1. WELCOME! Primary Care Update: A Practical Approach to Common Problems 1

2. Skin Cancers Robert A. Baldor, M.D. FAAFP Professor, Family Medicine and Community Health University of Massachusetts Medical School 2

3. Learning Objectives by the end of the session you will be able to recognize the precursor lesions and common features for skin cancers and understand primary care diagnosis and treatment modalities for these common skin cancers. 3

4. Predisposing Factors Fair skin Poor tanning ability Predilection to burn Excessive solar radiation exposure 4

5. Classification of Sun-Reactive Skin Types Blue eyes Red hair Gray eyes Blond hair Brown eyes & hair Brown/Black eyes & hair 5

6. Basal Cell Cancer (BCC) 6

7. Epidermis Junction Dermis Stratum corneum Keratinocytes Basal cells Melanocytes 7

8. Basal cell carcinoma (BCC) Most common form of skin cancer The most common of all cancers! 1 million Americans diagnosed annually Associated with childhood sunburns Sunscreens in later adulthood do not appear to prevent 8

9. Location Areas of chronic sun exposure Predilection for head (ears) and neck (90%) A persistent, non-healing sore But…. 9

10. A Reddish Patch or irritated area 10

11. A Shiny, pearly bump or nodule 11

12. A white, yellow or waxy scar-like area 12

13. Rodent ulcer 13

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15. Squamous Cell Cancer (SCC) Second most common skin cancer > 250,000 new cases annually Elderly (mean age 70 years) Common in sun exposed areas rim of ear, lower lip, face, bald scalp, neck, hands Occurs on all areas (mucous membranes, genitals) Skin with signs of sun damage pigmentation change, wrinkling,,loss of elasticity 15

16. Sun Damage and…. Environmental exposure – arsenic, radiation, petroleum products Smoking Inflammatory dermatosis Sunscreens are preventive 16

17. Epidermal Keratinocytic Atypia Actinic keratosis Bowen’s disease Squamous cell cancer 17

18. Epidermis Junction Dermis Stratum corneum Keratinocytes Basal cells Melanocytes 18

19. Actinic Keratosis UV light induced Circumscribed rough lesions Pinpoint to plaque (most 3-6 mms) Variety of colors May form horns Blend to background skin 19

20. Actinic Keratosis 20

21. Actinic Keratosis 21

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23. Precancerous Although < 20% transformed to SCC Slow process, very rare mets 23

24. Bowen’s Disease Erythematous plaque Sharp, irregular border Hyperkeratosis Erosions, ulcerations Not just sun exposed 24

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27. Bowen’s Disease Suspect in any persistent chronic plaque Confused with psoriasis or eczema May transform to SCC Treat like actinic keratosis 27

28. Squamous Cell Ca 28

29. Actinic keratosis Squamous Cell 29 Basal Cell

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31. Metastatic Potential 2-3% rate to regional nodes Local destruction 31

32. BC/SC Treatment Goals Remove cancerous tissues Preserve normal tissue Preserve optimal cosmetic result 32

33. Punch Biopsy 33

34. Shave biopsy 34

35. Office Treatment Modalities Electrodesiccation and curettage Cryotherapy Excision Topical agents 35

36. Curettage & Electrodesiccation Cure rates approaching surgical excision Not useful if in high-risk or difficult sites. No biopsy 36

37. Cryosurgery Freezing with liquid nitrogen x 2 Lesion scabs over; falls off within weeks Cure rates 85-90% No biopsy Not recommended for SCC – deeper portions of the tumor may be missed – scarring might obscure a recurrence. 37

38. Excision biopsy Remove the entire growth along with a thin margin of normal skin Cure rates around 90% Biopsy available 38

39. Topical treatment modalities 5-Fluorouracil 5% cream Imiquimod 5% cream Diclofenac 3% gel 39

40. 5-Fluorouracil (5-FU) FDA-approved for superficial BCC & AK Used to treat Bowen’s disease Cure rates 80-90 % BID for 3-6 weeks Normal skin minimally effected Significant Inflammatory response… 40

41. Imiquimod FDA-approved for superficial BCC & AK Used for treatment of Bowen’s disease 5X a week for 6 + weeks Stimulates the immune system 41

42. Diclofenac 3% gel FDA-approved for superficial BCC & AK BID x 2-3 months Less effective than 5-FU/Imiquimod 42

43. Referrals Radiation – Difficult surgical locations – Elderly in poor health Laser (Not FDA approved for BCC or SCC) Photodynamic therapy – for multiple BCC (not FDA approved) 43

44. Mohs Micrographic Surgery Saves the greatest amount of healthy tissue Highest overall cure rate — up to 99% For poorly demarcated & hard-to-treat tumors around the eyes, nose, lips, and ears. May require reconstructive closure 44

45. QUESTIONS ABOUT NON- MELANOTIC SKIN CANCERS??? 45

46. Melanoma The incidence has increased 690% since 1950 69,000 new cases of melanoma annually 8,700 deaths – 99% 5-year survival for localized disease – 15% 5-year survival for metastatic disease Genetic predisposition 46

47. Sites 83% arise de novo 80% trunk and extremities Most common site in men is the upper back Most common sites in women are the lower legs and upper back 47

48. A Moles Life cycle… 48 Simple Lentigo Junctional NevusCompound NevusIntradermal Nevus

49. epidermis dermis Epidermal/dermal junction melanocytes 49 Junctional Nevi change in adolescent years < 6 mms macules; sun exposed skin Simple Lentigo arise in childhood < 5 mms, round macule

50. epidermis dermis Epidermal/dermal junction melanocytes 50 Seen in early adulthood < 6 mms; macular, gradually elevate Smooth or rough surface (excess hair) Compound Nevi

51. epidermis dermis Epidermal/dermal junction melanocytes Intradermal Nevi Frequently disappear later in life A new mole that develops after the age of 40 is abnormal! 51

52. Halo Nevus 52

53. Solar Lentigo Uniformed tan to brown macules Sun damaged skin ‘Liver spots’ 53

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56. Seborrheic Keratosis Verrucal, warty, raised surface Brown to black Stuck on appearance, sharply demarcated Few mm to several cms Face, neck, trunk 56

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60. “I have a suspicious looking mole on my shoulder.” 60

61. Dysplastic Nevi Markers of MM prone individuals Precursor lesions 61

62. Dysplastic Nevus Syndrome Multiple heterogenous lesions Familial 62

63. Management Examine entire skin - watch scalp Biopsy worst looking lesion Patient education/sunscreens Follow up 3-12 months – Excise suspicious lesions 63

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65. Melanoma Evaluation Asymmetry Border Color Diameter 65

66. Asymmetry A line drawn through the middle will not create matching halves 66

67. Border Uneven scalloped or notched edges 67

68. Color Variable shades of brown or black hues of blue, grey, white, pink or red 68

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70. Diameter > 6 mm (pencil eraser) 70

71. Malignant Melanoma Superficial spreading melanoma (70%) Nodular melanoma (15%) Acrolentiginous melanoma (10%) Lentigo maligna melanoma (5%) 71

72. Superficial Spreading Melanoma 70% of all melanomas – most common type in light-skinned people Peak incidence 40-60 yrs Usually a mole changing slowly (1-5 years) Commonly affects areas with the greatest nevus density - upper backs & lower legs 72

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74. Characteristics SSM subtype usually has the classic early signs of melanoma (ABCDs) Borders are often very irregular Absence of pigmentation often represents regression of the melanoma 74

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77. Nodular Melanoma 2 nd most common subtype of melanoma (15% ) Median age at onset is 53 years A uniform blue-black, blue-red, nodule (E) Most common sites are trunk, head, and neck Usually begin in normal skin rather than in a preexisting lesion Rapid growth is a hallmark of nodular melanoma 77

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80. Acral lentiginous melanoma 10% of melanomas overall Most common types among Japanese, African, Latin, and Native Americans Median age 65 years; equal gender distribution. Palms or soles; beneath the nail plate – sole is the most common site in all races – not associated with sun exposure Average size at diagnosis is 3 cm (? delayed Dx) 80

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82. Lentigo maligna (melanoma in situ) Least common subtype (5% of all melanomas) Occurs on sun-damaged atrophic skin – Head & neck (nose and cheek most common) Median age at diagnosis is 65 years Usually quite large (3 to 6 cm or greater) A tan irregular macule that extends peripherally 1/3 rd progress to lentigo maligna melanoma Grow slowly for 5 -15 years before invading 82

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84. Treatment – Excision < 0.5 mm thick: 1 cm margin 0.5-1 mm thick: 1-2 cm margin 1 mm thick: 3 cm margin w/underlying fat/fascia <.76 mm thick: no mets - 99.5% 10 yr survival > 3 mm thick: 48% 10 yr survival 84

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86. DNA Damage UV light damages epidermal DNA Age related decline in ability to repair DNA 20-30 years of exposure for tumor development 86

87. Ultraviolet Radiation 87

88. Epidermis Junction Dermis Stratum corneum Keratinocytes Basal cells Melanocytes 88

89. Ultraviolet Light UVB causes sunburn and skin cancer UVA penetrates deeply, causing photo-aging (wrinkling, leathering, sagging) UVA exacerbate UVB carcinogenic effects and likely plays a role on it’s own Tanning Booths……. – Why pay for skin cancer, when you can get it for free! 89

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92. Photo aging treatment options Retin A – best evidence for improvement Sunscreens… 92

93. Sun Protection Factor (SPF) It takes 10 minutes for unprotected skin to start turning red, SPF 15 sunscreen prevents reddening 15 times longer — about 2 1/2hrs – SPF 15 blocks 93 % of incoming UVB rays – SPF 30 blocks 97 % – SPF 50 blocks 98 % 93

94. And for how long? no sunscreen is effective longer than 2 hours without reapplication So SPF-15 is good for 2.5 hours….. I recommend SPF-30 – every 2 hours 94

95. Sunscreens Vary in their ability to protect against UVA and UVB Usually 3 active ingredients… UVB absorption (eg PABA derivatives) UVA short-waves (b enzophenones ) Remaining UVA spectrum ( Parsol, zinc oxide) 95

96. New FDA labeling Change to UVB sunburn protection factor – Low protection (SPF 2-15) – Medium protection (SPF 15-29) – High protection (SPF 30-50) – Highest protection (SPF >50) Added 4-star rating for UVA protection – 1 star lowest to 4 stars highest protection 96

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