Cancer 1

I’ve long believed that the war on smoking will only ever end when it’s finally and conclusively proved that smoking doesn’t cause lung cancer, and that something else does. The police are looking for a serial killer, and they’ve arrested Mr Tobacco, because Mr Tobacco was present at 90% of the crime scenes, right inside the lungs where the dirty deed was done, and Mr Tobacco is a man of known bad character, who spends his days with Mr Booze and Mr Curry and Mr Pizza and other ne’er-do-wells of the Fast Food franchise. It’s going to need a Lieutenant Columbo to show that Mr Tobacco couldn’t have done it, and that the real killer was… somebody else. And he has to do it soon, because Mr Tobacco is now facing the electric chair.

Columbo, in this case, is going to have to be a cancer researcher. But who’s researching lung cancer these days? Hardly anybody. And why aren’t they researching lung cancer? Well, because everybody knows that Mr Tobacco was the culprit, and the case is closed.

So who’s going to find out what really causes lung cancer? Nobody, it seems. Mr Tobacco is just going to have to fry. And so are all the smokers.

But what if a few amateur investigators decide to find out for themselves? Why wait for highly-paid researchers in universities? Smokers have all the skills of such researchers. They’re biologists and microbiologists and geneticists and chemists and physicists and mathematicians and engineers and artists and historians. They can do anything. What’s to stop a bunch of people with these diverse skills from setting up their own research programme? Particularly when the professionals seem to be completely stuck, and getting nowhere fast.

Over the next few days I’d like to outline a research programme. I’m not going to ask for volunteers. I’m just going to try to explain why I’ve become utterly fascinated by cancer over the past few months, and why I can see the hazy outlines of a research project emerging.

It all started over 20 years ago, when I got interested in living things, and doing what I always do whenever I get interested in something – I started building computer simulation models. These were simple models of exponentially growing populations of theoretical critters whose numbers grew 1, 2, 4, 8, 16, 32 and so on. Sometimes the critters were plants, and sometimes grazers, and sometimes predators. And sometimes they were just tiny cells.

And I had a puzzle back then I couldn’t solve. It was the puzzle of how one cell grows and divides to become two cells. I wasn’t asking how two biological cells divided in two, but how a bag of water grew and divided in two. It wasn’t a biological puzzle: it was a geometrical puzzle. Because I thought of cells as being little plastic bags full of water. The problem was that there had to be just enough water and just enough plastic sheet to make two cells (and no more), and the growing cell also had to somehow divide in two.

And I couldn’t figure it out. But it didn’t really matter, because it didn’t really affect my models. So I’d pick up the problem every now and then, and have another shot at it, and get nowhere again.

Until last March, that is, when I picked up the ancient and seemingly insoluble problem once again, and had a new idea. I noticed that when a cell has grown from one sphere or cube to become two spheres or cubes of exactly the same size as the parent cell, the two daughter cells have the exactly twice the surface area and twice the volume as the parent cell. And I thought: what if a cell maintains the same ratio of surface area to volume throughout the whole cell cycle? Could that be done? Was there a geometric configuration whereby the ratio of surface area to volume stayed constant?

I remembered that real biological cells form a notch when they grow and divide, and so I started fooling around with pencil drawings of a growing cubical cell which formed a notch in it, working out the surface area and volume. Pretty soon, I’d written yet another computer programme to explore it numerically.

And it rapidly emerged that, yes, it was possible for a cubical cell with a notch in it to grow in such a way that it kept the same ratio of surface area to volume as it grew. What was really astonishing was that, if it did that, it automatically divided in two.

I had solved my insoluble puzzle! Delighted, I posted my discovery on my blog on 1 April 2012, All Fools’ day.

A month or two later I adapted a 3D display programme to show the entire sequence of cell growth and division. It’s shown at right. The cell starts off cubical, and I’ve coloured the different surfaces in different colours, so that you can see how the sizes of them change. If you wind the page up and down with a mouse wheel, it gives the appearance of an animation.

The important thing about this sequence of images is that they are all of a cell which maintains the exact same ratio of surface area to volume from start to finish.

At the end of the growth cycle, the two halves of the cell are connected only by the vertex of a pyramid: they are connected by nothing at all. The cells have divided to become two cells.

And in this particular case, the cell hasn’t divided into two cells exactly the same size as the parent cell, but into ones which are in total 1.76 times the volume of the parent. A new kind of cell has been produced, a bit smaller than the parent.

Further investigation showed that two exact replicas were only ever produced if the width of the notch was kept to zero. If the notch was a bit wider, the daughter cells were smaller than the parent cell. If the notch was wider still, the daughter cells were larger than the parent. In fact, they could be huge. And yet they all had exactly the same ratio of surface area to volume.

So these kinds of cells could grow and divide to form an entire zoo of different cells, some bigger, some smaller, some long and thin, some wide and flat.  Yet while there were some ways that they could grow, and there were lots more ways in which they couldn’t grow. For example, a cube with side length 1 and volume 1 and surface area 6  and A/V ratio 6 couldn’t become a cube with side length 2, because the volume would have become 8 and the surface area would have become 24, and the A/V  ratio 24/8 or 3 – which was not allowed. Cubes couldn’t grow into bigger cubes. Spheres couldn’t grow into bigger spheres.

Now, this was just me wondering how a cubical polythene bag of water could grow to become two cubical bags. But the more I looked at this model of cell growth and division, the more I thought: Never mind bags of water, this must be how real biological cells grow and divide. And as far as I could make out from watching online videos of dividing cells, they usually developed a very narrow notch between their two halves.

All of which was quite interesting in an academic sort of way, until I came across the following photo of dividing cells online one day.

And I looked at these dividing cells and immediately thought: The fluffy ends of these cells are a bit strange, but the middle bits of those cells are just like the pyramidal middle bits of many of my theoretical cells. Like the ones I’ve just shown growing and dividing.

But… these cells were cancer cells.

To be continued tomorrow….

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38 Responses to Cancer 1

  1. timbone says:

    Frank. You know that I am a regular visitor, and occasional contributor to your blog. I am sure you will also realise by now that I have deep respect for your articulate arguments against what has become our enemy, the tobacco control explosion.I do however have a problem with this ‘smoking does not cause lung cancer’ premise. I have, and totally agree with Dr Siepmann’s article ‘Smoking DOES NOT cause lung cancer’, – this however is an argument against the use of the word ’cause’. As I am sure you know, he argues that smoking is one of many possible contributors.

    I believe there was much discussion following the Doll publication in 1953, as the lung cancer epidemic in the first half of the 20th century also cooincided with a sudden rise in diesel as well as cigarette smoking. Whilst it is wrong to ignore other causes, the fact that the majority of lung cancers are in those who do, or have been cigarette smokers cannot be ignored.

    You know that I speak as a person who smokes cigarettes, and enjoys the experience greatly. I am also fully aware of the risk, which includes lung cancer.

    • harleyrider1978 says:

      The one problem doctors are around all the time is viral sickness from patients and I highly doubt Dolls study confounded for that. Is smoking a contributer,sure just as much as breathing in normal air everyday air. The one chemical smokers get more of is BENZO-A-PYRENE. But if you pump your own gas or live by a refinery or some other chemical plant you will no doubt get as much as a smoker or more. Im sure theres plenty of other sources but it still doesnt explain why 94% of life long smokers dont get LC at all…….

      • harleyrider1978 says:

        One other thought on this, it would be pretty apparent that in those who develop LC that something in their immune system went haywire and allowed possibly an environmental chemical to start a cancer to begin or it could be their own genetics caused it to happen. Its really the only explanation there is after we look at everything. And if thats true then a trail can be found in their genetic sequencing to see what happened. There in lies where a study should be conducted mapping 10 or 20 peoples genetic code all the way down and then if they ever get cancer cross examine a new mapped genetic code of that individual to see where a diference occured. Maybe thats to simple but its a place simple to start with.

    • west2 says:

      This, from 2002, is worth a read. It compares Japanese/American smokers. Unfortunately it is let down somewhat, as in some cases the control is younger. It does attempt to explain the ‘Paradox’ of higher smoking rates/Lower LC rates in Japan vs lower smoking rates/ higher LC rates in the US.

      Is there a more recent study perhaps?

    • Pat Nurse says:

      That is my view too Tim. I don’t say smoking is the only factor that COULD cause lung cancer – because too many never smokers who have not been in contact with smokers also get cursed – but we have to accept that it is a factor. My problem is that like Frank says, blaming Mr Tobacco closes the case without looking at the other suspects and that is why the whole war on smokers is just plain wrong – esp when those smokers know the risks, take a calculated risk, and decide based on their own informed knowledge, that they will continue to smoke.

      It is the scams of SHS and THS that we need to attack and expose because based on these concepts, they are moving on to criminalise our grandchildren simply because they can. It’s not, as we know, about health at all but hate campaigning against a group that powerful bigots personally dislike.

  2. harleyrider1978 says:

    Frank I have a feeling they already know what can make cancer happen,viruses and I believe theyve harnessed this viral compound. But I was actually reading about HPV and cervical cancer and they actually have no proof to connect the end points! Yet theyve created a vaccine they say. How do we know theyre vaccine wont cause cancer later in life? Its simple we dont know and neither do they……or do they actually know. Also HPV has been implicated in LC and oral cancers…… may just be in the decades to come that viruses are shown in a genetic chain of events to actually change cell structures and create cancerous lesions. Its anybodys guess right now. But I agree theyve given up trying to prove smoking and a cancer connection. I believe the last hype study they tried was back in 1999 and made the claim but was never replicated by anyone as usual.

    Ive become very very cynical over the last decade with what were normal viruses of the flu that simply lasted a few days or a week and was gone. But todays variety are like mini super viruses striking everyone. Lasting weeks and weeks and like this Adeno 14 virus discovered back in the 1950s and not seen since and it shows up out of nowhere but its symptons can last up to a year or more.

    Now if Pharma isnt creating the bugs or the govmnt labs or the terrorists then it has to be immigration causing it…………

  3. harleyrider1978 says:

    The Surgeon General Lies About Cancer
    Among the few specific conclusions of the 2010 Surgeon General report concerning the mechanisms by which smoking supposedly causes cancer: “7. There is consistent evidence that smoking leads to the presence of promoter methylation of key tumor suppressor genes such as P16 in lung cancer and other smoking-caused cancers.” It claims that “Researchers detected P16 methylation in specimens from 25 of 137 biopsy procedures (18 percent) classified as histologically normal, metaplasia, or mild dysplasia. In contrast, no P16 methylation was found in biopsy specimens obtained from lifetime nonsmokers…. (Belinsky et al. 1998).” (A Report of the Surgeon General: How Tobacco Smoke Causes Disease, Chapter 5 Cancer, p. 304 [pdf p. 84], and p. 292 [pdf p. 72 & 73].)
    Aberrant methylation of p16(INK4a) is an early event in lung cancer and a potential biomarker for early diagnosis. SA Belinsky, KJ Nikula, WA Palmisano, R Michels, G Saccomanno, E Gabrielson, SB Baylin, JG Herman. Proc Natl Acad Sci USA 1998 Sep 29;95(20):11891-11896. This study doesn’t mention never-smokers.

    The Surgeon General report commits flagrant scientific fraud by ignoring the evidence that methylation of P16 is solidly associated with infections by human papillomaviruses, Epstein-Barr virus, hepatitis viruses, and even Helicobacter pylori – all of which are known human carcinogens

    You will notice nowhere in the SG reports does it mention if any of the study subjects were tested for EBV,CMV or HPV nor were histories of bacterial infections mentioned……..It got so bad because the case controls were evenly matched in the findings they went out and got some selected non-smokers post mortem to toss into the study!

  4. harleyrider1978 says:

    But it seems cancer is really a disease of the old,striking when old immune systems breakdown!

    I saw one age study and death the other day about smokers and non on heart disease starting at the age of 50. The study found no real diference in heart disease between smoker sand non but they said smokers tended to die 5 years earlier than non smokers. So I dug thru and found most of the folks with no heart disease at age 50 lived into their 90s meaning 85-88 was the average age of smoker deaths!

  5. harleyrider1978 says:

    sorry Frank Im getting long winded again!

  6. harleyrider1978 says:

    Pfizer caught running global bribery network
    Thursday, August 30, 2012 by: J. D. Heyes

  7. Frank Davis says:

    In these few essays, I’m not looking at what causes cancer. I’m looking at what cancer is.

    Tomorrow I’m going to carry on looking at what it is, because I think that we’ll only ever get anywhere when we understand what it is.

    I have no idea what causes it. And I’m not going to be offering any hypothesis about what causes it over the next couple of days. I’m just going to be looking at cancer, and trying to understand how it works.

  8. Junican says:

    I’ve seen a couple of these videos of cells dividing (probably linked by you!). There seems to be some stretching involved in cell division. So perhaps your construction is a sort of dynamic calculus or fractal necessity. I understand that cells only divide if there is room for them to do so (apart from cancer cells, which is what causes the problem). If there is some sort of fractal, ‘differences’ based growth in cells, it is not difficult to see that this process can only occur if marginal opportunities exist for it to occur.
    There again, I could start speaking English….

    • Frank Davis says:

      I understand that cells only divide if there is room for them to do so (apart from cancer cells, which is what causes the problem).

      That’s exactly how I see it, and which will be the principal springboard for tomorrow’s essay.

  9. Rose says:


    Chaos looms over cigarette ruling

    “Chaos is expected at airports over the weekend as customs officials seize an estimated 400,000 cartons of cigarettes as new regulations kick in.

    Travellers entering Australia from tomorrow will only be allowed to bring in 50 duty free cigarettes each, drastically less than the 250 previously permitted. Only by paying $100 in duty will they be allowed to keep their goods.

    Stand and Deliver!

    • beobrigitte says:

      “This change will cause an unprecedented level of confusion and mayhem in arrivals halls, frustrating and complicating the arrival experience for all international visitors,” TTF chief executive John Lee said. “This reform has been rushed through with little or no concern for the impact on the tourism industry.”

      There is a solution to the problem: avoid Australia and choose another, more friendly, holiday destination.

      • nisakiman says:

        I certainly won’t set foot in the place again. You think UKBA are bad? I’ve never come across such a bunch of arrogant Nazis as I found in Australian Customs and immigration. Tin-pot tyrants to a man. They will absolutely love taking all those fags off people. I bet they’re wetting themselves with excitement at the prospect.

        • Rose says:

          Long queues and passenger anger mark introduction of new Australian duty free tobacco allowances

          “AUSTRALIA. Inbound travellers have faced lengthy queues and product seizures as the country’s sharply reduced tobacco allowances took effect today.

          From today, 1 September, the new limit is 50 cigarettes or 50 grams of tobacco, compared to 250 cigarettes or 250 grams of tobacco formerly.

          The news has major commercial repercussions not only for travel retailers in Australia whose Arrivals business will be hit badly but for any overseas airport (or airline) serving Australia-bound traffic.

          The regulatory change – due to both its severity and short lead time – represents one of the most fundamental changes to airport retail trading conditions in industry history.”

  10. Margo says:

    Yes, well you know what I think. The powers that be know full well what’s responsible for the massive increase in cancer since 1950 (incidence of some cancers up by 100% – see Cancer Prevention Coalition), but they don’t want us to know. They want us to think it’s our own fault if we get it.
    Secrecy, lies, cover-ups, minimalisation of effects – that’s the story of nuclear power and other industrial accidents. They don’t want us to know, and they’re not going to change a thing.
    As to the mechanism of cancer, what it actually is and how it works, not much seems to be known so I reckon your pursuit, Frank, is a very worthy one.
    You could maybe check out the Low Level Radiation Campaign website and Alice Stewart (the scientist whose career Doll was to some extent responsible in suppressing – if he hadn’t succeeded in doing that and getting those Smoking Study commissions back in the 1950s, the world would now think of smoking as a possible secondary, not primary, cause of lung cancer, and that wouldn’t be in the least bit useful to the powers that be).

    • harleyrider1978 says:

      Margo thats a home run…….a secondary cause or no cause at all simply a victim to cover up something else say like defective human immuno systems. Now I sound like a eugenicist!

      • harleyrider1978 says:

        Maybe its always been a Eugenics game,if you cant prove cause on anything and you blame everything calling them carcinogens in the environment. Theres really nothing left to blame except the victim as the cause. That my friends would be saying defective herd members must be removed! If your family history is diseased by xxx% you gone to SOILENT GREEN LAND!

      • Margo says:

        Well, a ‘secondary cause’, maybe, in the sense that it may be the straw that breaks the camel’s back – something else has already damaged the cells and the ‘secondary cause’ prevents them repairing themselves. That’s how I read it, anyway. I don’t think anyone’s suggesting people with damaged immune systems should be shot, are they?

        • harleyrider1978 says:

          Well in 1937 when hitler enacted smoking bans nobody else thought about shooting jews either except the ban enforcers.

          How do you switch tactics overnite to go after the folks who get cancer……..simply run the propaganda machine again…..and make them the cause! The same way they make smokers the cause thru shs/ets!

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  12. garyk30 says:

    “they said smokers tended to die 5 years earlier than non smokers.”

    The smokers probably do die at a younger age.

    ALL people in the lower social/economic classes do and that is where most smokers are found.

    They have worse living and working conditions and less access to preventative and curative health care.

    The upper economic/social classes tend to be mostly non-smokers.

    As for cell division, let’s look inside the cell at the nucleus.

    First the nucleus must divide by stretching into two new nucleuses.
    That leads to a thinning in the middle of both nucleus and then the cell.

    The thinnig continues until the cell membrane comes in contact with itself and then it will part into two new cells.

    Maybe cancer is more of a mutation, for whatever reason, of the cells into a slightly different form of cells.
    That leads to all sorts of crap.

    As for smoking and lung cancer, one side of the coin is that smoking ’causes’ lung cancer because smokers are more apt to get lung cancer.

    But, the other side of the coin is that smoking can not ’cause’ lung cancer because smokers and non-smokers have the precise same chance of not dying from lung cancer.

    The ratio is 1 to 1.002 and when you have to go to 3 decimal places to find a difference, that difference is not significant.

    • Frank Davis says:

      As for cell division, let’s look inside the cell at the nucleus.

      First the nucleus must divide by stretching into two new nucleuses.
      That leads to a thinning in the middle of both nucleus and then the cell.

      The thinnig continues until the cell membrane comes in contact with itself and then it will part into two new cells.

      Why does the stretching of the nucleus lead to thinning in the middle? Shouldn’t stretching of the nucleus lead to stretching in the middle?

      • harleyrider1978 says:

        Gets out electron microscope hands to Frank and walks away………to deep for me.

        But awaits the laymans explanation.

      • garyk30 says:

        “Why does the stretching of the nucleus lead to thinning in the middle? Shouldn’t stretching of the nucleus lead to stretching in the middle?”

        To a point.

        A sheet of rubber when pulled from both ends at the same time will stretch/elongate and then get thinner in the middle.

        The dividing nucleus does not, as such, stretch the cell, it pushes the cell apart from the inside.

        Like the formation of a drop of water that stretches out/elongates, then it thins at the connecting point, and then it comes loose in a more or less circular shape

        .A dividing nucleus would achieve much the same effect by pushing out against the walls of the cell in two opposite directions at the same time.

        • Frank Davis says:

          A sheet of rubber when pulled from both ends…

          What makes you think a cell is like a sheet of rubber?

          Like the formation of a drop of water…

          Water isn’t a bit like rubber. It’s more or less incompressible.

          I think you’re offering some slightly contradictory intuitive arguments. We can all offer any number of intuitive approaches, comparing cells to this or that. Why not a candy floss cell?

  13. Barbara says:

    During my daughters cancer I learned the following from doctors, nurses and researchers
    1 Cancer is the same process where ever it starts which is similar to the process that happens when you cut yourself, the cells grow to fill in the gap then stops when the job is done but cancer cell just keep multiplying and don’t get the message to stop.
    2 Your own body can deal with random cancer cells when your immune system is at optimum levels
    3 Most lung cancers are secondary cancers; primaries are somewhere else in your body. Cancers follow a well know route depending where they start but usually end up in the lungs.
    4 Your immune system drops dramatically during stress, or by an unhealthy diet ( which is why I think that people on low incomes suffer more than others)
    5 It is important to eat organic food that is free from pesticides; these also cause a dramatic drop in your immune system.
    6 Your mental attitude plays an important role in your treatment and life expectancy
    7 Avoid dairy products

    Sadly my daughter didn’t make it, we have no cancer on my side so it was not in the mitochondria but her father and grandfather died early from cancer

  14. harleyrider1978 says:

    Lord I wish I had 3 lifetimes to live at once,Id love to become a cancer researcher simply because its a challenge probably the greatest challenge ever.

    • harleyrider1978 says:

      Mind you not one of these Prohibitionists docs I want to find a real cure simply so that you can do whatever you want to do and should you get cancer,We got ya covered.

      What would happen overnite if the headline read cure for cancer found!

      TC and every other public health group would be out of a job OVERNITE!

  15. garyk30 says:

    “What makes you think a cell is like a sheet of rubber?

    Like the formation of a drop of water…

    Water isn’t a bit like rubber. It’s more or less incompressible.”

    The stretching of rubber was just a visual aid.

    The comparison was not of water drops to rubber; but, of water drop formation to the splitting of cells.
    After all, cells are mostly water and would behave in much the same way.

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