Meditations of an oncology geek

Archive for October, 2012

Experimental Obesity Contributes to Cancer

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24 October 2012

Overweight people get certain types of cancer more frequently; It’s been known from epidemiological association studies for a long time (1). However, that alone does not necessarily mean that obesity causes cancer. The media frequently conflates correlation and causation. Just because the mean ocean temperature and the number of pirate attacks have both increased in the last decade does not mean that warmer water is causing more piracy, or that pirates are making the earth warm. It could be that obesity causes cancer, or that there is something in the environment that causes both cancer and obesity.

Without causation studies (i.e. experimental research) it’s impossible to know if obesity causes cancer. The CDC reports that more than 35% of U.S. adults are obese, and that this rate is rising! (2) Given this alarming health trend, it’s a startling hypothesis that this already detrimental chronic health condition could influence another deadly health epidemic: cancer.

This morning I came across a paper by Mikhail G. Kolonin and colleagues that caught my attention. (3)

The authors used a strain of mice that are genetically “identical”. I.e. the mice have been inbred to the point where genetic differences in phenotypes of individual mice will be minimal. The authors then induced obesity in mice environmentally by feeding a test group a high fat diet (HFD) while a control cohort of mice was fed a regular diet. The authors then took the test mice off the HFD, and proceeded to implant mouse tumor cells into the breast of both groups of mice.

The result? The tumor cells implanted into the obese group of mice developed tumors that grew more than twice as fast! The authors analyzed the tumors and found that the increased white adipose tissue (fat) of the host allowed for the tumors to recruit more adipose stromal cells (non tumor cells from the host) to help the tumors form new blood vessels to help the tumors hijack energy and resources from the bloodstream.

Tumors are not a solid mass of tumor cells. They consist of blood vessels recruited from the host, and stromal (non-tumor cells) that are recruited from surrounding tissues that are normally used to do things like heal wounds and repair tissue. It appears that, at least in this model of tumor growth, that the physiological environment associated with obesity can promote tumor growth.

One part of this study that I really liked was the fact that both sets of mice had the same diet during the phase of tumor growth. If we are to extrapolate these findings to humans, it would indicate that a diet intervention of already diagnosed cancer patients might not be effective. I.e. it’s not the fat in the diet itself and the greater availability of fat resources in the blood that’s fueling the cancer growth; it’s the effects of the stored fat in tissues that’s making the tumors grow faster. I also liked the fact that the same strain of mice had obesity induced experimentally to rule out confounding genetic influences on the process: environmental influences lead to a chronically obese condition, and the physiological changes accompanying the obese condition are what allowed tumor cells to grow faster.

Cancer is not a single disease, but a blanket classification used to describe many diseases with similar properties; cancer is a very heterogeneous disease. No two people’s cancer is exactly alike on a molecular scale. It’s important to note that these studies were done with one cancer cell line, and performed in mice. The same mechanisms might or might not exist in humans, or all types of human cancers for that matter.

Nonetheless, this paper provides fresh evidence to the causation hypothesis (obesity increases cancer risk) and that the two conditions are perhaps not caused by a third, unknown confounding factor.

It is in the opinion of this scientific apprentice that the mechanism presented needs to be further analyzed by other scientific groups (isn’t that what scientists always say?). But, it is one more piece of understanding about the world that we can use to better our lives and those around us. It comes back to a similar theme: the United States (and many other first world countries) are facing a dire health epidemic stemming from metabolic syndrome. The good news is that the influences of metabolic syndrome and the result (obesity, and perhaps some cancers) are environmental, and as opposed to our genes, these are things we can control. That is not to say it is easy‚Ķ

If you or a friend are overweight or obese, it is my hope that this article will be a little bit of motivation to make positive health choices.

Peace and Health!
Ryon

note: I’ve also written about the positive effects of exercise on reducing cancer risk as well: http://ryongraf.com/2012/03/can-exercise-help-prevent-cancer/

References:
1) http://www.nature.com/nrc/journal/v4/n8/full/nrc1408.html
2) http://www.cdc.gov/nchs/data/databriefs/db82.pdf
3) http://cancerres.aacrjournals.org/content/72/20/5198

Written by Ryon

October 24th, 2012 at 9:37 am

Posted in Science Blog

I’m authoring a textbook chapter

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20 October 2012

It’s been a busy month for me (do I sound like a broken record yet?). Alas, I have some good news: I will soon have a new academic publication. And even better news: the publication will be open access, so anyone with an internet connection can check it out.

My research lab investigates mechanisms of tumor metastasis, or HOW cancer is able to spread through the body of a cancer patient. Our primary cancers of expertise are breast cancer, ovarian cancer, and neuroblastoma. Neuroblastoma affects about 650 new children in the U.S. every year, and is a particularly precarious cancer to treat. Neuroblastoma does not get not as much attention as other cancers, but there are many physician scientists that are very dedicated to improving clinical outcomes of these extremely brave kids.

When the opportunity arose to contribute a chapter to a textbook on neuroblastoma, our laboratory jumped on it. Together with my professor Dr. Dwayne Stupack and Shanique Young, another graduate student in our lab, we authored a chapter on neuroblastoma and integrins: how neuroblastoma (and by extension, their metastases) interact with their environment. It is our hope that our expertise will be put to good use by the courageous physician-scientists out there that are applying our theories and experimental laboratory insights in the clinic.

Often overlooked is the importance of communication in science. A remarkable scientific discovery is completely irrelevant to society if it is not communicated, and communicated properly. The nature of scientific understanding is very nuanced, and the more nuanced the understanding, the more critical the communication. As such, I take this opportunity to communicate science with great pride.

The science communication skills I’ve practiced here (as per my science communication blog) the last two years have helped me tremendously in my efforts to communicate the most clear and accurate version of the research to those that will put it to use. It would be impossible without my readers, so I would like to thank you as well.

peace and clarity,
Ryon

Written by Ryon

October 20th, 2012 at 8:47 am

Posted in Science Blog