1. Dermatology for Primary Care:
Recognizing Common Skin Tumors
Albert G. Caruana Jr., MD
Resident’s Conference
April 23, 2004
Presbyterian Hospital of Dallas

2. Acrochordon
Have various names: fibroepithelial polyp, skin tag, squamous papilloma.
Oval skin excrescence on a broad or narrow stalk, can be brown or flesh colored.
A pedunculated tumor.
Occur more frequently in obese patients.
Location: axilla (48%), neck (35%), also inguinal region.
Majority of patients (78%) have less than 3 lesions per area.
They begin to appear after 2nd decade of life.
They cease growing after the 5th decade of life.

3. Acrochordon
Composed mainly of loose fibrous tissue (like superficial dermis), covered by thin layer of epidermis.
They are benign.
Can be irritating to patients (caught in clothes and jewelry).
Treatment:
Can be snipped off by scissors
electrocautery

4. Acrochordon
Acrochordon: “skin tags.” Round, black-colored, fleshy excrescences on a
broad or narrow stalk (left). Clustering of lesions, the groin here, is common
in patients with obesity.

5. Acrochordon
Acrochordon: “skin tags.” Can present on or around the eyelid (left) or often
in the axilla (right). Axilla and neck are most common locations.

6. Seborrheic Keratosis
The most common benign skin neoplasm. No malignant potential.
Origin is unknown.
Become more frequent as we age.
Diagnosis is easy to make clinically, biopsy is usually not necessary.
Study has shown clinical diagnostic accuracy of 99% by dermatologists.
Tend to occur on trunk most often, but can appear on head and extremities.
Lesions contained entirely in epidermis, treat with cryosurgery or curettage.

7. Seborrheic Keratosis Appearance:
Size can range from 0.2 to 3.0 cm in diameter.
Can have smooth surface or be rough and cracked.
Characteristic “stuck-on” appearance.
Color can be tan, brown, or black.
The height of the lesion can vary.
Can resemble melanoma (SK has uniform surface appearance).
Key to visual diagnosis is identification of horn cysts
Black or pearly-white cysts either embedded in or on the surface of the lesion.
These are dilated follicular ostia filled with keratin.

8. Seborrheic Keratosis
Seborrheic Keratoses: tend to occur in sun-exposed areas. These patients
have many on the back, but none on the buttocks.

9. Seborrheic Keratosis
Seborrheic Keratosis: May be flat with some scale (left) or
raised (right) with deep cracks.

10. Seborrheic Keratosis
Seborrheic Keratosis: have characteristic horn cysts. They can
be white and deeper seated (left) or black and superficial (right).

11. Seborrheic Keratosis
Seborrheic Keratoses: flat lesions are often brown, can often form near hairline
(left). They also commonly can be found under the breasts, where they can
Become red and macerated (right).

12. Seborrheic Keratosis: Melanoma Look-Alikes
Seborrheic Keratosis: Has dark pigmentation, irregular borders, and
some variation of color, but horn cysts help to make diagnosis clinically.

13. Seborrheic Keratosis: Melanoma Look-Alikes

14. Seborrheic Keratosis Inflammed SK’s:
Have swollen and irregular borders.
Develop an erythematous base.
Can develop nummular dermatitis around edges.
Common in intertriginous areas where skin is macerated.
Itching
Develop inflammation around other SK’s that are not mechanically aggravated.
Severely affected lesions can appear like oozing, red masses with a friable surface. Confused with melanoma or pyogenic granuloma.
Treat with topic steroids or remove all lesions.

15. Seborrheic Keratosis: Inflammed SK’s
Seborrheic Keratosis: Often only one lesion is inflammed, but many can
become inflamed at once (left). This lesion has minimal inflammation
at the base (right).

16. Seborrheic Keratosis: Inflammed SK’s
Seborrheic Keratosis: As inflammation worsens, scale may obscure
typical features (left). With severe inflammation, mass may ooze
And lose all typical features (right).

17. Dermatosa Papulosa Nigra
Multiple brown to black dome-shaped papules.
Occur on face of young to middle-aged African Americans.
Thought to be a type of seborrheic keratosis.

18. Keratoacanthoma A common benign epithelial tumor.
Thought to be a variant of squamous cell carcinoma.
Unknown etiology.
Incidence 104 per 100,000.
Mean age of onset is 64 years. Disease of elderly.
Seasonal association implies role of UV radiation in development.
Will appear on sun-exposed areas most commonly, followed by the trunk.
Also develops at sight of previous trauma.
Most rapidly grow and eventually regress.
There are rare variants (2%) which are destructive.

19. Keratoacanthoma Appearance & Natural History:
Rapid growth phase: starts as a small domed-shape papule that may mimic molluscum contagiosum.
Will progress in weeks to grow 1-2cm and often develop a central keratin-filled crater with crusting.
Untreated, will stop growing in about 6 weeks
Stable phase: will remain unchanged for a variable length of time.
Regression phase: will diminish in size, eventually disappearing, leaving behind a scar. Often regresses in 2 to 12 months.

20. Keratoacanthoma
Can be difficult to distinguish from squamous cell carcinoma (particularly nodular SCC).
This lesion retains a smooth surface, unlike SCC.
This can be treated medically or surgically, as it is a scarring lesion.
Large KA on face may require Mohs’ surgery.
Medical therapy options:
5-FU creams (Efudex, Carac). Remove crust prior to application or pretreat with a 40% urea cream (Vanamide). Response in 1-6 wks.
5-FU intralesional injection. Less efficacious on slow growing lesions.
Intralesional methotrexate. Treat monthly.
Imiquimod (Aldara) – QOD for weeks.

21. Keratoacanthoma
Keratoacanthoma: smooth, dome-shaped papules or nodules, often with a
central keratin plug.

22. Dermatofibroma Common benign lesion.
Most commonly occur on anterior surface of legs.
Fibrous reaction to insect bite, truama, viral infection.
Can be asymptomatic, painful, or slightly pruritic.
Raised, pink or brown papule.
Can be hard, scaly.
“Dimpling test”
Will retract beneath the skin surface when compressed.

23. Sebaceous Hyperplasia
Common small tumors of enlarged sebaceous glands.
Start as pale, yellow papules on forehead, cheeks, nose.
Develop telangectasias and central umbilication.
Occur after age 30 in 25% of the population.
May look like BCC. But lesions of SH are soft to palpation.
Can express sebum.
Treated with electrocautery.

24. Actinic Keratosis Also called solar keratosis.
Squamous cell carcinoma confined to the epidermis.
Commonly thought of as a “pre-cancerous” lesion.
Induced by sun-exposure, years of cumulative exposure are required.
Lesions increase with age.
Can spontaneously regress if sun-exposure is removed.
Lesions have increased vascularity (erythematous).
Develops adherent white or yellowish scale.
Can bleed if picked.
Many lesions are more readily identified by rough texture than appearance.

25. Actinic Keratosis
Actinic Keratosis: classic appearance with scale and crust on an
erythematous base (left). Many AKs on the face, the surrounding
skin has irregular pigmentation and some dilated vessels (right).

26. Actinic Keratosis
Actinic Keratosis: Larger lesions may have significant depth (left).
Large lesions like this one may take years to develop (right).

27. Actinic Keratosis
Can progress to SCC: intra-epithelial lesion spreads to involve the papillary or reticular dermis.
Risk of transformation is 0.085% per lesion per year.
60% of SCC develop from actinic keratosis.
AK can be difficult to distinguish from SCC, particularly thickened hypertrophic AK’s.
Worrisome signs: induration, oozing, inflammation.
Clinical variants:
Cutaneous horn
Spreading pigmented AK (can resemble SK or melanoma)
Actinic chelitis (scaling, red lesion on lower lip with cracking or ulceration).

28. Actinic Keratosis
Actinic Keratosis: thicker lesions can develop into squamous cell
carcinoma (left). AK’s can often clinically appear like SCC (right).

29. Actinic Keratosis: Pigmented AK’s
Pigmented Actinic Keratosis: Can resemble a scaling lentigo, a
SK, or a melanoma in some cases.

30. Actinic Keratosis Treatment: Regular use of sunscreen is essential.
Cryosurgery is preferred since this method separates epidermis from the dermis. It may leave hypopigmented lesions.
For many lesions, topical 5-FU therapy may be preferred.
Incorporated into rapidly growing cells, causing cell death. Normal cells unaffected.
Duration of therapy depends on location (2-8 weeks).
Treatment causes marked inflammation in phases:
Early inflammatory phase (erythema)
Late inflammatory phase (burning, edema, stinging, oozing)
Lesion disintegration phase (erosion, ulceration, eschar formation, re-epithelialization)

31. Actinic Keratosis: Treatment
Actinic Keratosis: Treatment with topical 5-FU follows a predictable clinical progression of inflammation of lesions. Right: 3 weeks after starting treatment.

32. Basal Cell Carcinoma Most common type of skin cancer.
Commonly presents as recurring bleeding or scabbing wound.
Can occur at any age, but most common after age 40.
Locally invasive, aggressive, and destructive.
Limited capacity to metastasize.
Often occurs in areas not sun-exposed (behind ears, medial canthus).
Weaker causal relationship with UV exposure than SCC.
85% located on head and neck, 25-30% on the nose alone.
Tumor arises from basal keratinocytes and the surrounding adnexal structures (hair follicles, eccrine sweat ducts).

33. Basal Cell Carcinoma Nodular BCC:
Progression unpredictable: long periods of stability followed by rapid progression or regression.
Clinical types: nodular, pigmented, sclerosing, superficial.
Nodular BCC:
Most common type of BCC.
Pearly-white or pink, dome-shaped papule.
They may be flat.
Often has telangectasia.
Center may ulcerate, bleed, and develop crust and scale (“rodent ulcer”).
Any non-healing ulcer that fails to respond to treatment should be biopsied to rule out BCC.

34. Basal Cell Carcinoma
Classic appearance of nodular BCC: pink or pearly dome shaped papules
with telangectasias.

35. Basal Cell Carcinoma
Nodular BCC: “Rodent-Ulcer” with central scaling and crusting.

36. Basal Cell Carcinoma Nodular BCC: small lesions can be easy
To miss on physical exam.
Nodular BCC: On leg. Consider when
A chronic ulcer fails to improve with
therapy.

37. Basal Cell Carcinoma Pigmented BCC: Sclerosing (Morpheaform) BCC:
Contains melanin.
May resemble melanoma or seborrheic keratosis.
Look for pearly-white, transluscent borders.
Sclerosing (Morpheaform) BCC:
Innocuous surface appearance which can mask deep and wide extension.
Pale-white to yellow, waxy, firm, flat to slightly-raised.
Can look like localized scleroderma.
Borders are indistinct.
Requires wide excision.

38. Basal Cell Carcinoma
Pigmented BCC: Can have variable amounts of melanin. Look for elevated,
Pearly-white borders.

39. Basal Cell Carcinoma
Sclerosing (morpheaform) BCC: flat, firm, waxy, resembling a scar or
localized scleroderma

40. Basal Cell Carcinoma Superficial BCC: Least aggressive variety.
Most often seen on trunk or extremeties.
Can occur on the face.
Well-circumscribed, oval to round, red and scaling plaque.
Tend to bleed easily.
May resemble eczema or psoriasis.
Examine borders, which will be raised and pearly-white.
Tension on surrounding skin may make border characteristics more obvious.

41. Basal Cell Carcinoma
Superficial BCC: well circumscribed, with raised pearly-white borders, red,
scaly, and sometimes resembling eczema.

42. Basal Cell Carcinoma
Treatment Algorithm:

43. Mohs’ Micrographic Surgery

44. Squamous Cell Carcinoma
Unlike BCC, these lesions have significant chance of metastasis.
Risk Factors: childhood sun exposure, blistering sunburns, light skin, outdoor occupations, freckling, hazel/blue eyes.
UV radiation is involved in the pathogenesis of SCC.
Found in sun-exposed areas (scalp, back of hands, pinna).
Actinic keratosis is most common precursor lesion.
Capacity for metastasis related to lesion size and location.
Thickness of lesion best predictor:
One study found recurrent tumors always at least 4mm thick and all fatal tumors at least 10mm thick.
Surgical margins 2-4mm depending on grade.

45. Squamous Cell Carcinoma
A nodular lesion that had been previously treated with cryotherapy.
A red, keratotic papule with
surface scale. Resembles AK.

46. Squamous Cell Carcinoma
SCC on the lip of a patient who has spent years working outdoors.

47. Squamous Cell Carcinoma
Treatment Algorithm

48. Malignant Melanoma
Malignancy of melanocytes with high metastatic potential.
Increasingly common: incidence in Caucasians has tripled in last 40 years.
Lifetime risk in 1987 was 1 in By 2010 will be 1 in 50.
Incidence in African Americans 1/20 that of Caucasians, in Hispanics, 1/6.
Causes 75% of cancer deaths in the United States.
Median age of diagnosis is 53.
Significant association with UVA exposure ( nm).
Risk highest to those that tan poorly and get intermittent sun exposure.
Four major clinical subtypes: superficial spreading, lentigo maligna melanoma, nodular, acral-lentiginous melanoma.

49. Malignant Melanoma: Risk Factors
(Greatly Increased Risk)
Risk Status:
Relative Risk:
History of atypical moles, family hx of MM, having more than moles 35
Previous Nonmelanoma skin cancer 17
Congenital Nevus (>20cm)
5-15
History of previous melanoma
9-10
Family hx of melanoma in first degree relative 8
Immunosuppression
6-8

50. Malignant Melanoma: Risk Factors
(Moderately Increased Risk)
Risk Status:
Relative Risk:
Atypical nevi (2-9)
5-7
Many nevi (50-100)
3-5
Many nevi (26-50)
Chronic tanning with UVA (including PUVA for psoriasis)
5.4

51. Malignant Melanoma: Risk Factors
(Mildly Increased Risk)
Risk Status:
Relative Risk:
Repeated Blistering Sunburns:
Three Events
3.8
Two Events
1.7
Freckling
3.0
Fair skin, inability to tan
2.6
Red or blonde hair
2.2
Single atypical nevus
2.3

52. Malignant Melanoma: Recognizing Suspicious Nevi
The evolution of the benign mole (acquired nevi):
Lentigo simplex (freckle)
Pigmented junctional nevus (flat)
Pigmented compound nevus (elevated)
Flesh-colored intradermal nevus (more elevated)
This occurs over decades

53. Malignant Melanoma: Recognizing Suspicious Nevi
The ABCD’s of moles:
Asymmetry
Borders
Scalloped edges
Color
Uneven pigmentation
Various shades brown, black, red
Diameter
Greater than 6mm

54. Malignant Melanoma: Recognizing Suspicious Nevi
Sign:
Implication:
Changes in Color
Sudden darkening (brown or black)
Increased number of tumor cells, with varying density (and thus pigmentation)
Spread of color onto previously normal skin
Tumor cells migrating through epidermis (horizontal spread)
Red color
Vasodilation and inflammation
White color
Areas of regression, inflammation (hypopigmentation) or even “halo” effect
Blue color
Pigment deep in the dermis, a sign of increasing depth of tumor

55. Malignant Melanoma: Recognizing Suspicious Nevi
Sign:
Implication:
Changes in Borders
Irregular outline (scalloping)
Malignant cells migrating horizontally at different rates
Satellite pigmentation
Malignant cells migrating past borders of the primary tumor
Development of halo
Destruction of the melanocytes by immunologic reaction and inflammation
A halo nevus.

56. Malignant Melanoma Superficial Spreading Melanoma (SSM)
Comprises 70% of melanomas.
More immature histologically than lentigo maligna.
Rapid phases of radial growth and regression.
Most common in 4th to 5th decade of life.
Can occur anywhere on body.
Most common on back of either sex or the legs of women.
Known for random combinations of colors.
Color becomes more varied as time progresses.
Radial growth phase can last months to years.
Nodules can appear as lesion get larger than 2.5cm

57. Malignant Melanoma Superficial Spreading Melanoma (SSM)
SSM: note irregular borders and varied color patterns. There are
also white areas of tumor regression.

58. Malignant Melanoma Superficial Spreading Melanoma (SSM)
SSM: Angular notching occurs as tumor regresses. These later
lesions show thickened areas that imply vertical growth phase.

59. Malignant Melanoma Nodular Melanoma (NM)
Comprises 15-20% of melanomas.
Poorly-differentiated histologically. Does not respect histologic boundaries of skin.
Male to female ratio 2:1.
Most often dark brown, red-brown, red-black.
Can be amelanotic (1.8-8% of NM).
Dome-shaped, polypoid, or pedunculated.
Most common on trunk and legs.
Most commonly mis-diagnosed subtype (mistaken for hemangioma, dermatofibroma, dermal nevus).
Often ulcerates and bleeds.

60. Malignant Melanoma Nodular Melanoma (NM)
NM: Thickened nature of lesions reveal its tendency for vertical
growth. Color may vary.

61. Malignant Melanoma Nodular Melanoma (NM)
NM: Often ulcerate and bleed. Note the amelanotic (flesh-colored)
lesion pictured to the right.

62. Malignant Melanoma Lentigo Maligna Melanoma (LMM)
Comprises 4-15% of melanomas.
Presents in 6th to 7th decades of life.
Radial growth phase called lentigo maligna (Hutchinson’s Freckle), which may last for years.
Some LM never progress.
Risk of progression related to age:
For 45yo patient, lifetime risk of progression 4.7%.
For 65yo patient, lifetime risk of progression 2.2%.
Tend to have bizarre shape from years of growth and regression.
Nodules do not develop until lesions as large as 5-7cm.

63. Malignant Melanoma
Lentigo Maligna Melanoma (LMM)

64. Malignant Melanoma
Lentigo Maligna Melanoma (LMM)

65. Malignant Melanoma Acral Lentiginous Melanoma (ALM)
Comprises 2-8% of melanomas for Caucasians, but 30-75% for Hispanics, African Americans, and Asians.
Most often seen in males over age 60.
Appears on palms of hands, soles of feet (most common), mucous membranes, or terminal phalanges.
Grows slowly over years.
Similar presentation to LM and LMM.
These tend to be flat and are ignored by patients early on. Can be deeply invasive.
Usually presents late when nodule forms. Poor prognosis.
Hutchinson’s sign: pigmented band at proximal nail fold.

66. Malignant Melanoma Acral Lentiginous Melanoma (ALM)
ALM: Most commonly presents on sole of foot in non-whites.
Looks like LM or LMM.

67. Malignant Melanoma Acral Lentiginous Melanoma (ALM)
ALM: Pigmented band starting at proximal nail fold is called
Hutchinson’s sign. Can have peri-ungual spread (right).

68. Malignant Melanoma Treatment

69. Malignant Melanoma Treatment

70. References
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Fitzpatrick T. Johnson R.A. Wolf K. Color Atlas and Synopsis of Clinical Dermatology: Common and Serious Diseases. Third Edition, 1997 McGraw-Hill.
Habif: Clinical Dermatology, 4th ed., 2004 Mosby, Inc.
Vargo N. Basal cell and squamous cell carcinoma. Seminars in Oncology Nursing. 19(1):12-21, 2003 Feb.
Wong CS. Strange RC. Lear JT. Basal cell carcinoma. BMJ. 327(7418):794-8, 2003 Oct 4.