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Medicine Science

Method For Fooling Cancer Cells Into Fat Cells Can Stop Cancer's Spread (technologynetworks.com) 83

Researchers from the University of Basel in Switzerland have discovered that they can prevent the formation of metastases by fooling breast cancer cells into fat cells. The proof-of-concept study was published in the journal Cancer Cell. Technology Networks reports: Malignant cells can rapidly respond and adapt to changing microenvironmental conditions, by reactivating a cellular process called epithelial-mesenchymal transition (EMT), enabling them to alter their molecular properties and transdifferentiate into a different type of cell (cellular plasticity). Cancer cells can exploit EMT -- a process that is usually associated with the development of organs during embryogenesis -- in order to migrate away from the primary tumor and form secondary metastases. Cellular plasticity is linked to cancer survival, invasion, tumor heterogeneity and resistance to both chemo and targeted therapies. In addition, EMT and the inverse process termed mesenchymal-epithelial transition (MET) both play a role in a cancer cell's ability to metastasize.

Using mouse models of both murine and human breast cancer the team investigated whether they could therapeutically target cancer cells during the process of EMT -- whilst the cells are in a highly plastic state. When the mice were administered Rosiglitazone in combination with MEK inhibitors it provoked the transformation of the cancer cells into post-mitotic and functional adipocytes (fat cells). In addition, primary tumor growth was suppressed and metastasis was prevented. Since both drugs used in the preclinical study were FDA-approved the team are hopeful that it may be possible to translate this therapeutic approach to the clinic.

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Method For Fooling Cancer Cells Into Fat Cells Can Stop Cancer's Spread

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  • by Anonymous Coward

    English as a fifteenth language, or just the vocabulary of a screaming monkey?

  • Fooling? (Score:5, Insightful)

    by RyanFenton ( 230700 ) on Tuesday January 15, 2019 @05:42AM (#57964510)

    I think they mean 'turning'.

    Fascinating science in the actual article - really odd use of language in the article. 'Fooling' is kind of anthropomorphizing the cancer cells - they're changing based on mechanisms, they never really make decisions to be fooled on, and that's why the actual study doesn't really use the word.

    Ryan Fenton

    • Hacking (Score:5, Interesting)

      by Errol backfiring ( 1280012 ) on Tuesday January 15, 2019 @05:57AM (#57964542) Journal
      I would call it hacking. They are hacking the process started by the cancer cells. Just like digital hackers, biohackers can be good guys.
    • by Anonymous Coward

      Instead of runaway cancer, you get runaway obesity? Then you die of a massive coronary.

      FAIL

      • by Anonymous Coward

        Just compare the size of a metastasis to the amount of fat that makes you morbidly obese. If you have a tumor the size of an average American's potbelly you're probably terminal already.

      • Instead of runaway cancer, you get runaway obesity? Then you die of a massive coronary.

        FAIL

        Since we don't measure obese people with a 5-year survival scale and stage-rate their decline, I'd say it's rather obvious which one is more dangerous.

        And obesity is pretty much 100% curable. I'd much rather take those chances and work on losing the weight than be dead.

  • by froggyjojodaddy ( 5025059 ) on Tuesday January 15, 2019 @07:59AM (#57964814)
    fat? :)

    Serious question - I understand everyone has fat cells, just that in obese people, they are larger than in lean people. However, if we turn cancer cells into fat cells, and that person adopts a healthy lifestyle to reduce the size of the fat cell, is that a win-win? Or is this a different type of fat cell that has other consequences?
    • by Gilgaron ( 575091 ) on Tuesday January 15, 2019 @08:45AM (#57965016)
      The idea is to make the cancer behave like a fat cell, so it'll not metastasize or grow uncontrollably. It'll still be well-behaved cancer so depending on where it is, age and so on you still may want to have further treatment but it is much easier to treat cancer if it isn't metastatic. Even if this was a light sci-fi comedy, it'd be better to get fat than to have metastatic cancer.
      • I read it as the cancer cells turns into a fat cell, not just behaves like a fat cell.
        • Kinda... you can't really undo the genetic damage that made it cancer, but you can force the 'be a fat cell' genes to get loud and in charge, apparently.
    • Re: (Score:2, Insightful)

      by jellomizer ( 103300 )

      Fat itself isn't that bad. People can be very healthy and overweight. However issues on where the fat is forming in excess is where the problems happen. If the Fat is gathering around your organs then your organs are being restricted and will not function properly. Or if you put on too much weight that affects your physical activity then health issues from lack of mobility and getting proper exercise. Also people get fat from an improper diet, so while they are getting fat they are also malnourished.

      Peop

      • by jabuzz ( 182671 )

        Except after smoking obesity is the second largest cause of cancer in the UK at least.

        https://www.cancerresearchuk.o... [cancerresearchuk.org]

        For an intro into the science as to why

        https://www.cancerresearchuk.o... [cancerresearchuk.org]

        The basics are that there is no such thing as being fat and healthy.

      • There are often appearing slim, people who have a lot of health problems because while the fat isn't showing outwardly with a big belly, it is collecting underneath the rib cage squeezing your their internal organs.

        [Citation needed]

      • Re: (Score:2, Informative)

        by mspohr ( 589790 )

        The "fit and fat" hypothesis has been disproved.
        Fat is not healthy (BMI should be 25)
        Heart disease, stroke, diabetes, cancer rates all higher in fat people.

    • by mspohr ( 589790 )

      You just get "skinny" fat cells.
      Fat cells can be large or small depending on how much fat they have to store.

    • Be cancer free with bigger breasts?

      Ducks...

  • by Applehu Akbar ( 2968043 ) on Tuesday January 15, 2019 @08:08AM (#57964870)

    Because Basel is a major center for pharma research, with several major firms headquartered there, it nurtures a university/manufacturing complex that makes it the Silicon Valley of the drug trade. Switzerland has its own regulatory apparatus that is notably faster and more responsive than our FDA, with the same high standards. And as a non-EU country, Switzerland is not subject to regulatory luddism from Brussels. If genetic engineering turns out to be part of the next big cancer treatment, it will flourish in Switzerland.

    https://www.pharmaceutical-tec... [pharmaceut...nology.com]

  • While excited. I hope it works out.
    • It sounds like it is very timing critical, to catch the cancer cells at the exact right moment.

      Also, although it says that EMT is usually associated with embryonic cells, does it mean that there are no normal cells that would be affected ? I'd hate to have my brain suddenly turn to fat like the rest of my body.

  • Turn cancer cells into fat cells

    Good news for everyone except Hollywood starlets, who'd rather have the cancer.

  • by pesho ( 843750 ) on Tuesday January 15, 2019 @01:54PM (#57967140)
    I am a bit suspicious of the value of studies that have not been replicated for more than one case. This is one of those. It is very clever work but I don't think the chances that it will lead to a cancer therapy are particularly high. The idea behind the work is that cells from breast cancer are one type (epithelial), but they need to convert into another type (mesenchymal) so they can leave the tumor and form metastasis. The clever part is that they nudge the mesenchymal cells to convert to fat cells and stop dividing. The problem is that the occurrence of the epithelial to mesenchymal transition in tumors is a bit of a controversial topic. The idea has a devoted cult following, but it has not been convincingly shown to be true. We know that the breast cancer tumors are epithelial and we know that their metastasis are epithelial. Genetic tagging to detect the transition in actual tumors so far have failed to do so and have shown that you don't need this transition to form metastasis. We also can see epithelial cells leaving the tumor without the need to convert to a different cell type. In the work, they use cell lines (cell cultured in a dish) that either readily undergo the epithelial to mesenchymal transition when exposed to a hormone that is abundant in the tissue and the blood (TGF-Beta), or a cell line that is mesenchymal (MDA-MB-231). These experiments show that when you inject these cell lines in a mouse you can reprogram them into fat cells. To make sure the reprogramming also works on tumors they use a human patient derived tumor that is grown in mice. Here is where my major problem with the work is. There are hundreds of these patient derived tumors that are available but they do the experiments on just one. Why just one? Why this particular one? If you are developing a cancer therapy one of the major questions is what are the chances that it will work. You answer that question by testing as many tumors as you can.
  • Fat cancer sounds terrifying.
  • No, don''t get up, I'll show myself out
  • But cancer wants to become fat cells, it just can't remember how without our helpful hints.

  • All my cancer cells turned into fat!

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