making cancer in a can?

March 28, 2009

It’s been a long running staple of science fiction movies. A biochemical giant finds an amazing new business opportunity. Some compound or plant in an exotic location is able to alter or remove the limits on cell division in the human body. The “scientists” in the R&D department declare that turning whatever this infinite cell divider is into a pill would create a multi-billion dollar market and help extend human lifespan to extremes we could only dream of. But those are movies. In real life what those “scientists” would be doing is creating something like cancer in a can. There’s a good reason to let our cells stop dividing.

t-virus

Cell division in humans, and all other animals, is regulated by telomeres; regions of redundant hereditary material on the ends of a chromosome. Without them, chromosome ends for a new cell would come unraveled and all the codons it contains would be lost. But as cells divide, their telomeres shorten until they start unraveling. When they do, their home cell stops dividing and might even commit suicide when there’s too much damage to the chromosomes. And that’s a key component in suppressing cancerous tumors. Cancerous cells can regenerate their telomeres and as they grow out of control, they form tumors which invade nearby tissues and metastasize to spread throughout the body.

This isn’t so cut and dry though. We don’t know how humans would respond to a treatment of compounds that lengthen their telomeres. We only know that nematodes with longer telomeres would have longer lifespans and their offspring would inherit the extended telomeres, also with the longer lifespan seen in their parents. But would the same apply to humans? Human aging is rather complex and just having longer telomeres might not do all that much for us. And there would always be a concern that some of our cells would overdose on the treatment to become cancerous and create tumors. Either way, having us take pills to dramatically change how many times our cells could divide or giving these cells immortality is not a good idea. In fact, it may be an effective way of causing cancers on demand.

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  • http://hplusbiopolitics.wordpress.com/ Joshua

    I blogged about some interesting research in this vein, showing that mice can live longer if they over-express both telomerase AND anti-cancer genes: http://hplusbiopolitics.wordpress.com/2008/11/15/anti-ageing-telomerase-with-cancer-resistance-too/

  • Greg Fish

    Joshua,

    It seems to me that the researchers were doing the study on mice which had enhanced p53 pathways that would already provide tumor suppression. So in effect, they’re balancing their abilities to suppress tumors over the risk of cells becoming cancerous after over-expressing telomerase. And that sounds like it could potentially work.

    My focus was a little more narrow. I was just trying to show that the old sci-fi movie staple about just boosting or eliminating limits on cell division would be very dangerous.

  • Anonymous

    Cell division in humans, and all other animals, is regulated by telomeres; regions of redundant hereditary material on the ends of a chromosome. Without them, chromosome ends for a new cell would come unraveled and all the codons it contains would be lost. But as cells divide, their telomeres shorten until they start unraveling. When they do, their home cell stops dividing and might even commit suicide when theres too much damage to the chromosomes.

    And thats a key component in suppressing cancerous tumors. -> How does it suppress tumors again?

  • http://hplusbiopolitics.wordpress.com/ Joshua

    And thats a key component in suppressing cancerous tumors. -> How does it suppress tumors again?

    In most cells, each time a cell divides the telomeres get shorter. Eventually, the cell will have divided so many times that the telomeres are too short for the cell to divide again (this number of cell division is known as the ‘Hayflick limit’).

    Cancer is unregulated cell division, where the cells keep dividing uncontrollably. In most cases, cells will divide out of control then hit the Hayflick limit and stop/die. But if a mutation also stops the telomeres from shortening, then there will be no Hayflick limit to stop the tumor growth.

  • macd

    It’s new to my knowledge that telomeres also restrict the actual rate of cell division.

    As far as I know, cancerous cells occur when more than just one mistake in their “program” happen at the same time. These are (thats not a complete list):

    – The gain/activation of telomerase, an enzyme that extends telomeres. It is usually only active within certain parts of meiosis and inactive in adult cells.

    – The loss of one or several precautions to avoid unbraked multiplication, e.g. the factor that “healthy” cells won’t multiply themselves if there are to much neighbouring cells around them.

    – The deactivation of apoptosis.

    It’s rather common that cells develop one or a few malfunctions. Commonly, these are simply eliminated via various ways our body has developed. E.g. a cell incidentially activating telomerase might be destroy itself via apoptosis. Another common Method is that immune cells (T helpers for example) devour or destroy malfunctioning cells if those won’t do it themselves.

    Cancer happens to a person if to much malfunctions intersect with each other, making them to resistant to be eliminated by our body on its own. (In my college exams in Biology, a task was about a certain cancer variation carrying a certain enzyme on their hull which triggers the apoptosis of immune cells dedicated to destroy the cancer cell. (“Duh!” said the T-cell ;D))

    Having this knowledge in mind I’d like to disagree with your simple idea of “longer telomeres lead to cancer”. Of course, and as gen manipulators had to learn yet, it’s quite rare that a certain gene or operon can simply be chanced in order to chance *one* feature without changing some or even a lot other features unintendedly as well. Thus the scifiic idea of just prolonging man’s life by extending our telomeres is bulls*it of course but, at least in my eyes, such research might lead us to helpful knowledge of our own bodies and could also create new methods of medical treatment.

    (I’m dreadfully sorry for any grammatical mistakes, my English is a little rusty right now – I’m German)

    greetings

    macd