Pharma Strategy Blog

While reading the latest Cancer Research journal, I was surprised to learn that:

“Nonmelanoma skin cancer is the most common cancer in the United States, where DNA-damaging ultraviolet B (UVB) radiation from the sun remains the major environmental risk factor.”

Ming et al., (2011)

In fact, more than one million new cases are diagnosed in the US annually, which accounts for 40% of all new cancer cases.  That’s a lot of skin cancer!

Source: s_manca: Great Barrier Reef

The bigger question, though, is what are the genetic underpinings of the disease?  These non-melanoma skin skin cancers tend to derive from the epidermal basal layer in response to DNA damage from sunlight.

From an incidence perspective, I would suspect that those with pale skin who are subject to harsh sunlight such as Australia would be particularly susceptible.

Researchers from the University of Chicago may have identified a role for PTEN, a known tumour suppressor, in removing DNA damage derived from UVB radiation, see Ming et al., (2011) in the references below.  UVB radiation is a known risk factor for non-melanoma skin cancer.

In previous research, the group discovered laboratory mice with reduced levels of PTEN were more likely to have UVB-induced skin cancers.  They therefore decided to test the idea in human cells to see if the finding could be replicated.

In the latest research, they reported what happened when they exposed skin cells to UVB radiation and examined the rates of DNA repair. Those with lower PTEN levels had slower rates of DNA repair, because of loss of the key DNA repair protein xeroderma pigmentosum C (XPC).

What was most interesting was what happened when the scientists restored the levels of XPC?  In that situation, the rates of DNA repair went up as well.

Overall, the current research in human cell lines suggests that cells without adequate levels of PTEN were not able to repair sufficiently, confirming the results seen in the mice.

Given a greater understanding of the molecular mechanisms underpining non-melanoma skin cancer potentially means that chemoprevention strategies can be developed down the road.  In other words, if we could identify those most at risk due to low PTEN levels, then supplements or therapeutics might be useful as a protection strategy.

Photo Credit: s_manca

References:

Ming, M., Feng, L., Shea, C., Soltani, K., Zhao, B., Han, W., Smart, R., Trempus, C., & He, Y. (2011). PTEN Positively Regulates UVB-Induced DNA Damage Repair Cancer Research, 71 (15), 5287-5295 DOI: 10.1158/0008-5472.CAN-10-4614