Monthly Archives: April 2015

Melanin: Friend or Foe?

Sue Skin Cancer Post April 20 2015

Did you know you can still get skin cancer hours after you are out of the sun? The culprit: melanin.

Spring has finally arrived for Canadians and we are eager to bask in the sun. We all know that too much sun exposure increases our risk of getting skin cancer. However, a recent study found that the damaging effect of the sun’s ultraviolet (UV) radiation on our skin continues hours after we are out of the sun (1).

Let me back track and first describe why UV light exposure – from both the sun and tanning beds – is harmful.

Direct exposure to UV light leads to the creation of lesions within the DNA of our skin cells. These lesions are called cyclobutane pyrimidine dimers (CPDs) and form rapidly (trillionths of a second). It is thought that most skin cancers arise from mutations caused by these rapid-forming DNA lesions.

Our body possesses safety mechanisms to reduce the harmful effects of UV light. For instance, melanin (the pigment that makes our hair, eye and skin color) helps protect our DNA by absorbing UV energy. In the skin, only cells called melanocytes can produce melanin. Unfortunately, melanocytes account for a mere 10% of all skin cells! So how are the other skin cells protected? Melanocytes help their neighbours by giving some melanin to them, which in turn acts as an umbrella to cover and protect their DNA.

But there is a twist to the story- melanin can also be our foe.

Researchers from Yale University recently discovered that melanin could actively participate in the formation of CPDs (1). It was found that in melanocytes, UV causes melanin to break down into fragments. These melanin fragments contain lots of energy, which can then get transferred to DNA and cause damage. This creates what is called “dark CPDs” since they are generated more than 3 hours after initial UV exposure. What this means is that not only do we need to protect ourselves from the DNA damage that occurs during direct sun exposure, but also hours after we are out of the sun. The good news is that since dark CPDs takes longer to form, it allows time for intervention such as developing “evening-after” sunscreens to block the formation of dark CPDs.

The moral of the story? Don’t depend too much on your melanin for protection from the sun. Continue to limit your exposure to UV light to reduce your risk of skin cancer. Remember that DNA damage from the sun builds up with each exposure and is permanent. So while you are enjoying warm weather don’t forget to practice sun safety! For sun-safe tips check out these guidelines from the Canadian Cancer Society.

References:

  1. Premi S et al. (2015). Chemiexcitation of melanin derivatives induce DNA photoproducts long after UV exposure. Science. 347(6224):842-7.

This article was written by Sue Li. Sue has a PhD from the University of Toronto and is currently working at Princess Margaret Hospital developing new drugs to treat prostate cancer. To find out more about Sue and her research check out her bio on the Members page.

Getting to the Root of the Problem: Cancer Stem Cells

Cancer Stem Cell Blog Picture

If cancer is like a dandelion, cancer stem cells are considered the root of the dandelion. You can cut off the top of the dandelion, but unless you destroy the roots, the weed will grow back and spread.

One of the biggest challenges in the cancer field that has fueled decades of research is “how do cancers grow and spread?” The cancer stem cell hypothesis is one model that scientists are studying to answer this question

Stem cells are the only cells in our body that have the ability to form some or all different types of cells (i.e. breast, brain, blood). They are the cells responsible for humans to grow as well as heal after injury.

Similarly, cancer stem cells are thought to be the only cells within a tumor that are capable of forming another tumor. A helpful way to look at cancer and cancer stem cells is to think of them as dandelions. Cancer stem cells are the root of the dandelion- sure you can cut off the top, but unless you also destroy the roots, the weed will grow back and spread.

Because of this, scientists often refer to cancer stem cells as “tumor initiating cells”. They are thought to be the reason why cancer often returns after treatments, such as chemotherapy. The reason being is that cancer stem cells are highly resistant to chemotherapy. These drugs are designed to target rapidly dividing cells, however, just like normal stem cells, cancer stem cells do not divide very often, allowing them to evade these therapies. As a result, cancer stem cells may be primarily responsible for disease relapse.

Toronto has a strong heritage in stem and cancer stem cell research since 1961 when Drs. James Till and Ernest McCulloch first discovered stem cells at the Ontario Cancer Institute. Since then, Dr. John Dick discovered the first cancer stem cell in leukemia, kicking off this exciting field of research. With many intelligent and clever scientists (and students!), Toronto will continue to be a global leader in cancer stem cell research in years to come.

My lab, along with many others, are helping to get to the root of the problem! We are studying brain cancer stem cells so we can identify what makes them so unique. Our goal is to learn how to specifically target these cells to treat and prevent cancer from coming back.

References and further reading:

The Sleeping Cancer Cell

http://www.nytimes.com/2010/10/31/magazine/31Cancer-t.html

Nguyen, L.V., Vanner, R., Dirks, P., and Eaves, C.J. (2012). Cancer stem cells: an evolving concept. Nat. Rev. Cancer 12, 133–143.

Reya, T., Morrison, S.J., Clarke, M.F., and Weissman, I.L. (2001). Stem cells, cancer, and cancer stem cells. Nature 414, 105–111

This article was written by Mike Pryszlak. Mike currently completing the second year of his PhD at the University of Toronto. He studies how normal stem cell genes are changed in cancer stem cells. To learn more about Mike and his research check out our members page.