Everybody’s Free To Wear Sunscreen…And Prevent Skin Cancer

Our last article discussed using sunscreen to help protect skin against damaging UV radiation. When used properly, sunscreen prevents sunburn and sun-induced skin aging, and protects from skin cancer. Studies have shown that sunscreen use reduces the incidence rate of squamous cell carcinoma (SCC) and melanoma, but currently no evidence supports a protective role against basal cell carcinoma (BCC).

While some people, including supermodel Gisele Bundchen, believe sunscreen is dangerous (she declared “I cannot put that poison on my body”) experts such as The Skin Cancer Foundation and the American Academy of Dermatology—and even Cosmopolitan magazine—disagree with her and other skeptics.

A large, randomized controlled trial examined the effect of daily sunscreen use on the development of skin cancers. Researchers followed 1621 Australians from 1992-2006. From 1992-1996, participants were randomly placed in a group and instructed to either use the study-provided broad spectrum SPF 16 sunscreen daily on face, arms, neck and hands, or to continue personal discretionary use of sunscreen. At the 2004 follow up, researchers noted that the daily sunscreen use group had a 35% rate reduction in the incidence of SCC (considering all SCCs that appeared throughout the entire study). However, the incidence of BCC was not statistically different between the two groups. More recent studies corroborate these results.

US Senator and 2008 Republican Presidential Candidate John McCain has had multiple melanomas removed. Other political figures have battled skin cancer, including former Presidents Jimmy Carter (metastatic melanoma) and Bill Clinton (BCC), and former First Lady Laura Bush (SCC).

In 2006, researchers followed up again, this time looking for melanoma. The overall incidence rate of melanoma was 50% less in the sunscreen intervention group than the discretionary use group (out of approximately 800 people in each group, 11 people in sunscreen group and 22 in the control group developed melanoma). It should be noted that these results had borderline statistical significance, with a P value of 0.051 (P = 0.05 is the accepted cutoff for significance). This essentially translates to a 5.1% probability of these findings being due to chance, rather than to the actual sunscreen intervention. Also, there was a 73% lower rate of invasive melanoma in the sunscreen group. Although there was no significant difference in number of melanomas diagnosed at the prescribed intervention sites, it is possible that sunscreen use reduced the risk, as participants in the sunscreen intervention group reported more frequent use of sunscreen over the whole body after the intervention terminated.

Although these results are not the most compelling, they nonetheless point to a protective role of sunscreen. Many factors may contribute to a less than straightforward outcome. First, the sunscreen intervention was in adults and lasted 4.5 years. Melanoma and BCC are thought to result from both long term sun exposure and intense, intermittent episodes (sunburns), whereas SCC is mainly caused by cumulative UV exposure (both natural and indoor tanning bed). Furthermore, blistering childhood sunburns are a risk factor for melanoma. One study that examined sunscreen use in children found a significant protective benefit. Regular use (applied any time sun exposure would exceed 30 min) of a broad-spectrum SPF 30 sunscreen over a 3-year period resulted in significantly fewer newly developed moles, the number of which is a risk factor for melanoma.

Second, participants in the non-sunscreen intervention group continued their discretionary use of sunscreen. No trial in humans could ever prohibit sunscreen use or provide a placebo for ethical reasons. Therefore, perfectly delineating the protective effect of sunscreen is difficult.

Many questionnaire-based studies that rely on participants’ memory of sunscreen use suffer from recall bias. Some of these studies showed no benefit of sunscreen for melanoma prevention but memory limits the reliability of these results. The bottom line is that sunscreen protects from UV radiation, a known human carcinogen.

The skin consists of two layers, the dermis and epidermis. The epidermis contains a variety of cell types, including squamous cells, basal cells and melanocytes. These are the sources for squamous cell carcinoma, basal cell carcinoma and melanoma, respectively.

UV radiation is implicated in up to 90% of nonmelanoma skin cancers, squamous cell carcinoma (SCC) and basal cell carcinoma (BCC). Mutations consistent with UV radiation were also found in the genomes of melanoma tumors; UV radiation is thought to be responsible for the majority of melanoma. Whereas SCC and BCC are more frequent, melanoma is more often fatal. While UV radiation is the single most important risk factor for skin cancer, it’s worth noting that it is not responsible for all skin cancers. Aside from environmental carcinogens, cancer can arise due to a person’s genetics (familial effect) or random mutations.

Acral melanoma is a type of skin cancer not caused by UV radiation and is genetically distinct from UV-induced cutaneous malignant melanoma. Bob Marley’s acral melanoma metastasized and ultimately claimed his life.

UVA radiation primarily damages the components of skin cells by generating reactive oxygen species, or ROS. These highly active molecules can cause single-strand breaks in the DNA or crosslink DNA to protein, resulting in mutations or improper functioning. Both UVA and UVB can cause a more significant type of DNA damage called pyrimidine dimers, where two adjacent pyrimidine nucleotides (the “C” and “T” of DNA; the “A” and “G” are purines) fuse together. Because the higher energy UVB is absorbed directly by DNA, UVB can cause other modifications that compromise the integrity of DNA, leading to instability of the genetic code.

Indeed, the cell has repair mechanisms to fix pyrimidine dimers and other errors, but sometimes the very genes encoding the repair mechanisms are mutated. UV-induced DNA damage can result in highly characteristic mutations in critical genes, for example in the tumor suppressor gene p53. As the “guardian of the genome”, the p53 protein is involved in directing the repair of mutations and guiding the cell through its controlled death pathway, called apoptosis. Mutations in p53 are thought to be among the first steps in development of non-melanoma skin cancer. Formation of malignant melanoma is more complicated and not fully understood.

Yes, p53 has its own superhero persona. That’s how cool (and significant) it is. Image by Susanne Harris.

Cells that carry mutations in p53 proliferate uncontrollably, a hallmark of cancer. In some cases, the immune system will recognize malignant cells as a threat and effectively eliminate them. However, UV radiation is also known to suppress the immune system by at least two mechanisms. One is by diminishing the production of antigen-presenting cells, which engulf foreign-looking cells and display an alert to activate the immune system). The other is by inducing the production of an immune suppressive cytokine, interleukin-10. Additionally, some skin cancer cells display proteins on their surface that prevent the immune cells from killing them. Thus, in addition to mutations in key genes, immune suppression and immune evasion contribute to the development of skin cancer.

Even the mutant Wolverine wears sunscreen! In this Instagram post, Hugh Jackman urged his fans to use sunscreen. He became a fervent sunscreen proponent after having a BCC removed from his nose.

Contributed by: Julia van Rensburg, Ph.D.
Follow Julia on Twitter.

van der Pols JC, Williams GM, Pandeya N, Logan V, & Green AC (2006). Prolonged prevention of squamous cell carcinoma of the skin by regular sunscreen use. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 15 (12), 2546-8 PMID: 17132769

Lee TK, Rivers JK, & Gallagher RP (2005). Site-specific protective effect of broad-spectrum sunscreen on nevus development among white schoolchildren in a randomized trial. Journal of the American Academy of Dermatology, 52 (5), 786-92 PMID: 15858467

Koh HK, Geller AC, Miller DR, Grossbart TA, & Lew RA (1996). Prevention and early detection strategies for melanoma and skin cancer. Current status. Archives of dermatology, 132 (4), 436-43 PMID: 8629848

Leiter U, & Garbe C (2008). Epidemiology of melanoma and nonmelanoma skin cancer--the role of sunlight. Advances in experimental medicine and biology, 624, 89-103 PMID: 18348450

Brenner M, & Hearing VJ (2008). The protective role of melanin against UV damage in human skin. Photochemistry and photobiology, 84 (3), 539-49 PMID: 18435612

Might you like a water mite named after you?

It is estimated that nearly 9 million species share the Earth but only 2 million of them have been named. In scientific parlance, organisms are named using binomial nomenclature with the first word referring to the genus and the second word the species (e.g., humans = Homo sapiens). Typically, the scientists who discover the new species get the pleasure of naming it. Often, the species’ name refers to the location where it was found, or it refers to a peculiar trait the organism possesses. Or, it may simply be the music that was playing at the time of the discovery.

Famed singer/actress/dancer Jennifer Lopez provided the inspiration for the name of a newly discovered species of water mite found near Puerto Rico, Litarachna lopezae. Some have speculated that this is due to an uncanny resemblance between their posteriors, but the scientists claim that they were listening to her music while analyzing the mites (nothing like a little “Booty” piping through the lab to stimulate the intellectual rigor that goes into experimental design). But biologist Vladimiar Pesic, who made the discovery, contends, "The reason behind the unusual choice of name for the new species is simple: J Lo's songs and videos kept the team in a continuous good mood when writing the manuscript and watching World Cup Soccer 2014”.

Litarachna lopezae, also known as "L.Lo".
Why the extra “ae” at the end of “lopez”? To make it sound more science-y, of course.

In the scientific world, it is considered an honor to have a species named after you. Think about having your name forever linked to a beautiful flower or a majestic beast that rules the jungle – that would be pretty awesome. But as noted above, not all creatures are pleasant to look at or even possible to look at without a microscope. Some creatures make us sick or even kill us. Who’d want to be named after such a critter?

Well, President Barack Obama was the motivation behind the naming of Paragordius obamai, a newly described parasitic worm. I’m sure there are many people chomping at the bit to crack a joke about this, but the researchers claim that the name stems from the fact that they discovered the worm in Kenya, the native country of Obama’s father. There is also a trapdoor spider, Aptostichus barackobamai, named after our current president, presumably in recognition of his confessed love of Spiderman comics. Well on his way to having the most species named after him than any other president, Barack Obama’s namesake has also been used for a lichen (Caloplaca obamae) and an extinct lizard (Obamadon gracilis). Oh, and who can forget about the “Obamafish” (Etheostoma obama)?

A politician named after a worm. And not just any worm – a parasitic worm. Live bait for any comedian.

The names of other presidents and politicians have been adapted for binomial nomenclature, although surprisingly, no species of newt has been named after Newt Gingrich yet. George W. Bush, along with Dick Cheney and Donald Rumsfeld, all have a species of the Agathidium slime-mold beetle named after them (Agathidium bushi, A. cheneyi, and A. rumsfeldi). Both Teddy and Franklin D. Roosevelt, as well as Thomas Jefferson, have multiple species named after them. Clinton, Gore, and Carter have each been named after a species of Etheostoma (a genus of freshwater fish). And last but not least, George Washington served as the inspiration behind the name of Washingtonia, a genus of palm trees.

Let’s see if you can guess which celebrity is associated with the following species pictured below (answers at the bottom).



One

Two

Three



Four



Five

Six

The answers:

1. Echiniscus madonnae, a microscopic waterbear named after Madonna. These critters are virtually indestructible and have lived forever.

2. Gnathia marleyi, a fish parasite named after Bob Marley that is only found in the Caribbean Sea.

3. Eristalis gatesi, a flower fly named after Bill Gates. Yes, it crashes a lot.

4. Kootenichela deppi, a pre-historic arthropod that reminded the scientist of Edward Scissorhands, so he named it after Johnny Depp. Ironically, the scientist who discovered this many footed creature is named Dr. Legg!

5. Aleiodes gaga, a parasitoid wasp from Thailand named after Lady Gaga.

6. Sylvilagus palustris hefneri, a marsh rabbit named after the founder of Playboy, Hugh Hefner (Playboy bunny, get it?).

So where did we get this system to name all of the life on Earth (a science known as taxonomy)? Some say it formally started with Aristotle's classification scheme as early as 300 BC. First, an organism was divided into the plant or animal group. Second, animals were subdivided into those that had blood and those that did not. Third, animals were further divided into things that walked, flew, or swam. Aristotle's system gets confusing because a duck can do all of these things, but his scheme was good enough to last 2000 years.

In the 1700s, Carl Linnaeus revised this system to include more categories that grouped organisms based on their morphology (body form). He was also the one who perfected the binomial nomenclature with the genus and species names. Written properly, the genus is always capitalized and the species always in lower case, and the entire name should be in italics or underlined. Latin is used because it is a universal and "dead" language, meaning it is no longer in use and therefore immutable. Plus, it sounds very scholarly. The Linnaeus system is so elegant and effective, it is still used today.

Contributed by:  Bill Sullivan

Follow Bill on Twitter: @wjsullivan

Hanelt, B., Bolek, M., & Schmidt-Rhaesa, A. (2012). Going Solo: Discovery of the First Parthenogenetic Gordiid (Nematomorpha: Gordiida) PLoS ONE, 7 (4) DOI: 10.1371/journal.pone.0034472