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May be associated with tuberous sclerosis if multiple
Lipoma
Benign fatty tumor that may be present at any age
Clinical presentation: painless, soft, flesh-colored nodule
Anatomic location: commonly found on the trunk and
extremities
Treatment: simple excision
Dermatofibrosarcoma protuberans
Appears in middle age.
Clinical presentation: reddish-brown, firm, slow-growing
nodular plaque.
Anatomic location: more commonly found on trunk,
extremities.
*Treatment is radical excision (>3 cm margins) given
locally aggressive behavior.
Local recurrence is common; however, metastasis is
rare.
Neurofibroma
Composed of Schwann cells and endoneurial fibroblasts.
May appear at any age.
Clinical presentation: soft, flesh-colored or pink nodules;
button-hole sign (invaginate when compressed).
Anatomic location: more common on the trunk and
extremities.
Treatment: observation, excision.
Multiple neurofibromas may be associated with
neurofibromatosis type I or II.
*Type I—café au lait spots, Lisch nodules (iris
hamartomas), and optic nerve glioma
Type II—bilateral acoustic neuroma
OTHER DISORDERS
Calciphylaxis
Metastatic calcification of blood vessels and necrosis of
surrounding tissue
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Associated with renal failure; may appear at any age; more
common in women
Clinical presentation: painful necrotic ulcerations; red-blue
mottling of skin (livedo reticularis)
Anatomic location: fat-bearing locations on trunk and
extremities
Treatment: pain control, correct underlying electrolytes,
intravenous sodium thiosulfate, or excision (although
relatively contraindicated as often results in progressive
calcification)
Hidradenitis Suppurativa
Clinical presentation: chronic inflammation of apocrine
sweat glands, which can progress to chronic draining sinus
tracts and abscesses
Anatomic location: most commonly the axillae, breasts,
perineum, and buttocks.
Treatment: topical clindamycin, oral or IV antibiotics,
biologics (TNF-alpha inhibitors), wide local excision and
skin grafting, unroofing
Dystrophic Epidermolysis Bullosa
Hereditary disease with bulla formation of skin/mucosa
following minor trauma
May result in encasement of digits with scar tissue
Treatment: scar release/Z-plasty, topical steroids,
avoidance of trauma
Cutis Laxa
Defect in elastic fibers; wound healing unaffected.
Skin hangs loose from folds; premature aging.
Blepharoplasty and face lift can be beneficial.
Pseudoxanthoma Elasticum
Affects elastic fibers and collagen; wound healing is normal.
Skin thickens and appears cobblestoned; later becomes
wrinkled and lax.
Ehlers-Danlos Syndrome (Cutis Hyperelastica)
Autosomal recessive or x-linked causing genetic defects in
collagen.
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Hyperextensible skin, severe joint laxity, delicate blood
vessels.
*Wound healing is abnormal: approach surgery with
caution.
Acne Vulgaris
Appears in younger patients.
Clinical presentation: comedones, inflammatory papules,
deep-seated cysts.
Anatomic location: face.
Treatment: topical retinoids, topical and oral antibiotics and
oral isotretinoin (accutane). Isotretinoin—risk of birth
defects; patients must have two forms of contraception.
Avoid if planning aesthetic facial rejuvenation with lasers or
peels.
Rosacea
Clinical presentation
Facial flushing (increased vascularity), thickened skin
erythema, telangiectasia
Acne rosacea (papules and pustules)
Rhinophyma—nasal skin becomes erythematous with
telangiectatic changes
Anatomic location: affects forehead glabella, malar region,
nose, chin
Treatment: oral antibiotics, retinoic acid, dermabrasion,
cryotherapy, laser (CO2), tangential excision (for
rhinophyma)
Reconstruct with secondary contraction vs skin graft
Pyoderma Gangrenosum
Clinical presentation: superficial abscesses with significant
ulceration and skin necrosis.
Consult dermatology for biopsy to evaluate, although a
diagnosis of exclusion.
Treatment: systemic corticosteroids, immunosuppressants.
Given pathergy, avoid surgery, debridement or skin grafts
(can induce PG at donor sites).
*Associated with IBD—refer to gastroenterologist for
endoscopy.
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SKIN MALIGNANCIES
Generally grouped into three types
Basal cell carcinoma (BCC) > squamous cell carcinoma
(SCC) > melanoma.
The ratio of BCC to SCC to melanoma is ≈40:10:1.
Incidence of all three types is increasing; fortunately, the
more common types (BCC and SCC) are far less
aggressive than melanoma.
More than 20% of the U.S. population develops a skin
cancer during their lifetime.
There are more skin cancers in the U.S. population than all
other cancers combined.
BASAL CELL CARCINOMA
EPIDEMIOLOGY
Incidence
BCC is the most common skin cancer, accounting for ≈80%
of all skin cancers.
Roughly 3.6 million new cases per year in the United
States.
Risk Factors
UV exposure (eg, PUVA) or ionizing radiation, fair skin,
chemical exposure (eg, arsenic), immunosuppression
(transplant patients), nevus sebaceus
Syndromes associated with BCC
Basal cell nevus syndrome (Gorlin syndrome)
Autosomal-dominant inheritance
Palmoplantar cysts, early-onset BCCs, jaw cysts
(odontogenic keratocysts), skeletal anomalies,
medulloblastomas, fibromas (ovarian and cardiac)
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Xeroderma pigmentosum (XP): patients have
increased incidence of BCC, SCC, and malignant
melanoma (see below in melanoma section).
Autosomal recessive disorder affecting DNA repair
Treatment: avoidance of sunlight, isotretinoin, 5-
fluorouracil, or excision
BCC DISEASE BIOLOGY AND
CHARACTERISTICS
Basal keratinocytes are the cell of origin, residing in the basal
layer of the epidermis at the dermoepidermal junction.
No universal clinical precursor lesion.
BCC is most common in areas with high concentrations of
pilosebaceous follicles and thus >90% are found on the head
and neck.
Metastasis is rare.
Morbidity is caused by invasion of the tumor into underlying
structures, including the sinuses, orbit, and brain. Typically, only
a problem if neglected for many years.
Types of BCC
Nodular BCC
The most common type, usually presenting as a single
lesion consisting of pearly papules with telangiectasias,
pruritus, and occasional bleeding.
Lesion breakdown over time leads to nodulo-ulcerative
BCC (“rodent ulcer”).
Histology demonstrates palisading nuclei.
Superficial spreading BCC
Slow-growing, erythematous, minimal induration, and
located primarily on the trunk.
It is easily confused with other scaly, eczematous
dermatoses.
Shallow lesions with horizontal growth pattern; can
become invasive.
Morpheaform (sclerosing, fibrosing) BCC
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Flat, scarlike, white to yellow to pink plaque with scale,
erosion.
The true extent of the lesion is usually greater than the
clinical appearance.
High incidence of recurrence or incomplete excision
due to “fingerlike” extensions.
Margins of 1 cm or Mohs surgery is warranted.
Pigmented BCC: similar to nodular BCC; easily confused
with melanoma due to its deep pigmentation and nodularity.
Adnexal BCC
Uncommon and found in older individuals.
Tumors arise from sweat glands, and although they
exhibit slow growth, they are locally invasive, with a
high incidence of local recurrence.
TREATMENT OF BCC
Standard Surgical Techniques: ≈95% cure rate
Wide local excision of BCC: 3- to 5-mm margins
Frozen sections may be used to confirm negative
margins intraoperatively. False negatives are common.
Surgeon must have confidence in
pathologist/laboratory.
Mohs surgery: sequential horizontal excision with
immediate frozen section testing by dedicated Mohs
dermatopathologist; ~99% cure rate for primary BCC.
*Indications include morpheaform BCC and/or
lesions in aesthetically sensitive areas (nose,
eyelid, lip, etc.).
Advantages are tissue preservation and confirmation of
complete excision.
Field Therapies
Curettage and electrodessication can be used for
superficial, low-risk BCCs.
Cryotherapy, PDT, topical imiquimod, or fluorouracil if poor
surgical candidate.
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Radiation is effective but requires multiple visits. High cure
rates (≈90%), but recurrence is relatively common many
years (10-15) later.
Topical Pharmaceuticals
Imiquimod: immune stimulant. FDA approved only for
superficial BCCs, with cure rates between 80% and 90%.
The 5% cream is applied 5 times per week for 6 weeks or
longer.
5-Fluorouracil (5-FU): chemotherapy. FDA approved for
superficial BCCs, with similar cure rates to imiquimod. Five
percent liquid or ointment is rubbed onto the tumor 2 times
per day for 3-6 weeks.
Adjuvant Radiation Therapy (after surgery): useful for
advanced, deeply invasive BCC
Metastatic Disease: rare, can treat with SMO inhibitors
(vismodegib or sonidegib)
SQUAMOUS CELL CARCINOMA
EPIDEMIOLOGY
Incidence
Second most common skin cancer after BCC
Roughly 1.8 million new cases annually in the United States
Risk Factors
UV exposure (eg, PUVA) or ionizing radiation, fair skin,
chemical exposure (eg, arsenic), immunosuppression
(transplant, HIV), viral infection (HPV, HSV), Marjolin ulcer:
SCC arising in a chronic wound (ie, chronic burn scars and
pressure sores) secondary to genetic changes caused by
chronic inflammation
Syndromes: xeroderma pigmentosum, oculocutaneous
albinism, dystrophic EB
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SCC DISEASE BIOLOGY AND
CHARACTERISTICS
Precursor Lesions
Actinic keratoses (AKs, or solar keratoses)—risk of
malignant transformation is ~10%.
Erythematous macules and papules with coarse,
adherent scale.
Histologically resembles SCC in situ (premalignant).
Bowen disease (SCC in situ)
Exhibits full-thickness cytologic atypia of the
keratinocytes.
Erythroplasia of Queyrat is SCC in situ of the glans
penis.
Leukoplakia: white patch on oral or other mucosa;
malignant transformation in 15%.
Keratoacanthoma: resembles SCC, rapid growth followed
by involution.
Types of SCC
Verrucous carcinoma (well-differentiated SCC): slow-
growing; exophytic; less likely to metastasize; found on
plantar feet, genitalia or in oral cavity.
Ulcerative SCC: grows rapidly and is locally invasive.
Ulcerative SCC has very aggressive growth
characteristics, raised borders, and central ulceration.
Around <50% 5-year survival if spread to lymph nodes
in the head and neck.
Marjolin ulcer: arises within chronic wound or scar (burn,
ulcer or fistula tracks).
SCC TREATMENT OPTIONS
Standard Surgical Techniques: 90%-95% cure rates; similar
to BCC options
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Wide local excision of SCC: 4- to 6-mm margins are
usually sufficient. Frozen sections may be used to confirm
negative margins intraoperatively.
If <2 cm, low grade and extends to dermis, 4-mm
margin
If >2 cm, grade 2-4, high risk or extension into fat, 6mm margin
Mohs surgery: sequential horizontal excision with frozen
section testing. Highest cure rate for SCC: ~97%
Indications include recurrent, high-risk SCC, and/or
lesions in aesthetically sensitive areas (nose, eyelid,
lip, etc.).
Advantages are tissue preservation and confirmation of
complete excision.
Field Therapies
Curettage, electrodessication, and cryotherapy are less
used SCC treatment than in BCC due to risk of missed
deep tumor portions and scarring obscuring SCC
recurrences.
Radiation is reserved for unresectable lesions or for the
very elderly. Cure rates vary widely. Must consider cosmetic
damage and long-term risks.
Management of Nodal Disease
SLN biopsy: considered for high-risk SCC without palpable
nodes (controversial).
Aggressive resection indicated for histologically positive
(palpable) lymph nodes.
Adjuvant Radiation Therapy: postexcision for high-risk
cutaneous SCC or if positive nodes
Chemotherapy: cisplatin alone or combined with 5-FU or EGFR
inhibitors
Immunotherapies: cemiplimab (PD-1 inhibitor) FDA approved
for metastatic SCC
MELANOMA
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EPIDEMIOLOGY
Incidence is increasing, faster than any other cancer in
Western world.
A total of 106 000 new cases diagnosed in the United
States in 2021; annual increase ~3%-7%.
Less than 1% of all skin cancers, but cause majority of skin
cancer-related deaths.
Prognosis of metastatic disease has doubled since 2004
given treatment advancements.
Five-year risk of developing a second melanoma following
primary is 8%.
Median age of diagnosis is 65.
Risk Factors: genetics, personal or family history of melanoma,
history of UV exposure (both UVA and UVB), indoor tanning,
blistering burns, fair skin (Fitzpatrick I and II) (Table 7-1) and red
hair, large number nevi and/or lentigines, immunosuppression.
TABLE 7-1 Fitzpatrick Classification of Skin Type
Race: incidence is lower, but prognosis is worse for African-
Americans, due to delayed diagnosis and/or worse disease
subtype.
Family History: vast majority of melanomas are sporadic;
however, some hereditary forms exist (see also Genetics
section below).
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