in which cancer kills is very important. For example, if a person gets a ‘tumour’ (which, ignorant as I am, I take to be a lump of tissue) in their windpipe, then that tumour might block the air passage and thus, in effect, suffocate that person. But a cancer in the liver might work quite differently. If that tumour means that the the ‘useful’ part of the liver shrinks or is destroyed, then toxins will accumulate and the person will, in effect, be poisoned.
    Having said that, it is OK for me to guess what happens, but what in fact actually causes a tumour to kill?

  9. Pingback: A Polyhedral Cell Model | Frank Davis

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