Skin Cancer Prevention Strategies: TRIED, TRUE, & NEW

By Ronald L. Moy, MD, and Shannon Famenini

Skin cancer is the most common cancer in the US. In 2013, more than two million people will be diagnosed with nonmelanoma skin cancers (NMSC),1 and almost 77,000 will develop potentially deadly melanomas.2 The total direct cost associated with the treatment for NMSC, primarily basal and squamous cell carcinomas, was $1.4 billion in 2004.3

Risk factors for skin cancer include fair complexion, weakened or suppressed immune systems, family history and genetic predisposition, having many moles or any typical moles, and a history of sunburns or skin cancer.4 Overall risk increases with age and ultraviolet (UV) radiation exposure. Additionally, some people simply have decreased DNA repair capability. For example, xeroderma pigmentosum patients have a rare genetic defect that prevents their DNA repair enzymes from undoing the damage caused by UV radiation, leaving them highly vulnerable to skin cancers.

Despite all these potential risk factors, skin cancer remains one of the most preventable diseases. The vast majority of the time, it can be avoided by protecting the skin from UV radiation emitted by the sun and tanning machines. Some effective protection methods include avoiding UV tanning; shade-seeking, especially between 10 AM and 4 PM; wearing protective clothing, and using sunscreen. There are also many other effective forms of skin cancer prevention. Everyone should be aware of the following tried and true or new prevention methods.

Prevention Strategy: Sunscreen Use

Sunscreens protect against skin cancer by deflecting or absorbing UV radiation, keeping it from reaching the skin and causing DNA damage. Consistent sunscreen use has been shown to result in significantly fewer new precancers, squamous cell carcinomas, and melanomas.5,6 Although most public health agencies recommend reapplying sunscreen every 2-3 hours, one study showed that doing a first reapplication after 20 minutes outdoors significantly reduces UV exposure.6 Some experts now recommend applying sunscreen both 30 minutes before UV exposure, and again after 15 to 30 minutes of continuous UV exposure. Further reapplications should be done after another two hours outdoors, or immediately after swimming or heavy sweating.

It’s also essential to apply a sufficient amount of sunscreen. Most people simply apply too little. A 2012 study suggested that a double application might help users attain the thickness needed to achieve the SPF (sun protection factor) value on the label.7 But applying enough sunscreen is just part of the equation, since only broad-spectrum (UVA- and UVB-filtering), high-SPF sunscreens (SPF 15+ for brief daily sun exposures and SPF 30+ for extended or intense exposures) can prevent or significantly reduce UV-induced skin damage.8 New FDA labeling regulations, which permit manufacturers to use the term “broad-spectrum” only on products containing sufficient UVA and UVB protection, should help consumers find appropriate sunscreens.

Prevention Strategy: Your Diet

Some research has shown that diets low in fat and high in fruits and vegetables can reduce the risk of all cancers, including skin cancer. In the
1990’s, Black and colleagues declared that a lowfat diet was associated with fewer actinic keratoses (common skin precancers) and NMSCs in skin cancer patients,9,10 while in 2004, subjects treated with an antioxidant derived from a fern experienced less redness and DNA damage following UV exposure.11 Antioxidants are substances such as vitamin C or E that remove potentially damaging toxins called “free radicals” from the body, and fruits and vegetables are full of these substances.

Prevention Strategy: Topical DNA Enzymatic Therapy

Our skin cells have built-in protective mechanisms that use DNA repair enzymes, which are molecules that prompt chemical changes, to repair UV damage. Scientists can now encapsulate such enzymes in certain fat cells so that they can be topically applied, allowing them to penetrate the skin and supplement its natural protective abilities. Topically applied DNA repair enzymes can reverse free radical damage caused by UV exposure and decrease the number of gene errors (mutations) that can lead to cancers.12,13 Although these enzymes are not FDA approved for the prevention of skin cancer, evidence suggests they can prevent precancerous lesions such as actinic keratoses.

Prevention Strategy: Retinoids

Retinoids, which are vitamin A derivatives, may prevent skin cancer in people particularly vulnerable to skin cancers.14,15,16 The oral retinoid isotretinoin(Roaccutane) improves wrinkles and other sun-induced skin damage, while actinic keratoses and basal cell carcinomas treated with the topical retinoid tretinoin, sometimes marketed as Renova or Retin-A,17,18,19 have completely regressed. Although such results may be temporary,20 tretinoin .05 percent does reduce some signs of skin aging (such as fine facial wrinkles, brown spots, and roughness) associated with chronic sun exposure. Used with topical DNA repair enzymes, it may help treat actinic keratoses and prevent basalcell and squamous cell carcinomas.

Prevention Strategy: Resurfacing Procedures

The use of resurfacing procedures and acid peels to treat skin precancers and prevent skin cancer has produced promising results — and fewer recurrences 21,22 than treatment with the topical chemotherapy drugs 5-fluorouracil and imiquimod.23,24 Dermabrasion, a resurfacing technique that uses abrasives to remove the top layers of the skin (which often contain many precancerous cells), and trichloroaceticacid peels have been used for years to treat severe actinic damage and prevent its progression to squamous cell carcinoma. More recently, treatment with fractional lasers, which permit a very careful and controlled delivery of light, has also reduced the number of actinic keratoses. One fractional laser is FDA-approved for this purpose.25,26,27


While more research on some of the newer strategies remains to be done, all of these methods should be considered when you’re exploring ways to prevent skin cancer.

Ronald L. Moy, MD, practices dermatology, Mohs micrographic surgery, and cosmetic surgery in Beverly Hills, CA. Dr. Moy completed his residency training at UCLA and his surgical fellowship with Dr. John Zitelli in Pittsburgh. He has been Editor in- Chief of Dermatologic Surgery, President of the American Society for Dermatologic Surgery and is a Past President of the American Academy of Dermatology. Dr. Moy is a Vice President of The Skin Cancer Foundation.

Shannon Famenini received her BA in biology from UCLA in 2009 and will graduate from the David Geffen School of Medicine in 2014. She is currently doing a clinical research fellowship at Kaiser Permanente Los Angeles Medical Center as well as assisting Dr. Moy in clinical studies.

Published on October 28, 2014


  1. Rogers, HW, Weinstock, MA, Harris, AR, et al. Incidence estimate of nonmelanoma skin cancer in the United States, 2006. Arch Dermatol 2010; 146(3):283-287.
  2. American Cancer Society. Cancer Facts & Figures 2012.
  3. The Lewen Group, Inc. The burden of skin diseases 2005. The Society for Investigative Dermatology and the American Academy of Dermatology Association. 2005.
  4. Moy RL, Taheri DP, Ostad A. Practical Management of Skin Cancer. 1st ed. Philadelphia, PA: Lippincott-Raven Publications, 1999.
  5. Thompson SC, Jolley D, Marks R. Reduction of solar keratoses by regular sunscreen use. N Engl J Med 1993; 329(16):1147-51.
  6. Diffey BL. When should sunscreen be reapplied? J Am Acad Dermatol 2001; 45(6):882-885.
  7. Teramura T, Mizuno M, Asano H, et al. Relationship between sun-protection factor and application thickness in high-performance sunscreen: double application of sunscreen is recommended. Clin Exp Dermatol 2012 Oct 10. [Epub ahead of print]
  8. Moyal DD, Fourtanier AM. Broad-spectrum sunscreens provide better protection from solar ultraviolet-simulated radiation and natural sunlight-induced immunosuppression in human beings. J Am Acad Dermatol 2008; 58(5 Suppl 2):S149-54.
  9. Black HS, Herd JA, Goldberg HH, et al. Effect of a low-fat diet on the incidence of actinic keratosis. N Engl J Med 1994; 330(18):1272-5.
  10. Black HS. Influence of dietary factors on actinically-induced skin cancer. Mutat Res 1998; 422(1):185-90.
  11. Middelkamp-Hup MA, Pathak MA, Parrado C, et al. Oral polypodium leucotomos extract decreases ultraviolet-induced damage of human skin. J Am Acad Dermatol 2004; 51(6):910-8.
  12. Stege H. Effect of xenogenic repair enzymes on photoimmunology and photocarcinogenesis. J Photochem Photobiol B 2001; 65(2-3):105-8.
  13. Russo GG. Actinic keratoses, basal cell carcinoma, and squamous cell carcinoma: uncommon treatments. Clin Dermatol 2005; 23(6):581-6.
  14. Kraemer KH, DiGiocanna JJ, Peck GL. Chemoprevention of skin cancer in xeroderma pigmentosum. J Dermatol 1992; 19(11):715-8.
  15. Bouwes Bavinck JN, Tieben LM, Van der Woude FJ, et al. Prevention of skin cancer and reduction of keratotic skin lesions during acitretin therapy in renal transplant recipients: a double-blind, placebo-controlled study. J Clin Oncol 1995; 13(8):1933-8.
  16. Harwood CA, Leedham-Green M, Leigh IM, Proby CM. Low-dose retinoids in the prevention of cutaneous squamous cell carcinomas in organ transplant recipients: a 16-year retrospective study. Arch Dermatol 2005; 141(4):456-64.
  17. Bollag W, Ott F. Retinoic acid: topical treatment of senile or actinic keratoses and basal cell carcinomas. Agents Actions 1970; 1(4):172-5.
  18. Peck GL. Hypertrophic scar after cryotherapy and topical tretinoin. Arch Dermatol 1973; 108(6):819-22.
  19. Belisario JC. Recent advances in topical cytotoxic therapy of skin cancer and precancer. In: Melanoma and Skin Cancer. Sydney, Australia: Proceedings of the International Cancer Conference. Sydney; 1972:349-375.
  20. Bollag W, Ott F. Vitamin A acid in benign and malignant epithelial tumours of the skin. Acta Derm Venereol Suppl. Stockholm: 1975; 74:163-6.
  21. Ostertag JU, Quaedvlieg PJ, van der Geer S, et al. A clinical comparison and long-term follow-up of topical 5-fluorouracil versus laser resurfacing in the treatment of widespread actinic keratoses.Lasers Surg Med 2006; 38(8):731-9.
  22. Brodland DG, Roenigk RK. Trichloroacetic acid chemexfoliation (chemical peel) for extensive premalignant actinic damage of the face and scalp. Mayo Clin Proc 1988; 63(9):887-96. Rhavar M, Lamel SA, Maibach HI. Randomized, vehiclecontrolled trials of topical 5-fluorouracil therapy for actinic keratosis treatment: an overview. Immunotherapy 2012; 4(9):939-45.
  23. Strohal R, Kerl H, Shuster L. Treatment of actinic keratoses with 5% topical imiquimod: a multicenter prospective observational study from 93 Austrian office-based dermatologists. J Drugs Dermatol 2012; 11(5):574-8.
  24. Weiss ET, Brauer JA, Anolik R, et al. 1927-nm fractional resurfacing of facial actinic keratoses: a promising new therapeutic option. J Am Acad Dermatol 2012 Oct 2. [Epub ahead of print.]
  25. Togsverd-Bo K, Haak CS, Thaysen-Petersen D, et al. Intensified photodynamic therapy of actinic keratoses with fractional CO2 laser: a randomized clinical trial. Br J Dermatol 2012; 166(6):1262-9.
  26. Ostertag JU, Quaedvlieg PJ, Neumann MH, et al. Recurrence rates and long-term follow-up after laser resurfacing as a treatment for widespread actinic keratoses on the face and scalp. Dermatol Surg 2006; 32(2):261-7.
  27. JU, Quaedvlieg PJ, Neumann MH, et al. Recurrence rates and long-term follow-up after laser resurfacing as a treatment for widespread actinic keratoses on the face and scalp. Dermatol Surg 2006; 32(2):261-7.