Basal Cell Carcinoma
Author: Michael L Ramsey, MD, Director, Mohs Surgery Fellowship, Co-Director, Procedural Dermatology Fellowship, Department of Dermatology,
Geisinger Medical Center
Coauthor(s): Lindsay Dane Sewell, MD, Staff Physician, Department of Dermatology, Geisinger Medical Center
Contributor Information and Disclosures
Updated: Sep 11, 2009
Introduction
Background
Basal cell carcinoma (BCC) is the most common malignancy in humans. It typically occurs in areas
of chronic sun exposure. BCC is usually slow growing and rarely metastasizes, but it can cause
clinically significant local destruction and disfigurement if neglected or inadequately treated.
Prognosis is excellent with proper therapy.
Pathophysiology
Many believe that basal cell carcinomas (BCCs) arise from pluripotential cells in the basal layer of
the epidermis or follicular structures. These cells form continuously during life and can form hair,
sebaceous glands, and apocrine glands. Tumors usually arise from the epidermis and occasionally
arise from the outer root sheath of a hair follicle, specifically from hair follicle stem cells residing
just below the sebaceous gland duct in an area called the bulge.
The patched/hedgehog intracellular signaling pathway plays a role in both sporadic BCCs and in
nevoid BCC syndrome (Gorlin syndrome). This pathway influences differentiation of a variety of
tissues during fetal development. After embryogenesis, it continues to function in regulation of cell
growth and differentiation. Loss of inhibition of this pathway is associated with human malignancy,
including BCC.
The hedgehog gene encodes an extracellular protein that binds to a cell membrane receptor
complex to start a cascade of cellular events leading to cell proliferation. Of the 3 known human
homologs, Sonic hedgehog (SHH) protein is the most relevant to BCC. Patched (PTCH) is a
protein that is the ligand-binding component of the hedgehog receptor complex in the cell
membrane. The other protein member of the receptor complex, smoothened (SMO), is responsible
for transducing hedgehog signaling to downstream genes.1,2
When SHH is present, it binds to PTCH, which then releases and activates SMO. SMO signaling is
transduced to the nucleus via Gli. When SHH is absent, PTCH binds to and inhibits SMO.
Mutations in the PTCH gene prevent it from binding to SMO, simulating the presence of SHH . The
unbound SMO and downstream Gli are constitutively activated, thereby allowing hedgehog
signaling to proceed unimpeded. The same pathway may also be activated via mutations in the
SMO gene, which also allows unregulated signaling of tumor growth. How these defects cause
tumorigenesis is not fully understood, but most BCCs have abnormalities in either PTCH or SMO
genes. Some even consider defects in the hedgehog pathway to be requirements for BCC
development.
UV-induced mutations in the TP53 tumor suppressor gene, which resides on band 17p13.1, have
been found in some cases of BCC.3 Activated BCL2 (an antiapoptosis proto-oncogene) also is
commonly found in BCCs and may be detected immunohistochemically.
Frequency
United States
The annual incidence of basal cell carcinoma (BCC) is approximately 900,000 cases (550,000 in
men, 350,000 in women). The age-adjusted incidence per 100,000 white individuals is 475 cases
in men and 250 cases in women. The estimated lifetime risk of BCC in the white population is 3339% in men and 23-28% in women.
Mortality/Morbidity
Basal cell carcinoma (BCC) can cause clinically significant morbidity if allowed to progress.
Because this cancer most commonly affects the head and neck, cosmetic disfigurement is not
uncommon. Loss of vision or the eye may occur with orbital involvement. Perineural spread can
result in loss of nerve function and in deep and extensive invasion of the tumor. These neoplasms
are often friable and prone to ulceration; thus, they provide a nidus for infection. Death from BCC
is extremely rare.
Race
Basal cell carcinoma (BCC) is generally a disorder of white individuals, especially those with fair
skin. It is rare in dark-skinned individuals.
Sex
The male-to-female ratio for basal cell carcinoma (BCC) is approximately 3:2.
Age
Basal cell carcinoma (BCC) most commonly occurs in adulthood, especially in elderly persons.
Clinical
History
Basal cell carcinoma (BCC) patients often present with a nonhealing sore of varying duration. The
lesions are typically seen on the face, ears, scalp, neck, or upper trunk. Mild trauma, such as face
washing or drying with a towel, initially may cause bleeding. A history of chronic recreational or
occupational sun exposure is commonly elicited. Intense sun exposure often occurred in childhood
or young adulthood.
Physical
Several clinical and histologic subtypes of basal cell carcinoma (BCC) may exhibit different
patterns of behavior. Recognizing the various types is important because aggressive therapy is
often necessary for variants such as micronodular, infiltrating, or morpheaform BCC. When one
examines possible skin cancers, the best plan is to use good lighting and magnification. The
affected skin should be stretched, squeezed, and palpated to best estimate the size and depth of
the tumor. Oblique illumination of the tumor can highlight surface changes, such as a rolled border.
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Nodular BCC: This is the most common variety of BCC. Nodular BCCs most commonly
occur on the head, neck, and upper back. They may have some of the following features:
o Waxy papules with central depression (see Media File 2)
o Pearly appearance
o Erosion or ulceration
o Bleeding
o Crusting
o Rolled (raised) border (see Media Files 4-5)
o Translucency
o Telangiectases over the surface
o History of bleeding with minor trauma
Nodular basal cell carcinoma appearing as a waxy, translucent papule with central depression and a few small
erosions.
Scale, erythema, and a threadlike raised border are present in this superficial basal cell carcinoma on the trunk.
Large, superficial basal cell carcinoma.
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Pigmented BCC: In addition to features seen in lesions of nodular BCC, lesions of
pigmented BCC contain increased brown or black pigment and are most common in
individuals with dark skin (see Media File 7).
Pigmented basal cell carcinoma has features of nodular basal cell carcinoma with the addition of dark
pigmentation from melanin deposition. The pigmentation often has the appearance of dark droplets in the lesion,
as shown here.
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Cystic BCC: Lesions of cystic BCC are translucent blue-gray cystic nodules that may
mimic benign cystic lesions.
Superficial BCC: This variety appears as scaly patches or papules that are pink to redbrown, often with central clearing. A threadlike border is common. Erosion is less common
in superficial BCC than in nodular BCC (see Media File 1). Superficial BCC is common on
the trunk and has little tendency to become invasive. The papules may mimic psoriasis or
eczema, but they are slowly progressive and not prone to fluctuate in appearance.
Numerous superficial BCCs may indicate arsenic exposure.
This translucent pink papule has telangiectases and a crusted erosion, characteristic of nodular basal cell
carcinoma.
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Micronodular BCC: This aggressive BCC subtype has the typical BCC distribution. It is not
prone to ulceration, it may appear yellow-white when stretched, and it is firm to the touch.
It may have a seemingly well-defined border.
Morpheaform and infiltrating BCC: These are aggressive BCC subtypes with sclerotic
(scarlike) plaques or papules. The border is usually ill defined and often extends well
beyond clinical margins. Ulceration, bleeding, and crusting are uncommon. It may be
mistaken for scar tissue (see Media 8 and Media File 10).
This infiltrating basal cell cancer has ill-defined borders and telangiectases.
Large, scarlike morpheaform basal cell cancer.
Younger patients (<40 y) may have a lower prevalence of BCC on the head and neck and a higher
prevalence on the trunk, with greater tendency to superficial BCC, than in older patients.4
Childhood BCC is exceedingly rare in the absence of other underlying conditions. Only 107 cases
of de novo childhood BCC have been reported in the literature, but the majority (90%) occurred on
the head and neck, and aggressive subtypes were observed in 20% of the total cases.5
Causes
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UV radiation: This is the most important and common cause of basal cell carcinoma
(BCC). Short-wavelength UV radiation (290-320 nm, sunburn rays) is believed to play a
greater role in BCC formation than long-wavelength UVA radiation (320-400 nm, tanning
rays). In addition, chronic sun exposure appears to be important in the development of
BCC. A latency period of 20-50 years is typical between the time of UV damage and the
clinical onset of BCC.
Other radiation: X-ray and grenz-ray exposure are associated with BCC formation.
Arsenic exposure: Chronic exposure to arsenic is associated with BCC development.
Exposure may be medicinal, occupational, or dietary. A contaminated water supply is
most commonly implicated.
Immunosuppression: Immunosuppression is associated with a modest increase in the risk
of BCC.
Xeroderma pigmentosum: This autosomal recessive disease predisposes people to rapid
aging of exposed skin, starting with pigmentary changes and progressing to BCC,
squamous cell carcinoma, and malignant melanoma. The effects are due to an inability to
repair UV-induced DNA damage. Other features include corneal opacities, eventual
blindness, and neurologic deficits.
Nevoid BCC syndrome (basal cell nevus syndrome, Gorlin syndrome): Multiple BCCs
occur in this autosomal dominant condition, often starting at an early age. Odontogenic
keratocysts, palmoplantar pitting, intracranial calcification, and rib anomalies may be
seen. Various tumors, such as medulloblastomas, meningioma, fetal rhabdomyoma, and
ameloblastoma, can also occur. Mutations in the hedgehog signaling pathway, particularly
the PTCH gene, are causative.6
Bazex syndrome (Bazex-Dupre-Christol syndrome): This is an x-linked dominant condition
with features of follicular atrophoderma (ice-pick marks, especially on dorsum of the
hands), multiple BCCs, local anhidrosis (decreased or absent sweating), and congenital
hypotrichosis.7
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Rombo syndrome8 : This is an autosomal dominant condition distinguished by BCC and
atrophoderma vermiculatum, trichoepitheliomas, hypotrichosis milia, and peripheral
vasodilation with cyanosis.
History of nonmelanoma skin cancer (BCC or squamous cell carcinoma): Persons with
one nonmelanoma skin cancer are at increased risk of developing others in the future.
The rate of new nonmelanoma skin cancer is 35% at 3 years and 50% at 5 years after an
initial diagnosis of skin cancer.9
Basal Cell Carcinoma: Differential Diagnoses & Workup
Differential Diagnoses
Actinic Keratosis
Sebaceous Hyperplasia
Bowen Disease
Seborrheic Keratosis
Fibrous Papule of the Face Squamous Cell Carcinoma
Keratoacanthoma
Trichoepithelioma
Nevi, Melanocytic
Workup
The following clinical guideline summaries may be helpful:
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US Preventive Services Task Force - Screening for skin cancer: U.S. Preventive Services
Task Force recommendation statement10
Cancer Care Ontario - Screening for skin cancer: a clinical practice guideline11
Procedures
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Skin biopsy: Biopsy is required to confirm the diagnosis and to identify the histologic
subtype of the basal cell carcinoma (BCC). Shave or punch biopsy is usually performed.
Additional workup is rarely necessary, unless a genetic disorder is suspected.
o Shave biopsy suffices for the diagnosis of most BCCs. Avoid taking an
exceedingly superficial biopsy specimen because missing the tumor is possible.
For example, an ulcerated BCC may reepithelialize with normal epidermis while a
tumor is present at a deeper level. Part or all of the BCC may be sampled, but
avoid going beyond the clinical margins if the biopsy is only for diagnostic
purposes.
o Punch biopsy is an easy method to obtain a thick specimen. The most suspicious
area of a lesion may be sampled, or multiple biopsy samples may be taken if the
tumor has different appearances in different areas. Avoid punch biopsy if
curettage is planned for final treatment.
Histologic Findings
Tumor cells of nodular basal cell carcinoma (BCC), sometimes called basalioma cells, typically
have large, hyperchromatic, oval nuclei and little cytoplasm. Cells appear uniform, and, if present,
mitotic figures are usually few. Nodular tumor aggregates may be of varying sizes, but tumor cells
tend to align more densely in a palisade pattern at the periphery of these nests (see Media File 3).
Early lesions usually have some connection to the overlying epidermis, but such contiguity may be
difficult to appreciate in more advanced lesions. Increased mucin is often present in the
surrounding dermal stroma.
Nodular basal cell carcinoma. Nodular aggregates of basalioma cells are present in the dermis and exhibit
peripheral palisading and retraction artifact. Melanin is also present within the tumor and in the surrounding
stroma, as seen in pigmented basal cell carcinoma.
Cleft formation, known as retraction artifact, commonly occurs between BCC nests and stroma
because of shrinkage of mucin during tissue fixation and staining. Some lobules may have areas
of pseudoglandular change, and this is the predominant change in adenoid BCC. In other
instances, large tumor lobules may degenerate centrally, forming pseudocystic spaces filled with
mucinous debris. These changes are seen in the nodulocystic variant of BCC (see Media File 6).
Histology of superficial basal cell carcinoma. Nests of basaloid cells are seen budding from the undersurface of
the epidermis.
Numerous variants occur, including pigmented BCC, in which benign melanocytes in and around
the tumor produce large amounts of melanin. These melanocytes contain many melanin granules
in their cytoplasm and dendrites. Superficial BCC appears as buds of basaloid cells attached to the
undersurface of the epidermis. Nests of various sizes are often seen in the upper dermis. The
tumor cell aggregates typically show peripheral palisading.
The more aggressive morpheaform and infiltrating BCCs have growth patterns resulting in strands
of cells rather than round nests. Morpheaform BCC arises as thin strands of tumor cells (often only
1 cell in thickness) that are embedded in a dense fibrous stroma. The strands of infiltrating BCC
tend to be somewhat thicker than those seen in morpheaform BCC, and they have a spiky,
irregular appearance. Infiltrating BCC usually does not exhibit the scarlike stroma seen in
morpheaform BCC. Peripheral palisading and retraction are less pronounced in morpheaform and
infiltrating BCC than in less aggressive forms of the tumor, and subclinical involvement is often
extensive.
Another aggressive variant, micronodular BCC, appears as small, nodular aggregates of basaloid
cells. Retraction artifact tends to be less pronounced than in the nodular form of BCC, and
subclinical involvement is often significant. Basosquamous carcinoma, which exhibits features of
both BCC and squamous cell carcinoma, is also considered an aggressive skin cancer.
Basal Cell Carcinoma: Treatment & Medication
Treatment
Medical Care
Local therapy with chemotherapeutic and immune-modulating agents is useful in some cases of
basal cell carcinoma (BCC). In particular, small and superficial BCC may respond to these
compounds. In addition, they may be used for prophylaxis or maintenance in patients who are
prone to having many BCCs, such as those with basal cell nevus syndrome. See Medication. Also
see the clinical guideline summary from the British Association of Dermatologists, Guidelines for
the management of basal cell carcinoma.12
Surgical Care
The goal of surgical treatment of basal cell carcinoma (BCC) is to destroy or remove the tumor so
that no malignant tissue is allowed to proliferate further. Factors to consider when choosing
therapy include the histologic subtype of BCC, the location and size of tumors, the age of the
patient, the patient's ability to tolerate surgery, and the expense. Recurrent tumors are generally
more aggressive than primary lesions, and subclinical extension also tends to be increased.
Tumors that are aggressive and those occurring near vital or cosmetically sensitive structures are
best treated with methods that allow for an examination of the tissue margins.
The most common surgical methods are curettage, excision with margin examination, Mohs
micrographic surgery, and radiotherapy. Additionally, cryotherapy is sometimes used to treat these
tumors (see Media File 9).
Postoperative wound after Mohs micrographic surgery demonstrates extensive subclinical involvement typical of
many infiltrating and morpheaform basal cell carcinomas.
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Curettage (usually with electrodesiccation) for basal cell carcinoma13
o A looped blade (curette) is used to vigorously scrape tumor away from adjacent
normal skin. One may start with a larger curette to debulk the tumor and then
follow with a smaller curette to better remove smaller fragments of tumor from
surrounding stroma. This technique works best in nodular or superficial BCC
because these tumors tend to be friable and do not tend to be embedded in
fibrous stroma. The instrument is applied firmly and used in multiple directions
over the tumor and immediately adjacent skin. Curetting is most often followed by
electrodesiccation, and the entire process may be repeated 1-2 more times. If
electrodesiccation is not performed, vigorous and firm scraping in several
directions is especially important. Many recurrences after curettage are believed
to be due to insufficient aggressiveness on the part of the surgeon. The overall
cure rate exceeds 90% for low-risk BCCs. The method is quick, simple, and less
expensive than most other methods.
o Curettage is a blind technique in which the specimen cannot be examined for
margin control. This lack of microscopic margin control limits the usefulness of
curettage in high-risk areas, such as the face and ears. Furthermore, the
aggressive subtypes of BCC, such as morpheaform, infiltrating, micronodular,
and recurrent tumors, are usually not friable and therefore unlikely to be removed
by using the curette. The success of this treatment, even in nonaggressive
tumors in low-risk sites, highly depends on the operator's experience and
technique. Finally, healing by secondary intention (granulation) often leads to
atrophic, white scars that may not be satisfactory in aesthetically important areas.
Surgical excision for basal cell carcinoma14
o One may surgically excise the clinically apparent tumor and a margin of clinically
normal–appearing skin. This method can usually be performed in an ambulatory
setting and provides the pathologist with a specimen to examine the tissue
margins. Healing time is generally shorter with sutured closure than with
granulation, and cosmesis compares favorably with that of curettage.
o Surgical excision is more time-consuming and costly than curettage. In addition,
this method requires sacrifice of normal tissue to obtain acceptable cure rates.
Margins of at least 4 mm are needed, even with the least aggressive BCCs, to
achieve 95% cure rates. If standard bread-loaf tissue sectioning is used, areas of
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margin involvement may be missed under microscopy because only a small
sampling of the specimen is evaluated.
Mohs micrographic surgery for basal cell carcinoma15,16
o Mohs surgery involves removal of the clinically apparent tumor and a thin rim of
normal-appearing skin around the defect. This saucer-shaped tissue specimen
represents tissue adjacent to the tumor or the margin surrounding the tumor. This
margin specimen is sectioned and marked so that the entirety of the undersurface
and outer edges of the tumor are examined microscopically to minimize sampling
error. Use of the frozen-section technique allows for an examination of tissue
while the patient is in the office. Tissue is mapped microscopically so if any foci of
tumor persist, further excision can be directed to only those areas to spare the
normal tissue.
o With the Mohs technique, almost 100% of the tissue margins are examined,
compared with standard vertical (bread-loaf) sectioning, in which less than 1% of
the outer margins are examined. Because relatively thin layers are taken only in
areas of proven tumor, this technique is tissue sparing. Excision and repair can
usually be performed on the same day. Of most importance, Mohs micrographic
surgical excision has the best long-term cure rates of any treatment modality for
BCC. Cure rates for primary BCC are 98-99% with Mohs excision and 94-96% for
recurrent BCC.
o Massive, invasive BCC tumors may sometimes be treated with Mohs surgery to
clear peripheral margins with deeper aspects treated surgically by other
disciplines.17
o Chief disadvantages of Mohs surgery are its increased expense and time
requirement compared with curettage. Mohs excision compares favorably with
standard surgical excision when one factors in the savings of treating fewer
recurrences with this technique.
Radiation therapy for basal cell carcinoma18
o Radiation therapy is effective as primary treatment for a variety of BCCs. For
most BCCs, cure rates approach 90%. It is especially useful for patients who
cannot easily tolerate surgery, such as elderly or debilitated individuals.
Irradiation can also be a useful adjunct when patients have aggressive tumors
that were treated surgically or when surgery has failed to clear the margins of the
tumor. Radiation is also an excellent option in patients who refuse surgery
because of the size of a lesion or its proximity to vital structures.
o Initial cosmetic results tend to be good, and this therapy can be less disfiguring
than surgical excision. However, long-term results after several years can be
deforming. Another disadvantage of this technique is that surgical margins cannot
be examined. Tumors recurring in previously radiated sites tend to be aggressive
and difficult to treat and reconstruct. Radiation therapy remains an important,
feasible option in selected patients with BCC.
Cryotherapy for basal cell carcinoma
o Cryotherapy is also an effective treatment for most nonaggressive BCCs, with
cure rates near 90%. However, successful treatment is highly dependent on the
experience of the operator. Optimal cure rates are obtained when the depth,
duration, and temperature of treatment are measured with special
instrumentation, such as cryoprobes.
o Patients must be willing to endure the immediate posttreatment swelling, resultant
necrosis of treated areas, and unpredictable scarring that can occur with this
approach.
o This method is not commonly used for the treatment of BCC, except by a few
experienced cryosurgeons.
Medication
Imiquimod 5% cream19 has been used successfully to treat superficial basal cell carcinomas
(BCCs).19,20,21,22 Although its exact mode of action in treating BCC is not known, a few suggested
mechanisms follow. Lymphocytes, dendritic cells, and macrophages may be recruited into the area
of imiquimod application. These cells may be activated via toll-like receptors 7 and 8 (both of which
recognize imiquimod as a ligand) to release cytokines, particularly tumor necrosis factor-alpha,
interferon-alpha, and interleukin 6. Antitumor effects, such as apoptosis, may then proceed,
thereby inducing tumor regression.23 Induction of tumor suppressor function via the Notch signaling
pathway in superficial BCCs has also been suggested as a mechanism of imiquimod.21,24
The current recommended dosing frequency for the treatment of superficial BCC is 5 times per
week for 6 weeks, but the frequency and duration should be tailored to the individual patient's
response and ability to tolerate the medication. Many application schedules have been used,
ranging from 3 times per week to twice daily 7 d/wk. The duration of treatment varies from 6-16
weeks. Superficial BCC cure rates of 70-100% should be expected after a 6-week course of 5times-per-week application, as shown in studies. Topical imiquimod has also been used to treat
small, nodular BCCs in low-risk locations, but cure rates have been lower than those with
superficial BCCs.
Although successful use of imiquimod in immunosuppressed populations (eg, transplantation
patients) without systemic complications has been documented, it has not been widely studied, nor
have safety and efficacy been established. Imiquimod should be used cautiously in patients with
autoimmune disease. Additionally, its high cost may prohibit its use in some patients.
Topical 5-fluorouracil 5% cream25 is sometimes used to treat small, superficial BCCs. It is a
fluorinated pyrimidine that "blocks the methylation reaction of deoxyuridylic acid to thymidylic acid.
In this manner fluorouracil interferes with the synthesis of deoxyribonucleic acid (DNA) and to a
lesser extent inhibits the formation of ribonucleic acid (RNA). Since DNA and RNA are essential for
cell division and growth, the effect of fluorouracil may be to create a thymine deficiency which
provokes unbalanced growth and death of the cell."
In properly selected (eg, thin) tumors, cure rates of approximately 80% have been obtained. It is
generally applied twice daily and must be used for at least 6 weeks for the treatment of superficial
BCC. Percutaneous absorption of 5-fluorouracil is its major limiting factor; it penetrates only 1 mm
into the skin. New vehicles that may enhance absorption of 5-fluorouracil are being investigated.
One advantage of 5-fluorouracil use is that it can act on BCCs that are not large enough to be
seen with the unaided eye. Therefore, it may be used in patients with basal cell nevus syndrome or
in individuals prone to develop many BCCs to preemptively treat subclinical tumors. Patients with
BCCs that are treated with 5-fluorouracil should be monitored carefully because not all tumors
completely respond. Cosmetic results tend to range from good to excellent with the use of 5fluorouracil. Although it is not inexpensive, it does cost less than imiquimod.
Interferon alfa-2b has shown some success in treating small (<1 cm), nodular, and superficial
BCCs. It is administered intralesionally, 3 times per week for 3 weeks. The recommended dose is
1.5 million units per injection (total of 13.5 million U). In appropriate BCC tumors, cures rates of up
to 80% have been obtained. Interferon has not become a mainstay in BCC treatment because of
its cost, the inconvenience of multiple visits, the discomfort of administration, and its adverse
effects. Flulike symptoms, which are dose related, are common with the doses administered to
treat BCCs. Cardiovascular, myelodepressive, and neurologic adverse effects are less common
with this treatment than with others. Because interferon is an immune stimulant, it should not be
used to treat BCC in transplant recipients or in individuals with autoimmune diseases.
Photodynamic therapy (PDT) for BCCs has been used for more than 20 years.26 PDT is the
process of using specific wavelengths of light to photoexcite porphyrins that have been applied to
neoplastic and preneoplastic cells. This increased energy is rapidly absorbed by adjacent tissue
oxygen, causing the formation of singlet oxygen radicals. These radicals rapidly react with
adjacent tissue and destroy it. 5-Aminolevulinic acid (ALA-PDT) is the only US Food and Drug
Administration approved photoreactive molecule for PDT in the United States, and it is only
approved for actinic keratoses. It is photoactivated with blue light for 1000 seconds after 1 hour of
incubation.
Although its use is off label, PDT has been used for treatment and prevention of BCCs, including
patients with immunosuppression and nevoid BCC syndrome. Shallow tumors, such as superficial
BCCs, respond most consistently. Surgical excision has been shown to be significantly more
effective than ALA-PDT in the treatment of nodular BCC.27 The strongest support for PDT as a
modality for BCCs comes with data on thin lesions treated with methylaminolevulinate (used
outside the United States), but at least one long-term follow-up trial has also shown surgical
excision to be superior.28,29 Various protocols have been followed to achieve varying levels of
success—increasing the incubation time, increasing occlusion time, and using longer and/or
deeper-penetrating wavelengths of light (eg, red light or pulse-dye laser). Many patients continue
to prefer PDT because of its short healing time, excellent cosmesis, and relative affordability.
Also see the British Association of Dermatologists Therapy Guidelines and Audit Subcommittee’s
clinical guidelines summary, Guidelines for topical photodynamic therapy: update.30
Antineoplastic agents
Topical or intralesional antineoplastic agents may be administered depending on the type, location,
and stage of the basal cell carcinoma (BCC).
5-Fluorouracil (Efudex, Carac, Fluoroplex)
Used topically to manage superficial BCC (not on head or neck). Interferes with DNA synthesis by
blocking methylation of deoxyuridylic acid and inhibiting thymidylate synthetase and, subsequently,
cell proliferation.
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Dosing
Interactions
Contraindications
Precautions
Adult
Apply bid in amount sufficient to cover lesions; apply for at least 3 wk; only 5% strength
recommended; therapy might be required for up to 10-12 wk
Pediatric
Not established
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DosingInteractionsContraindicationsPrecautionsDosingInteractionsContraindicationsPrecautionsDosingInteractionsContraindicationsPrecautio
ns
Imiquimod (Aldara)
Precise mechanism for superficial BCC unknown. May increase tumor infiltration of lymphocytes,
dendritic cells, and macrophages. Indicated for biopsy-confirmed primary superficial BCC (not on
head or neck) in adults with normal immune systems. Tumors must not be >2 cm in diameter on
certain areas of body. Indicated only when surgical methods not appropriate.
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Dosing
Interactions
Contraindications
Precautions
Adult
Apply cream to treatment area (including 1 cm of skin around tumor) 5 d/wk at bedtime for 6 wk;
leave on for 8 h, then wash area
Pediatric
Not established
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DosingInteractionsContraindicationsPrecautionsDosingInteractionsContraindicationsPrecautionsDosingInteractionsContraindicationsPrecautio
ns
Interferon alfa-2b (Intron A)
Protein product manufactured with recombinant DNA technology. Mechanism of antitumor activity
not clearly understood; however, direct antiproliferative effects against malignant cells and
modulation of host immune response may be important. Investigational use for nodular BCC. Used
in a randomized, placebo-controlled multicenter study (172 subjects). Intralesional injections of 1.5
million U administered 3 times/wk for 3 wk yielded 86% complete-response rate; 29% for placebo.
Study included nodular BCCs; similar study did not show efficacy for morpheaform or aggressive
BCCs.
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Dosing
Interactions
Contraindications
Precautions
Adult
1.5 million U intralesional injection 3 times/wk for 3 wk
Pediatric
Not established
Basal Cell Carcinoma: Follow-up
Follow-up
Prognosis
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Basal cell carcinomas (BCCs) treated incompletely can recur.
All treated sites must be monitored after therapy.
Individuals with BCC have a 30% greater risk of having another BCC unrelated to the
previous lesion compared with the risk in the general population.
Patient Education
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Avoidance of exposure to UV radiation is encouraged to prevent basal cell carcinoma
(BCC). Helpful preventive measures include carefully planning outdoor activities before 10
am and after 4 pm, wearing a broad-brimmed hat during outdoor activities, and using
sunscreens with sun protection factor of 30 or higher.
For excellent patient education resources, visit eMedicine's Cancer and Tumors Center
and Burns Center. In addition, see eMedicine's patient education articles Skin Cancer,
Skin Biopsy, and Sunburn.
Basal Cell Carcinoma: Multimedia
Multimedia
Media file 1: This translucent pink papule has telangiectases and a crusted erosion,
characteristic of nodular basal cell carcinoma.
(Enlarge Image)
Media file 2: Nodular basal cell carcinoma appearing as a waxy, translucent papule
with central depression and a few small erosions.
(Enlarge Image)
Media file 3: Nodular basal cell carcinoma. Nodular aggregates of basalioma cells
are present in the dermis and exhibit peripheral palisading and retraction artifact.
Melanin is also present within the tumor and in the surrounding stroma, as seen in
pigmented basal cell carcinoma.
(Enlarge Image)
Media file 4: Scale, erythema, and a threadlike raised border are present in this
superficial basal cell carcinoma on the trunk.
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Media file 5: Large, superficial basal cell carcinoma.
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Media file 6: Histology of superficial basal cell carcinoma. Nests of basaloid cells are
seen budding from the undersurface of the epidermis.
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Media file 7: Pigmented basal cell carcinoma has features of nodular basal cell carcinoma with
the addition of dark pigmentation from melanin deposition. The pigmentation often has the
appearance of dark droplets in the lesion, as shown here.
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Media file 8: This infiltrating basal cell cancer has ill-defined borders and
telangiectases.
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Media file 9: Postoperative wound after Mohs micrographic surgery demonstrates
extensive subclinical involvement typical of many infiltrating and morpheaform basal
cell carcinomas.
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Media file 10: Large, scarlike morpheaform basal cell cancer.
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