Basal cell carcinoma recurrence after surgical excision

Overview

Practice Essentials

Basal cell carcinoma (BCC) is a nonmelanocytic skin cancer (ie, an epithelial tumor) that arises from basal cells (ie, small, round cells found in the lower layer of the epidermis). [1, 2] The prognosis for patients with BCC is excellent, but if the disease is allowed to progress, it can cause significant morbidity. [3]

The image below depicts BCC of the right lower lid.

See Nonmelanoma Skin Cancers You Need to Know, Can You Recognize Benign Skin Lesions From Cancerous Ones?, and Mole or Melanoma? Test Yourself With These Suspicious Lesions, Critical Images slideshows, to help correctly identify various lesions.

Signs and symptoms

Approximately 85% of BCCs occur on the face, head (scalp included), and neck; others appear on the trunk or extremities; rarely, they may occur on the hands. [3, 4] Other characteristic features of BCC tumors include the following:

• Waxy papules with central depression

• Pearly appearance

• Erosion or ulceration: Often central and pigmented

• Bleeding: Especially when traumatized

• Oozing or crusted areas: In large BCCs

• Rolled (raised) border

• Translucency

• Telangiectases over the surface

• Slow growing: 0.5 cm in 1-2 years

• Black-blue or brown areas

Periocular tumors most commonly involve the following:

• Lower eyelid: 48.9-72.1%

• Medial canthus: 25-30%

• Upper eyelid: 15%

• Lateral canthus: 5%

Clinicopathologic types of BCC, each of which has a distinct biologic behavior, include the following:

• Nodular: Cystic, pigmented, keratotic; the most common type of BCC; usually presents as a round, pearly, flesh-colored papule with telangiectases

• Infiltrative: Tumor infiltrates the dermis in thin strands between collagen fibers, making tumor margins less clinically apparent

• Micronodular: Not prone to ulceration; may appear yellow-white when stretched, is firm to the touch, and may have a seemingly well-defined border

• Morpheaform: Appears as a white or yellow, waxy, sclerotic plaque that rarely ulcerates; is flat or slightly depressed, fibrotic, and firm

• Superficial: Seen mostly on the upper trunk or shoulders; appears clinically as an erythematous, well-circumscribed patch or plaque, often with a whitish scale

See Presentation for more detail.

Diagnosis

Given that BCC rarely metastasizes, laboratory and imaging studies are not commonly clinically indicated in patients presenting with localized lesions. Imaging studies may be necessary when involvement of deeper structures, such as bone, is clinically suspected. In such cases, computed tomography scans or radiography can be used.

Biopsy

Types of skin biopsy that may be used to confirm the diagnosis and determine the histologic subtype of BCC include the following:

• Shave biopsy: Most often, the only biopsy that is required

• Punch biopsy: May be indicated in the case of a pigmented lesion if there is difficulty distinguishing between pigmented BCC and melanoma; ensures that the depth of the lesion can be determined if it proves to be a malignant melanoma

Histology

Histologically, BCC is divided into the following 2 categories:

• Undifferentiated: When there is little or no differentiation, the carcinoma is referred to as solid BCC; this form includes pigmented BCC, superficial BCC, sclerosing BCC, and infiltrative BCC (a histologic subtype)

• Differentiated: Differentiated BCC often has slight differentiation toward hair (keratotic BCC), sebaceous glands (BCC with sebaceous differentiation), and tubular glands (adenoid BCC); noduloulcerative (nodular) BCC is usually differentiated

See Workup for more detail.

Management

Surgery

In nearly all cases of BCC, surgery is the recommended treatment modality. [5, 6] Techniques used include the following [7] :

• Electrodesiccation and curettage

• Excisional surgery

• Mohs micrographically controlled surgery

• Cryosurgery

Radiation therapy

BCCs are usually radiosensitive; radiation therapy (RT) can be used in patients with advanced and extended lesions, as well as in those for whom surgery is not suitable. Postoperative radiation 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. [8]

Photodynamic therapy

Photodynamic therapy (PDT) as an adjunct is a reasonable choice in the following cases:

• Tumor recurrence with tissue atrophy and scar formation

• Elderly patients or patients with medical conditions preventing extensive oculoplastic reconstructive surgery

• Tumor with poorly defined borders based on clinical examination

• Tumor requiring difficult or extensive oculoplastic surgery

Pharmacologic therapy

Topical agents used in the treatment of superficial BCC include the following [7] :

• Topical 5-fluorouracil 5%: May be used to treat small, superficial BCCs in low-risk areas

• Imiquimod: Approved by the US Food and Drug Administration (FDA) for the treatment of nonfacial superficial BCC

• Tazarotene: Can also be used to treat small, low-risk BCCs

Oral agents approved by the FDA for advanced forms of BCC include the following Hedgehog pathway inhibitors (HHIs):

The checkpoint inhibitor cemiplimab (Libtayo) is approved for patients with locally advanced BCC and has been granted accelerated approval for metastatic BCC previously treated with an HHI or for whom an HHI is not appropriate.

See Treatment and Medication for more detail.

Background

Basal cell carcinoma (BCC) is the most common skin cancer in humans, yet it accounts for less than 0.1% of patient deaths from cancer. Basal cell skin cancer tumors typically appear on sun-exposed skin, are slow growing, and rarely metastasize (0.028-0.55%). BCC usually appears as a flat, firm, pale area that is small, raised, pink or red, translucent, shiny, and waxy, and the area may bleed following minor injury. Tumor size can vary from a few millimeters to several centimeters in diameter. (See Presentation.)

See the clinical images below of basal cell carcinoma.

BCC is a nonmelanocytic skin cancer (ie, an epithelial tumor) that arises from basal cells, which are small round cells found in the lower layer of the epidermis. Basal cells invade the dermis but seldom invade other parts of the body. The deoxyribonucleic acid (DNA) of certain genes is often damaged in patients with BCC; therefore, inheritance may be a factor. Most DNA alterations result from damage caused by exposure to sunlight. (See Pathophysiology.)

Body distribution of BCCs is as follows:

• Head and neck (most frequently on the face [9] ; most common location is the nose, specifically the nasal tip and alae) - 85%

• Trunk and extremities [3] -15%

• Penis, [10] vulva, [11, 12] or perianal skin - Infrequent

The anatomic distribution of BCCs correlates with embryonic fusion planes. After adjusting for surface area, BCC occurrence is greater than 4 times more likely on embryonic fusion planes than on other regions of the midface, a finding that supports the possibility of an embryologic role for BCC pathogenesis. [13]

BCC can develop on unexposed areas. In some patients, contributing factors are exposure to or contact with arsenic, [14] tar, coal, paraffin, [15] certain types of industrial oil, and radiation. BCC can also be associated with scars (eg, burn complications), [16] xeroderma pigmentosum, [17] , previous trauma. [18] vaccinations, or even tattoos. (See Etiology.)

A skin biopsy (most often a shave biopsy is sufficient) may be necessary to confirm the diagnosis and is often required to determine the histologic subtype of BCC. A punch biopsy may be used to obtain a thick specimen, especially when the clinical suspicion of a BCC is still present after shave biopsy results are negative. (See Workup.)

Neglected tumors can continue to grow and lead to significant local destruction and even disfigurement. Surgery, in almost all cases, is the recommended treatment, [5, 7] with treatments varying on the basis of cancer size, depth, and location. (See Treatment.)

Superficial BCCS have been successfully treated with imiquimod 5% cream, [19, 20, 21, 22, 23, 24] and topical 5-fluorouracil 5% cream may be used to treat small, superficial BCCs. [25] Several studies have shown success in treating small nodular BCCs with imiquimod 5% cream, although this is an off-label indication and patients should be informed of this fact. (See Medication.)

Pathophysiology

Although the exact etiology of BCC is unknown, a well-established relationship exists between BCC and the pilosebaceous unit, as tumors are most often discovered on hair-bearing areas.

Many believe that 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.

Signaling pathways

The patched/hedgehog intracellular signaling pathway plays a role in both sporadic BCCs and nevoid BCC syndrome (Gorlin syndrome). This pathway influences differentiation of various 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 homologues, 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. [26, 27]

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.

BCC most commonly develops on sun-exposed areas. Zhang et al reported that ultraviolet (UV)-specific nucleotide changes in PTCH, as well as the tumor suppressor gene TP53, are implicated in the development of early-onset BCC. [28]

UV-induced mutations in the TP53 tumor suppressor gene, which resides on band 17p13.1, have been found in some cases of BCC. [29]  A germline single-nucleotide polymorphism (SNP) in the TP53 gene, rs78378222, has also been associated with susceptibility to BCC. [29] In addition, frameshift mutations of the BAX gene (BCL2-associated X protein) have been found in sporadic cases of BCC. A reduction of bcl-2 proteins is observed in the aggressive, infiltrative type of BCC.

Radiation and immunologic origins

Radiation has proven to be tumorigenic by two mechanisms. The first entails the initiations of prolonged cellular proliferation, thereby increasing the likelihood of transcription errors that can lead to cellular transformation. The second mechanism is direct damage of DNA replication, leading to cellular mutation that may activate proto-oncogenes or deactivate tumor suppressor genes.

Immunologically, the mechanism by which prolonged ultraviolet radiation exposure leads to the development of BCC includes suppression of the cutaneous immune system and immunologic unresponsiveness to cutaneous tumors. This local effect includes a decrease in Langerhans cells, dendritic epidermal T cells, and Thy1+ cells. Furthermore, systemic proliferation of suppressor T cells and the release of immunosuppressive factors (eg, tumor necrosis factor-alpha [TNF-alpha], interleukin 1 [IL-1], prostaglandin [PG], interleukin 10 [IL-10]) are believed to be pathogenic to the development of BCC.

DNA mismatch repair proteins

DNA mismatch repair (MMR) proteins are a group of proteins that physiologically stimulate G2 cell cycle checkpoint arrest and apoptosis. Failure of MMR proteins to detect induced DNA damage results in the survival of mutating cells. MMR protein levels have been found to be higher in nonmelanoma skin cancers than in normal skin, and there is also some evidence of MMR dysregulation. [30]

Etiology

The exact cause of BCC is unknown, but environmental and genetic factors are believed to predispose patients to BCC.

Radiation exposure

Sunlight, particularly long-term exposure, is the most frequent association with development of BCC; risk correlates with the amount and nature of accumulated exposure, especially during childhood. Patient geographic location affects the risk of developing skin cancer. A latency period of 20-50 years is typical between the time of ultraviolet (UV) damage and BCC clinical onset.

The prevalence of BCC increases in areas of higher altitude and in areas of lower latitude. The incidence of BCC is rising, potentially because of atmospheric changes and the increased popularity of sunbathing.

Radiation exposure that contributes to BCC development may also include tanning booths and UV light therapy. Both short-wavelength UVB radiation (290-320 nm, sunburn rays) and longer wavelength UVA radiation (320-400 nm, tanning rays) contribute to the formation of BCC. UVB is believed to play a greater role in the development of BCC than UVA, however, and is the primary agent responsible for most skin cancer. [31]

UVB and UVC can modify unsaturated chemical bonds of nucleic acids, which may lead to mutations. UVC does not penetrate the atmospheric ozone layer. The UVA spectrum is absorbed by melanin and, through free-radical transfer, affects cellular deoxyribonucleic acid (DNA). Mutations caused by UV radiation typically include cytosine (C) to thymine (T), or CC to TT, translocation. This process can cause activation of oncogenes or inactivation of tumor suppressor genes, leading to tumor initiation and progression. [32]

The skin can repair superficial damage, but the underlying cumulative damage remains, including DNA damage. The damage worsens with each successive sun exposure, causing a lifetime progression. [33]

In a 2012 systematic review and meta-analysis of 12 studies with 9328 cases of non-melanoma skin cancer, Wehner et al found that indoor tanning was associated with a significantly increased risk of both basal and squamous cell skin cancer. The risk was highest among users of indoor tanning before age 25. The authors estimate that the population attributable risk fraction in the United States is 8.2% for squamous cell carcinoma and 3.7% for basal cell carcinoma, corresponding to more than 170,000 cases of non-melanoma skin cancer annually caused by indoor tanning. [34] In another 2012 study of 376 patients with basal cell carcinoma and 390 control patients with minor benign skin conditions, indoor tanning was strongly associated with early-onset basal cell carcinoma, particularly in women. [35]

X-ray and Grenz-ray exposure are also associated with basal cell carcinoma formation.

Gene mutations

Studies have demonstrated a high incidence of TP53 gene mutations in BCC. Researchers speculate that ultraviolet sunlight may play an important role in the genesis of this mutation; yet, genetic involvement has been demonstrated on chromosome 9 only in patients with familial basal cell nevus syndrome (Gorlin syndrome). Such mutation involves the patched (PTCH) gene, a tumor suppressor gene.

Inappropriate activation of the hedgehog signaling pathway is found in both sporadic and familial cases of BCC. This results in loss-of-function mutations in tumor-suppressor protein patched homologue 1 (PTCH1) and gain-of-function mutations in sonic hedgehog (SHH), smoothened (SMO), and Gli.

Arsenic exposure through ingestion

Arsenic has been used as a medicinal agent, predominantly the Fowler solution of potassium arsenite, which was used to treat many disorders, including asthma and psoriasis. Historically, a contaminated water source has been the most common source of arsenic ingestion. [14]

Immunosuppression

A modest increase in the lifetime risk of BCC has been noted in chronically immunosuppressed patients, such as recipients of organ or stem cell transplants and patients with AIDS.

Organ transplant patients must be instructed to limit sun exposure and alerted that skin cancer is a serious problem for them. In fact, immunosuppression and sun damage may cooperate to cause skin cancer. The skin cancer incidence is 10-fold higher in transplant patients than in the general population; up to 65-75% of patients with long-term immunosuppression develop skin cancer. Skin cancers can significantly alter and reduce the transplant recipients’ quality of life; some patients may develop more than 100 skin cancers per year.

Xeroderma pigmentosum

This autosomal recessive disease results in the inability to repair ultraviolet-induced DNA damage. Pigmentary changes are seen early in life, followed by the development of basal cell carcinoma, squamous cell carcinoma, and malignant melanoma. Other features include corneal opacities, eventual blindness, and neurological deficits.

Nevoid basal cell carcinoma syndrome

In addition to basal cell carcinoma, this autosomal dominant disorder can result in the early formation of multiple odontogenic keratocysts, palmoplantar pitting, intracranial calcification, and rib anomalies. Various tumors such as medulloblastomas, meningioma, fetal rhabdomyoma, and ameloblastoma also can occur. [36]

Odontogenic keratocysts, palmoplantar pitting, intracranial calcification, and rib anomalies may be seen. Mutations in the hedgehog signaling pathway, particularly the patched gene, are causative. [37]

Go to Nevoid Basal Cell Carcinoma Syndrome to see more complete information on this topic.

Bazex syndrome

Features of Bazex syndrome include follicular atrophoderma (so-called ice pick marks, especially on dorsal hands), multiple basal cell carcinomas, and local anhidrosis (decreased or absent sweating). [33]

Previous nonmelanoma skin cancer

Persons who have been diagnosed with one nonmelanoma skin cancer are at increased risk of developing tumors in the future. The risk of developing new nonmelanoma skin cancers is reported to be 35% at 3 years and 50% at 5 years after an initial skin cancer diagnosis. [38]

Skin type

Albinism has been implicated in BCC. The Fitzpatrick skin-type scale, which ranges from very fair (skin type I) to very dark (skin type VI), categorizes cutaneous sensitivity to ultraviolet radiation. It is based on the individual's tendency to burn and tan and is a good predictor of relative risk among whites.

Rombo syndrome

Rombo syndrome is an autosomal dominant condition distinguished by basal cell carcinoma and atrophoderma vermiculatum, trichoepitheliomas, hypotrichosis milia, and peripheral vasodilation with cyanosis. [39]

Alcohol consumption

A study among adults in the United States reports a strong association between excessive alcohol drinking and higher incidence of sunburn, suggesting a linkage between alcohol consumption and skin cancer. [40]

Hydrochlorothiazide use

The widely used diuretic hydrochlorothiazide (HCTZ) is a potent photosensitizer. Slightly increased risk for BCC (and dramatically increased risk for cutaneous squamous cell carcinoma [SCC]) was documented in a case-control study that cross-referenced 71,533 cases of BCC and 8629 cases of SCC from the Danish Cancer Registry with data on cumulative HCTZ exposure in these cases with that country’s National Prescription Registry. No association was found between nonmelanoma skin cancer and other antihypertensive drugs. [41]

The study results supported a dose-response relationship between HCTZ use and BCC, as follows [41] :

• High cumulative use of HCTZ (≥50,000 mg) increased the odds ratios (ORs) of BCC by 1.29.

• Patients with the highest HCTZ exposure (>200,000 mg) had an OR of 1.54 for BCC.

The association of BCC with HCTZ use was strongest in younger individuals (age 50 years and younger). In these patients, the OR was 1.91. Overall, the proportion of BCCs attributable to HCTZ use was 0.6%. HCTZ showed the strongest association with skin cancers on heavily sun-exposed sites such as the lower limbs (versus the trunk). [41]

Epidemiology

The American Cancer Society (ACS) reports skin cancer as being the most common cancer in the United States, with basal cell carcinoma (BCC) constituting the majority of cases. The ACS cites an estimate that about 5.4 million basal and squamous cell skin cancers are diagnosed each year in about 3.3 million persons in the US, with about 80% of those being BCCs. Although the number of these skin cancers has been increasing for years, death from them remains uncommon: non-melanoma skin cancers are estimated to cause about 2000 deaths annually, and that number has been decreasing in recent years. [42]

The estimated lifetime risk for BCC in the white population is 33-39% for men and 23-28% for women. BCC incidence doubles every 25 years.

In states near the equator, such as Hawaii, BCC incidence is approaching three-fold that of states in the Midwest, such as Minnesota. BCC incidence also varies globally. The highest rates of skin cancer occur in South Africa and Australia, areas that receive high amounts of UV radiation. [43] Australia has a trend toward increasing BCC incidence, while Finland has a low reported incidence that is approximately one quarter that in Minnesota; BCC incidence in Finland also appears to be increasing, however, especially among young women.

BCC is the least likely cancer to metastasize. BCC differs from squamous cell carcinoma, which accounts for 16% of skin cancers and is more life-threatening.

Race

Although BCC is observed in people of all races and skin types, dark-skinned individuals are rarely affected, and it is most often found in light-skinned individuals (type 1 or type 2 skin). Those with type 1 skin are very fair and have red or blond hair and freckles; these individuals always burn and never tan. Those with type 2 skin are fair and burn easily while tanning minimally. Whites of Celtic ancestry have the highest risk for BCC. Incidence is low in persons with type 5 and 6 skin. [44]

Sex

Historically, men are affected twice as often as women. The higher incidence in men is probably due to increased recreational and occupational exposure to the sun, although these differences are becoming less significant with changes in lifestyle. The current male-to-female ratio is approximately 2.1:1.

For tumors involving the periocular skin, Cook et al reported the incidence of BCC to be equal in men and women. [45] In addition, this investigative team found that the age-adjusted incidence rates for all malignant tumors of the eyelid in men and women, respectively, were 19.6 cases and 13.3 cases per 100,000 population per year. The age-adjusted incidence rates for BCC of the eyelid for men and women, respectively, were 16.9 and 12.4 cases per 100,000 population per year.

Age

The likelihood of developing BCC increases with age. Data indicate that BCC incidence is far higher (more than 100-fold) in persons aged 55-70 years than in those aged 20 years and younger. Patients 50-80 years of age are affected most often. The median age at diagnosis is 67 years and the mean age is 64 years.

Nevertheless, BCC can develop in teenagers and now appears frequently in fair-skinned patients aged 30-50 years. Approximately  5% to 15% of cases of BCC occur in patients aged 20- 40 years. Aggressive-growth types of BCC are more frequently noted in patients younger than 35 years than in older individuals.

Zhang et al reported an inverse association between body mass index (BMI) and onset of BCC before age 40 years. The multivariate odds ratio for early-onset BCC in obese versus normal individuals was 0.43 for adult BMI and 0.54 for BMI at age 18. [46]

Prognosis

The prognosis for patients with BCC is excellent, with a 100% survival rate for cases that have not spread to other sites. Nevertheless, if BCC is allowed to progress, it can result in significant morbidity, and cosmetic disfigurement is not uncommon.

Typically, basal cell tumors enlarge slowly, relentlessly and tend to be locally destructive. Periorbital tumors can invade the orbit, leading to blindness, if diagnosis and treatment are delayed. BCC arising in the medial canthus tends to be deep and invasive and more difficult to manage; this type of BCC can result in perineural extension and loss of nerve function.

Although BCC is a malignant neoplasm, it rarely metastasizes. The incidence of metastatic BCC is estimated to be less than 0.1%. The most common sites of metastasis are the lymph nodes, lungs, [47] and bones. [48]

Although treatment is curative in more than 95% of cases, BCC may recur, especially in the first year, or develop in new sites. Therefore, regular skin screenings are recommended. [49]

Recurrence

The 5-year recurrence rate is about 5%, but it depends on the histologic subtype and type of treatment; the recurrence rate is less than 1% for primary (previously untreated) BCCs treated with Mohs micrographic surgery. Most reports show that the distance to the closest resection margin is an important predictor of recurrence. [50]

The following is a list of treatments and their 5-year recurrence rates for primary (previously untreated) BCCs:

• Surgical excision - 10.1%

• Radiation therapy - 8.7%

• Curettage and electrodesiccation - 7.7%

• Cryotherapy - 7.5%

• All non-Mohs modalities - 8.7%

• Mohs micrographic surgery - 1%

These rates are probably affected by the fact that clinicians use cryotherapy, curettage, and desiccation mostly on smaller and better-demarcated lesions.

Pieh et al reported a recurrence rate of 5.36% after the first excision of the tumor; the rate increased to 14.7% after the second operation, and the rate reached 50% after the third and fourth operations. [51] The highest recurrence, approximately 60%, was seen with lesions arising from the medial canthus.

Recurrences usually occur 4-12 months after initial treatment. One meta-analysis found that the 3-year cumulative risk of devloping a second BCC after an index BCC is about 44%, which is a 10-fold increase over that of the general population. [52, 53] Tumors on the nose or T-zone of the face have a higher incidence of recurrence. Recurrence is most common on the nose and nasolabial fold, but this observation may be secondary to lack of adequate margins obtained in these areas. Infiltrative, micronodular, and multifocal types are more likely than nodular types to recur.

A recurrence of BCC should be suspected when one of the following conditions occurs:

• Nonhealing ulceration

• Tissue destruction

• Scar that becomes red, scaled, or crusted or enlarges with large adjacent telangiectasia

• Scar that slowly enlarges over time (months)

• Development of papule/nodule within a scar

Histologic types of BCC at higher risk for recurrence include morpheaform (sclerotic), micronodular, infiltrative, and superficial (multicentric). Other conditions that contribute to a higher recurrence rate include recurrent tumors that have been treated previously, large tumors (>2 cm), and deeply infiltrating tumors.

Patient Education

Adequate patient education is essential in the prevention of recurrence and spread of basal cell carcinoma. Patients should avoid possible potentiating factors (eg, sun exposure, ionizing radiation, arsenic ingestion, tanning beds). The regular use of sun-protecting clothing (eg, wide-brimmed hat, long-sleeved shirts, sunglasses with ultraviolet [UV] protection) is recommended when outdoors.

Instruct patients to avoid sun exposure particularly during the middle of the day (ie, 11 am to 3 pm), which is the most dangerous time. Also, the sun's rays are especially intense in sunny climates and at high altitudes, and UV radiation can also pass through clouds and water. Patients should be instructed to be careful on the beach and in the snow because sand, water, and snow reflect sunlight and increase the amount of received UV radiation. [54]

During the initial consultation, the patient should be counseled regarding the extent of resection, type of reconstructive procedure, and attendant morbidity. High importance should be attached to adequately preparing the patient regarding the cosmetic and functional result of treatment. During posttreatment follow-up, the patient should be counseled regarding sunlight exposure and the risk of developing additional primary skin tumors.

Sunscreen

Regular application and reapplication of sunscreen is recommended prior to sun exposure. People who use sunscreens have a 40% reduction in skin cancer incidence versus nonusers.

Note that the sun protection factor (SPF) ratings of sunscreens correspond to their ability to protect the skin from harmful UVB rays. The Centers for Disease Control and Prevention (CDC) recommends use of a sunscreen with an SPF rating of at least 15, [55] while the American Academy of Dermatology (AAD) advises use of a sunscreen with an SPF rating of at least 30. [56] Both organization recommend use of a broad spectrum sunscreen, which will also provide protection against UVA radiation.

Emphasize also that sunscreens must be applied generously, 20-30 minutes before going outside, and reapplied about every 2 hours, more often if swimming or sweating; the AAD recommends use of water resistant sunscreen, which maintains its SPF for 40 minutes of immersion (or, in the case of "very water resistant products, for 80 minutes). For lip protection, a lip balm with an SPF of 15 or higher should be applied.

Instruct parents to protect their children's skin with sunscreen or protective clothing to reduce the risk of BCC later in life. It has been estimated that intensive sun protection before age 18 years can reduce nonmelanoma skin cancer by 78%.

Advise parents not to expose children younger than 12 months to direct sunlight and to cover up children aged 12-24 months with a hat, shirt, and a small amount of sunscreen on the remaining exposed areas. Similarly, for children older than 2 years, instruct parents to consider using sunscreens, covering the child's skin with clothing, and, when possible, restricting the child to shaded areas.

Self-examination for skin changes

Educate patients on how to recognize any unexplained changes in their skin, especially changes that last for more than 3-4 weeks. Also, educate patients on how to examine their own and their partner's skin. The knowledge of mole distribution on the skin is helpful.

Tell the patient to first look at the front and back of his or her body in a full-length mirror, using a hand mirror. The patient also should use the hand mirror to look at the back of the neck and scalp, the back, and the breeches. The patient then should turn and look at each side of the body with the arms raised. Next, the patient should bend the elbows and look carefully at the forearms, the back of the upper arms, and the palms. Instruct the patient to sit down and check the backs of the legs and feet, including the spaces between the toes and bottoms of the feet.

The American Cancer Society recommends a dermatologic examination every 3 years for people aged 20-40 years and every year for people older than 40 years.

For patient education information, see Skin Cancer and Basal Cell Carcinoma.

1. Cameron MC, Lee E, Hibler BP, Barker CA, Mori S, Cordova M, et al. Basal cell carcinoma: Epidemiology; pathophysiology; clinical and histological subtypes; and disease associations. J Am Acad Dermatol. 2019 Feb. 80 (2):303-317. [QxMD MEDLINE Link].

2. Cameron MC, Lee E, Hibler BP, Giordano CN, Barker CA, Mori S, et al. Basal cell carcinoma: Contemporary approaches to diagnosis, treatment, and prevention. J Am Acad Dermatol. 2019 Feb. 80 (2):321-339. [QxMD MEDLINE Link].

3. Kim DP, Kus KJB, Ruiz E. Basal Cell Carcinoma Review. Hematol Oncol Clin North Am. 2019 Feb. 33 (1):13-24. [QxMD MEDLINE Link].

4. Loh TY, Rubin AG, Brian Jiang SI. Basal Cell Carcinoma of the Dorsal Hand: An Update and Comprehensive Review of the Literature. Dermatol Surg. 2016 Apr. 42 (4):464-70. [QxMD MEDLINE Link].

5. [Guideline] Dandurand M, Petit T, Martel P, Guillot B. Management of basal cell carcinoma in adults Clinical practice guidelines. Eur J Dermatol. 2006 Jul-Aug. 16(4):394-401. [QxMD MEDLINE Link].

6. [Guideline] Trakatelli M, Morton C, Nagore E, Ulrich C, Del Marmol V, Peris K, et al. Update of the European guidelines for basal cell carcinoma management. Eur J Dermatol. 2014 May-Jun. 24 (3):312-29. [QxMD MEDLINE Link].

7. [Guideline] National Comprehensive Cancer Network. NCCN Clinical Practice Guidelines in Oncology: Basal Cell Skin Cancer. NCCN. Available at http://www.nccn.org/professionals/physician_gls/pdf/nmsc.pdf. Version 1.2022 — November 17, 2021; Accessed: February 14, 2022.

8. Mendenhall WM, Amdur RJ, Hinerman RW, Cognetta AB, Mendenhall NP. Radiotherapy for cutaneous squamous and basal cell carcinomas of the head and neck. Laryngoscope. 2009 Oct. 119(10):1994-9. [QxMD MEDLINE Link].

9. Erba P, Farhadi J, Wettstein R, Arnold A, Harr T, Pierer G. Morphoeic basal cell carcinoma of the face. Scand J Plast Reconstr Surg Hand Surg. 2007. 41(4):184-8. [QxMD MEDLINE Link].

10. Shindel AW, Mann MW, Lev RY, et al. Mohs micrographic surgery for penile cancer: management and long-term followup. J Urol. 2007 Nov. 178(5):1980-5. [QxMD MEDLINE Link].

11. Mulvany NJ, Allen DG. Differentiated intraepithelial neoplasia of the vulva. Int J Gynecol Pathol. 2008 Jan. 27(1):125-35. [QxMD MEDLINE Link].

12. Kara M, Colgecen E, Yildirim EN. Vulvar basal cell carcinoma. Indian J Pathol Microbiol. 2012 Oct-Dec. 55 (4):583-4. [QxMD MEDLINE Link]. [Full Text].

13. Newman JC, Leffell DJ. Correlation of embryonic fusion planes with the anatomical distribution of basal cell carcinoma. Dermatol Surg. 2007 Aug. 33(8):957-64; discussion 965. [QxMD MEDLINE Link].

14. Karagas MR, Gossai A, Pierce B, Ahsan H. Drinking Water Arsenic Contamination, Skin Lesions, and Malignancies: A Systematic Review of the Global Evidence. Curr Environ Health Rep. 2015 Mar. 2 (1):52-68. [QxMD MEDLINE Link]. [Full Text].

15. Romao-Correa RF, Maria DA, Soma M, et al. Nucleolar organizer region staining patterns in paraffin-embedded tissue cells from human skin cancers. J Cutan Pathol. 2005 May. 32(5):323-8. [QxMD MEDLINE Link].

16. Ozyazgan I, Kontas O. Previous injuries or scars as risk factors for the development of basal cell carcinoma. Scand J Plast Reconstr Surg Hand Surg. 2004. 38(1):11-5. [QxMD MEDLINE Link].

17. Mohanty P, Mohanty L, Devi BP. Multiple cutaneous malignancies in xeroderma pigmentosum. Indian J Dermatol Venereol Leprol. 2001 Mar-Apr. 67(2):96-7. [QxMD MEDLINE Link].

18. Keyhani K, Ashenhurst M, Oryschak A. Periocular basal cell carcinoma arising in a site of previous trauma. Can J Ophthalmol. 2007 Jun. 42(3):467-8. [QxMD MEDLINE Link].

19. Aldara (imiquimod) Cream, 5% [package insert]. Bristol, TN: Graceway Pharmaceuticals. 2010. Available at [Full Text].

20. Geisse J, Caro I, Lindholm J, Golitz L, Stampone P, Owens M. Imiquimod 5% cream for the treatment of superficial basal cell carcinoma: results from two phase III, randomized, vehicle-controlled studies. J Am Acad Dermatol. 2004 May. 50(5):722-33. [QxMD MEDLINE Link].

21. Sapijaszko MJ. Imiquimod 5% cream (Aldara) in the treatment of basal cell carcinoma. Skin Therapy Lett. 2005 Jul-Aug. 10(6):2-5. [QxMD MEDLINE Link].

22. Micali M, Nasca MR, Musumeci ML. Treatment of an extensive superficial basal cell carcinoma of the face with imiquimod 5% cream. Int J Tissue React. 2005. 27(3):111-4. [QxMD MEDLINE Link].

23. Bilu D, Sauder DN. Imiquimod: modes of action. Br J Dermatol. 2003 Nov. 149 Suppl 66:5-8. [QxMD MEDLINE Link].

24. Wuest M, Dummer R, Urosevic M. Induction of the members of Notch pathway in superficial basal cell carcinomas treated with imiquimod. Arch Dermatol Res. 2007 Dec. 299(10):493-8. [QxMD MEDLINE Link].

25. Efudex (fluorouracil) [package insert]. Costa Mesa, CA: Valeant Pharmaceuticals. 2005. Available at [Full Text].

26. Bale AE, Yu KP. The hedgehog pathway and basal cell carcinomas. Hum Mol Genet. 2001 Apr. 10(7):757-62. [QxMD MEDLINE Link].

27. Wicking C, McGlinn E. The role of hedgehog signalling in tumorigenesis. Cancer Lett. 2001 Nov 8. 173(1):1-7. [QxMD MEDLINE Link].

28. Zhang H, Ping XL, Lee PK, et al. Role of PTCH and p53 genes in early-onset basal cell carcinoma. Am J Pathol. 2001 Feb. 158(2):381-5. [QxMD MEDLINE Link]. [Full Text].

29. National Center for Biotechnical Information. Tumor Protein p53; TP53. Available at http://www.ncbi.nlm.nih.gov/omim/191170. 11/07/2018; Accessed: March 23, 2021.

30. Young LC, Listgarten J, Trotter MJ, Andrew SE, Tron VA. Evidence that dysregulated DNA mismatch repair characterizes human nonmelanoma skin cancer. Br J Dermatol. 2008 Jan. 158(1):59-69. [QxMD MEDLINE Link].

31. Lim JL, Stern RS. High levels of ultraviolet B exposure increase the risk of non-melanoma skin cancer in psoralen and ultraviolet A-treated patients. J Invest Dermatol. 2005 Mar. 124(3):505-13. [QxMD MEDLINE Link].

32. Walling HW, Fosko SW, Geraminejad PA, Whitaker DC, Arpey CJ. Aggressive basal cell carcinoma: presentation, pathogenesis, and management. Cancer Metastasis Rev. 2004 Aug-Dec. 23(3-4):389-402. [QxMD MEDLINE Link].

33. Centers for Disease Control and Prevention (CDC). Sunburn prevalence among adults--United States, 1999, 2003, and 2004. MMWR Morb Mortal Wkly Rep. 2007 Jun 1. 56(21):524-8. [QxMD MEDLINE Link].

34. Wehner MR, Shive ML, Chren MM, Han J, Qureshi AA, Linos E. Indoor tanning and non-melanoma skin cancer: systematic review and meta-analysis. BMJ. 2012 Oct 2. 345:e5909. [QxMD MEDLINE Link]. [Full Text].

35. Ferrucci LM, Cartmel B, Molinaro AM, Leffell DJ, Bale AE, Mayne ST. Indoor tanning and risk of early-onset basal cell carcinoma. J Am Acad Dermatol. 2012 Oct. 67(4):552-62. [QxMD MEDLINE Link]. [Full Text].

36. Cohen MM Jr. Nevoid basal cell carcinoma syndrome: molecular biology and new hypotheses. Int J Oral Maxillofac Surg. 1999 Jun. 28(3):216-23. [QxMD MEDLINE Link].

37. Klein RD, Dykas DJ, Bale AE. Clinical testing for the nevoid basal cell carcinoma syndrome in a DNA diagnostic laboratory. Genet Med. 2005 Nov-Dec. 7(9):611-9. [QxMD MEDLINE Link].

38. Karagas MR. Occurrence of cutaneous basal cell and squamous cell malignancies among those with a prior history of skin cancer. The Skin Cancer Prevention Study Group. J Invest Dermatol. 1994 Jun. 102(6):10S-13S. [QxMD MEDLINE Link].

39. Michaelsson G, Olsson E, Westermark P. The Rombo syndrome: a familial disorder with vermiculate atrophoderma, milia, hypotrichosis, trichoepitheliomas, basal cell carcinomas and peripheral vasodilation with cyanosis. Acta Derm Venereol. 1981. 61(6):497-503. [QxMD MEDLINE Link].

40. Heal C, Buettner P, Browning S. Risk factors for wound infection after minor surgery in general practice. Med J Aust. 2006 Sep 4. 185(5):255-8. [QxMD MEDLINE Link].

41. Pedersen SA, Gaist D, Schmidt SAJ, Hölmich LR, Friis S, Pottegård A. Hydrochlorothiazide use and risk of nonmelanoma skin cancer: A nationwide case-control study from Denmark. J Am Acad Dermatol. 2018 Apr. 78 (4):673-681.e9. [QxMD MEDLINE Link].

42. Key statistics for basal and squamous cell skin cancers. American Cancer Society. Available at http://www.cancer.org/cancer/skincancer-basalandsquamouscell/detailedguide/skin-cancer-basal-and-squamous-cell-key-statistics. January 12, 2022; Accessed: February 14, 2022.

43. Marks R, Jolley D, Dorevitch AP, Selwood TS. The incidence of non-melanocytic skin cancers in an Australian population: results of a five-year prospective study. Med J Aust. 1989 May 1. 150(9):475-8. [QxMD MEDLINE Link].

44. Brasseur R, Lagesse Ch. [Contribution of psychometry of clinical evaluation of the therapeutic effect of "Solcoseryl" in states of intellectual weakness connected with chronic cerebral circulatory insufficiency (author's transl)]. Schweiz Rundsch Med Prax. 1977 Mar 8. 66(10):312-7. [QxMD MEDLINE Link].

45. Cook BE Jr, Bartley GB. Epidemiologic characteristics and clinical course of patients with malignant eyelid tumors in an incidence cohort in Olmsted County, Minnesota. Ophthalmology. 1999 Apr. 106(4):746-50. [QxMD MEDLINE Link].

46. Zhang Y, Cartmel B, Choy CC, Molinaro AM, Leffell DJ, Bale AE, et al. Body mass index, height and early-onset basal cell carcinoma in a case-control study. Cancer Epidemiol. 2017 Feb. 46:66-72. [QxMD MEDLINE Link].

47. Patel MS, Thigpen JT, Vance RB, Elkins SL, Guo M. Basal cell carcinoma with lung metastasis diagnosed by fine-needle aspiration biopsy. South Med J. 1999 Mar. 92(3):321-4. [QxMD MEDLINE Link].

48. Akinci M, Aslan S, Markoc F, Cetin B, Cetin A. Metastatic basal cell carcinoma. Acta Chir Belg. 2008 Mar-Apr. 108(2):269-72. [QxMD MEDLINE Link].

49. Mc Loone NM, Tolland J, Walsh M, et al. Follow-up of basal cell carcinomas: an audit of current practice. J Eur Acad Dermatol Venereol. Jul 2006. 20(6):698-701.

50. Kyrgidis A, Vahtsevanos K, Tzellos TG, Xirou P, Kitikidou K, Antoniades K, et al. Clinical, histological and demographic predictors for recurrence and second primary tumours of head and neck basal cell carcinoma. A 1062 patient-cohort study from a tertiary cancer referral hospital. Eur J Dermatol. 2010 May-Jun. 20 (3):276-82. [QxMD MEDLINE Link].

51. Pieh S, Kuchar A, Novak P, Kunstfeld R, Nagel G, Steinkogler FJ. Long-term results after surgical basal cell carcinoma excision in the eyelid region. Br J Ophthalmol. 1999 Jan. 83(1):85-8. [QxMD MEDLINE Link]. [Full Text].

52. Marcil I, Stern RS. Risk of developing a subsequent nonmelanoma skin cancer in patients with a history of nonmelanoma skin cancer: a critical review of the literature and meta-analysis. Arch Dermatol. 2000 Dec. 136(12):1524-30. [QxMD MEDLINE Link].

53. Levi F, Randimbison L, Maspoli M, Te VC, La Vecchia C. High incidence of second basal cell skin cancers. Int J Cancer. 2006 Sep 15. 119(6):1505-7. [QxMD MEDLINE Link].

54. Bruce AJ, Brodland DG. Overview of skin cancer detection and prevention for the primary care physician. Mayo Clin Proc. 2000 May. 75(5):491-500. [QxMD MEDLINE Link].

55. Centers for Disease Control and Prevention. Sun Safety. CDC. Available at http://www.cdc.gov/cancer/skin/basic_info/sun-safety.htm. April 28, 2021; Accessed: February 14, 2022.

56. How to select a sunscreen. American Academy of Dermatology. Available at https://www.aad.org/public/spot-skin-cancer/learn-about-skin-cancer/prevent/how-to-select-a-sunscreen. Accessed: February 14, 2022.

57. Betti R, Radaelli G, Mussino F, Menni S, Crosti C. Anatomic location and histopathologic subtype of basal cell carcinomas in adults younger than 40 or 90 and older: any difference?. Dermatol Surg. 2009 Feb. 35(2):201-6. [QxMD MEDLINE Link].

58. Griffin JR, Cohen PR, Tschen JA, et al. Basal cell carcinoma in childhood: case report and literature review. J Am Acad Dermatol. 2007 Nov. 57(5 Suppl):S97-102. [QxMD MEDLINE Link].

59. Gorlin RJ. Nevoid basal cell carcinoma (Gorlin) syndrome: unanswered issues. J Lab Clin Med. 1999 Dec. 134(6):551-2. [QxMD MEDLINE Link].

60. Bernardini FP. Management of malignant and benign eyelid lesions. Curr Opin Ophthalmol. 2006 Oct. 17(5):480-4. [QxMD MEDLINE Link].

61. Ly JQ. Scintigraphic findings in Gorlin's syndrome. Clin Nucl Med. 2002 Dec. 27(12):913-4. [QxMD MEDLINE Link].

62. Barton K, Curling OM, Paridaens AD, Hungerford JL. The role of cytology in the diagnosis of periocular basal cell carcinomas. Ophthal Plast Reconstr Surg. 1996 Sep. 12(3):190-4; discussion 195. [QxMD MEDLINE Link].

63. Orengo IF, Salasche SJ, Fewkes J, Khan J, Thornby J, Rubin F. Correlation of histologic subtypes of primary basal cell carcinoma and number of Mohs stages required to achieve a tumor-free plane. J Am Acad Dermatol. 1997 Sep. 37(3 Pt 1):395-7. [QxMD MEDLINE Link].

64. Cherpelis BS, Turner L, Ladd S, Glass LF, Fenske NA. Innovative 19-minute rapid cytokeratin immunostaining of nonmelanoma skin cancer in Mohs micrographic surgery. Dermatol Surg. 2009 Jul. 35(7):1050-6. [QxMD MEDLINE Link].

65. Ackerman AB, Gottlieb GJ. Fibroepithelial tumor of pinkus is trichoblastic (Basal-cell) carcinoma. Am J Dermatopathol. 2005 Apr. 27(2):155-9. [QxMD MEDLINE Link].

66. Bowen AR, LeBoit PE. Fibroepithelioma of pinkus is a fenestrated trichoblastoma. Am J Dermatopathol. 2005 Apr. 27(2):149-54. [QxMD MEDLINE Link].

67. Strauss RM, Edwards S, Stables GI. Pigmented fibroepithelioma of Pinkus. Br J Dermatol. 2004 Jun. 150(6):1208-9. [QxMD MEDLINE Link].

68. Mannor GE, Wardell K, Wolfley DE, Nilsson GE. Laser Doppler perfusion imaging of eyelid skin. Ophthal Plast Reconstr Surg. 1996 Sep. 12(3):178-85. [QxMD MEDLINE Link].

69. Prieto-Granada C, Rodriguez-Waitkus P. Basal cell carcinoma: Epidemiology, clinical and histologic features, and basic science overview. Curr Probl Cancer. 2015 Jul-Aug. 39 (4):198-205. [QxMD MEDLINE Link].

70. Babilas P, Landthaler M, Szeimies RM. Photodynamic therapy in dermatology. Eur J Dermatol. 2006 Jul-Aug. 16(4):340-8. [QxMD MEDLINE Link].

71. Foley P. Clinical efficacy of methyl aminolaevulinate photodynamic therapy in basal cell carcinoma and solar keratosis. Australas J Dermatol. 2005 Feb. 46 Suppl 3:S8-10; discussion S23-5. [QxMD MEDLINE Link].

72. Zimmermann A, Walt H, Haller U, Baas P, Klein SD. Effects of chlorin-mediated photodynamic therapy combined with fluoropyrimidines in vitro and in a patient. Cancer Chemother Pharmacol. 2003 Feb. 51(2):147-54. [QxMD MEDLINE Link].

73. Love WE, Bernhard JD, Bordeaux JS. Topical imiquimod or fluorouracil therapy for basal and squamous cell carcinoma: a systematic review. Arch Dermatol. 2009 Dec. 145(12):1431-8. [QxMD MEDLINE Link].

74. Ally MS, Ransohoff K, Sarin K, Atwood SX, Rezaee M, Bailey-Healy I, et al. Effects of Combined Treatment With Arsenic Trioxide and Itraconazole in Patients With Refractory Metastatic Basal Cell Carcinoma. JAMA Dermatol. 2016 Apr 1. 152 (4):452-6. [QxMD MEDLINE Link].

75. Berman B. Scientific rationale: combining imiquimod and surgical treatments for basal cell carcinomas. J Drugs Dermatol. 2008 Jan. 7(1 Suppl 1):s3-6. [QxMD MEDLINE Link].

76. Brownell I. Nodular basal cell carcinoma: when in doubt, cut it out. J Drugs Dermatol. 2007 Dec. 6(12):1245-6. [QxMD MEDLINE Link].

77. Farhi D, Dupin N, Palangie A, Carlotti A, Avril MF. Incomplete excision of basal cell carcinoma: rate and associated factors among 362 consecutive cases. Dermatol Surg. 2007 Oct. 33(10):1207-14. [QxMD MEDLINE Link].

78. van Kester MS, Goeman JJ, Genders RE. Tissue-sparing properties of Mohs micrographic surgery for infiltrative basal cell carcinoma. J Am Acad Dermatol. 2019 Jan 30. [QxMD MEDLINE Link].

79. [Guideline] Ad Hoc Task Force, Connolly SM, Baker DR, Coldiron BM, Fazio MJ, et al. AAD/ACMS/ASDSA/ASMS 2012 appropriate use criteria for Mohs micrographic surgery: a report of the American Academy of Dermatology, American College of Mohs Surgery, American Society for Dermatologic Surgery Association, and the American Society for Mohs Surgery. J Am Acad Dermatol. 2012 Oct. 67 (4):531-50. [QxMD MEDLINE Link].

80. Miller BH, Shavin JS, Cognetta A, et al. Nonsurgical treatment of basal cell carcinomas with intralesional 5-fluorouracil/epinephrine injectable gel. J Am Acad Dermatol. 1997 Jan. 36(1):72-7. [QxMD MEDLINE Link].

81. Greenway HT, Cornell RC, Tanner DJ, Peets E, Bordin GM, Nagi C. Treatment of basal cell carcinoma with intralesional interferon. J Am Acad Dermatol. 1986 Sep. 15(3):437-43. [QxMD MEDLINE Link].

82. Geisse JK, Rich P, Pandya A, et al. Imiquimod 5% cream for the treatment of superficial basal cell carcinoma: a double-blind, randomized, vehicle-controlled study. J Am Acad Dermatol. 2002 Sep. 47(3):390-8. [QxMD MEDLINE Link].

83. Garcia-Martin E, Gil-Arribas LM, Idoipe M, et al. Comparison of imiquimod 5% cream versus radiotherapy as treatment for eyelid basal cell carcinoma. Br J Ophthalmol. 2011 Oct. 95(10):1393-6. [QxMD MEDLINE Link].

84. Eigentler TK, Kamin A, Weide BM, et al. A phase III, randomized, open label study to evaluate the safety and efficacy of imiquimod 5% cream applied thrice weekly for 8 and 12 weeks in the treatment of low-risk nodular basal cell carcinoma. J Am Acad Dermatol. 2007 Oct. 57(4):616-21. [QxMD MEDLINE Link].

85. Stockfleth E, Ulrich C, Hauschild A, Lischner S, Meyer T, Christophers E. Successful treatment of basal cell carcinomas in a nevoid basal cell carcinoma syndrome with topical 5% imiquimod. Eur J Dermatol. 2002 Nov-Dec. 12(6):569-72. [QxMD MEDLINE Link].

86. Arits AH, Mosterd K, Essers BA, et al. Photodynamic therapy versus topical imiquimod versus topical fluorouracil for treatment of superficial basal-cell carcinoma: a single blind, non-inferiority, randomised controlled trial. Lancet Oncol. 2013 Jun. 14(7):647-54. [QxMD MEDLINE Link].

87. Bianchi L, Orlandi A, Campione E, Angeloni C, Costanzo A, Spagnoli LG, et al. Topical treatment of basal cell carcinoma with tazarotene: a clinicopathological study on a large series of cases. Br J Dermatol. 2004 Jul. 151(1):148-56. [QxMD MEDLINE Link].

88. Lewis JE. Keloidal basal cell carcinoma. Am J Dermatopathol. 2007 Oct. 29(5):485. [QxMD MEDLINE Link].

89. Cognetta AB, Howard BM, Heaton HP, Stoddard ER, Hong HG, Green WH. Superficial x-ray in the treatment of basal and squamous cell carcinomas: a viable option in select patients. J Am Acad Dermatol. 2012 Dec. 67(6):1235-41. [QxMD MEDLINE Link].

90. Piccinno R, Benardon S, Gaiani FM, Rozza M, Caccialanza M. .1080/09546634.2016.1274365. Dermatologic radiotherapy in the treatment of extensive basal cell carcinomas: a retrospective study. J Dermatolog Treat. 2017 Jan 29. 1-5. doi:10. [QxMD MEDLINE Link]. [Full Text].

91. Braathen LR, Szeimies RM, Basset-Seguin N, et al. Guidelines on the use of photodynamic therapy for nonmelanoma skin cancer: an international consensus. International Society for Photodynamic Therapy in Dermatology, 2005. J Am Acad Dermatol. 2007 Jan. 56(1):125-43. [QxMD MEDLINE Link].

92. [Guideline] Morton CA, McKenna KE, Rhodes LE. Guidelines for topical photodynamic therapy: update. Br J Dermatol. 2008 Dec. 159(6):1245-66. [QxMD MEDLINE Link].

93. Calzavara-Pinton PG, Szeimies RM, Ortel B, Zane C. Photodynamic therapy with systemic administration of photosensitizers in dermatology. J Photochem Photobiol B. 1996 Nov. 36(2):225-31. [QxMD MEDLINE Link].

94. Puccioni M, Santoro N, Giansanti F, et al. Photodynamic therapy using methyl aminolevulinate acid in eyelid basal cell carcinoma: a 5-year follow-up study. Ophthal Plast Reconstr Surg. 2009 Mar-Apr. 25(2):115-8. [QxMD MEDLINE Link].

95. Mosterd K, Thissen MR, Nelemans P, et al. Fractionated 5-aminolaevulinic acid-photodynamic therapy vs. surgical excision in the treatment of nodular basal cell carcinoma: results of a randomized controlled trial. Br J Dermatol. 2008 Sep. 159(4):864-70. [QxMD MEDLINE Link].

96. Rhodes LE, de Rie MA, Leifsdottir R, et al. Five-year follow-up of a randomized, prospective trial of topical methyl aminolevulinate photodynamic therapy vs surgery for nodular basal cell carcinoma. Arch Dermatol. 2007 Sep. 143(9):1131-6. [QxMD MEDLINE Link].

97. Christensen E, Mork C, Skogvoll E. High and sustained efficacy after two sessions of topical 5-aminolaevulinic acid photodynamic therapy for basal cell carcinoma: a prospective, clinical and histological 10-year follow-up study. Br J Dermatol. 2012 Jun. 166(6):1342-8. [QxMD MEDLINE Link].

98. Kempf RA. Systemic therapy of skin carcinoma. Cancer Treat Res. 1995. 78:137-62. [QxMD MEDLINE Link].

99. Von Hoff DD, LoRusso PM, Rudin CM, et al. Inhibition of the hedgehog pathway in advanced basal-cell carcinoma. N Engl J Med. 2009 Sep 17. 361(12):1164-72. [QxMD MEDLINE Link].

100. ERIVEDGE™ (vismodegib) capsule for oral use [package insert]. South San Francisco, CA: Genentech USA, Inc. 2012. Available at [Full Text].

101. Migden MR, Guminski A, Gutzmer R, Dirix L, Lewis KD, Combemale P, et al. Treatment with two different doses of sonidegib in patients with locally advanced or metastatic basal cell carcinoma (BOLT): a multicentre, randomised, double-blind phase 2 trial. Lancet Oncol. 2015 Jun. 16 (6):716-28. [QxMD MEDLINE Link].

102. Libtayo (cemiplimab) [package insert]. Tarrytown, NY: Regeneron Pharmaceuticals, Inc. February 2021. Available at [Full Text].

103. [Guideline] US Preventive Services Task Force, Bibbins-Domingo K, Grossman DC, Curry SJ, Davidson KW, Ebell M, et al. Screening for Skin Cancer: US Preventive Services Task Force Recommendation Statement. JAMA. 2016 Jul 26. 316 (4):429-35. [QxMD MEDLINE Link].

104. [Guideline] Moyer VA, U.S. Preventive Services Task Force. Behavioral counseling to prevent skin cancer: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. 2012 Jul 3. 157 (1):59-65. [QxMD MEDLINE Link].

105. [Guideline] Council on Environmental Health, Section on Dermatology, Balk SJ. Ultraviolet radiation: a hazard to children and adolescents. Pediatrics. 2011 Mar. 127 (3):588-97. [QxMD MEDLINE Link]. [Full Text].

106. [Guideline] American Cancer Society. Can basal and squamous cell skin cancers be prevented?. American Cancer Society. Available at http://www.cancer.org/cancer/skincancer-basalandsquamouscell/detailedguide/skin-cancer-basal-and-squamous-cell-prevention. July 26, 2019; Accessed: February 14, 2022.

107. [Guideline] Be Safe in the Sun. American Cancer Society. Available at http://www.cancer.org/cancer/cancercauses/sunanduvexposure/skincancerpreventionandearlydetection/index. Accessed: February 14, 2022.

108. [Guideline] Basal Cell Carcinoma Warning Signs. Skin Cancer Foundation. Available at http://www.skincancer.org/skin-cancer-information/basal-cell-carcinoma/bcc-prevention-guidelines. January 2021; Accessed: February 14, 2022.

109. American Academy of Dermatology. Free Skin Cancer Screenings. AAD. Available at https://www.aad.org/public/public-health/skin-cancer-screenings. Accessed: February 14, 2022.

110. [Guideline] Work Group., Invited Reviewers., Kim JYS, Kozlow JH, Mittal B, Moyer J, et al. Guidelines of care for the management of basal cell carcinoma. J Am Acad Dermatol. 2018 Mar. 78 (3):540-559. [QxMD MEDLINE Link]. [Full Text].

111. [Guideline] Lang BM, Balermpas P, Bauer A, Blum A, Brölsch GF, et al. S2k Guidelines for Cutaneous Basal Cell Carcinoma - Part 1: Epidemiology, Genetics and Diagnosis. J Dtsch Dermatol Ges. 2019 Jan. 17 (1):94-103. [QxMD MEDLINE Link]. [Full Text].

112. [Guideline] Kauvar AN, Cronin T Jr, Roenigk R, Hruza G, Bennett R, American Society for Dermatologic Surgery. Consensus for nonmelanoma skin cancer treatment: basal cell carcinoma, including a cost analysis of treatment methods. Dermatol Surg. 2015 May. 41 (5):550-71. [QxMD MEDLINE Link].

113. [Guideline] Nasr I, et al; British Association of Dermatologists’ Clinical Standards Unit. British Association of Dermatologists guidelines for the management of adults with basal cell carcinoma 2021. Br J Dermatol. 2021 Nov. 185 (5):899-920. [QxMD MEDLINE Link]. [Full Text].

114. [Guideline] Likhacheva A, Awan M, Barker CA, Bhatnagar A, Bradfield L, Brady MS, et al. Definitive and Postoperative Radiation Therapy for Basal and Squamous Cell Cancers of the Skin: Executive Summary of an American Society for Radiation Oncology Clinical Practice Guideline. Pract Radiat Oncol. 2020 Jan - Feb. 10 (1):8-20. [QxMD MEDLINE Link]. [Full Text].

• A pink, scaly lesion on the skin. Superficial basal cell carcinoma (BCC) is often misdiagnosed as eczematous dermatitis or guttate psoriasis and is often difficult to distinguish clinically from Bowen disease (squamous cell carcinoma in situ). Features that suggest the diagnosis of superficial BCC are the absence of significant white, adherent scale and a history of the lesion remaining unchanged for several months or years. Treatment options for this tumor include electrodesiccation and curettage, surgical excision, cryosurgery, 5-fluorouracil, 5% imiquimod cream, and superficial radiotherapy. Electrodesiccation and curettage is the modality most commonly used, with a cure rate of approximately 95%.

• Basal cell carcinoma.

• A 68-year-old patient presenting with an advanced basal cell carcinoma (BCC) of the right periorbital region, frontal view. Courtesy of M Abraham Kuriakose, DDS, MD.

• Lateral view of face showing extent of tumor. Courtesy of M Abraham Kuriakose, DDS, MD.

• Basal cell carcinoma of the right lower lid.

• Biopsy-proven basal cell carcinoma of the upper lid margin. Note the loss of cilia (madarosis) in the area of the tumor.

• Medial canthal/lower lid basal cell. Note the pearly nodular surface with characteristic telangiectatic vessels. Proximity to the lacrimal system will impact its treatment and reconstruction.

• Nodular basal cell carcinoma.

• 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.

• Basal cell carcinoma. Courtesy of Hon Pak, MD.

• Pigmented basal cell carcinoma.

• Pigmented basal cell carcinoma.

• 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.

• This infiltrating basal cell cancer has ill-defined borders and telangiectases.

• This translucent pink papule has telangiectases and a crusted erosion, characteristic of nodular basal cell carcinoma.

• Large, scarlike morpheaform basal cell cancer.

• 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.

• Histologic pattern of a well-differentiated basal cell carcinoma (original magnification X140). Courtesy of Prof Pantaleo Bufo, University of Foggia, Italy.

• Histologic pattern of a well-differentiated basal cell carcinoma (original magnification X250). Courtesy of Prof Pantaleo Bufo, University of Foggia, Italy.

• Micronodular basal cell carcinoma often has an absence of retraction artifact. The characteristic histology is small size and uniformity of the tumor nodules. Courtesy of Shang I Brian Jiang, MD.

• Infiltrative basal cell carcinoma. Tumor cells are arranged in narrow strands, and mucin-rich stroma is often present. Courtesy of Shang I Brian Jiang, MD.

• Keratotic basal cell carcinoma. Rare type characterized by keratocysts. Courtesy of Shang I Brian Jiang, MD.

• Basosquamous basal cell carcinoma. Foci of neoplastic cells with squamous differentiation are present. Courtesy of Shang I Brian Jiang, MD.

• Histology of superficial basal cell carcinoma. Nests of basaloid cells are seen budding from the undersurface of the epidermis. Courtesy of Michael L Ramsey, MD.

Author

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD<br/>Served as a speaker for various universities, dermatology societies, and dermatology departments.

Chief Editor

Mark S Granick, MD, FACS Professor of Surgery, Division of Plastic Surgery, Rutgers New Jersey Medical School; Professor of Surgery, Rutgers Robert Wood Johnson Medical School; Medical Director, University Hospital Wound Care Center

Mark S Granick, MD, FACS is a member of the following medical societies: American Association of Plastic Surgeons, American College of Surgeons, American Society of Plastic Surgeons, New Jersey Society of Plastic Surgeons, Northeastern Society of Plastic Surgeons, Phi Beta Kappa, Wound Healing Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: PolarityTE; Misonix<br/>Serve(d) as a speaker or a member of a speakers bureau for: Misonix, PolarityTE<br/>Received income in an amount equal to or greater than $250 from: Misonix, PolarityTE.

Additional Contributors

Andrew S Kennedy, MD, FACRO Physician-in-Chief, Radiation Oncology, Sarah Cannon; Director, Radiation Oncology Research, Sarah Cannon Research Institute

Andrew S Kennedy, MD, FACRO is a member of the following medical societies: Alpha Omega Alpha, American Association for Cancer Research, American Society for Radiation Oncology, American Society of Clinical Oncology, Americas Hepato-Pancreato-Biliary Association, Radiological Society of North America

Disclosure: Nothing to disclose.

Luigi Santacroce, MD Assistant Professor, Medical School, State University at Bari, Italy

Disclosure: Nothing to disclose.

Laura Diomede University of Bari School of Medicine, Italy

Disclosure: Nothing to disclose.

Acknowledgements

Sanjiv S Agarwala, MD Chief of Oncology and Hematology, St Luke's Cancer Center, St Luke's Hospital and Health Network; Professor, Temple University School of Medicine

Sanjiv S Agarwala, MD is a member of the following medical societies: American Association for Cancer Research, American Society for Head and Neck Surgery, American Society of Clinical Oncology, Eastern Cooperative Oncology Group, and European Society for Medical Oncology

Disclosure: BMS Honoraria Speaking and teaching; Novartis Consulting fee Consulting; Merck Consulting fee Consulting

Michael G Barkett, MD, MS Cardiovascular Diseases, Department of Medicine, Advocate Aurora Health

Disclosure: Nothing to disclose.

Daniel Berg, MD, FRCP(C) Professor of Dermatology, Director of Dermatologic Surgery, University of Washington School of Medicine

Daniel Berg, MD, FRCP(C) is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Mohs Micrographic Surgery and Cutaneous Oncology, and American Society for Dermatologic Surgery

Disclosure: Genentech Honoraria Review panel membership

Gregory Caputy, MD, PhD, FICS Chief Surgeon, Aesthetica Plastic and Laser Surgery Center, Inc

Gregory Caputy, MD, PhD, FICS is a member of the following medical societies: American Society for Laser Medicine and Surgery, International College of Surgeons, International College of Surgeons US Section, Pan-Pacific Surgical Association, and Wound Healing Society

Disclosure: Syneron Corporation Salary Speaking and teaching

Edward F Chan, MD Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania School of Medicine

Edward F Chan, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Robert A Copeland Jr, MD Chair, Professor, Department of Ophthalmology, Howard University College of Medicine

Robert A Copeland Jr, MD is a member of the following medical societies: American Academy of Ophthalmology

Disclosure: Nothing to disclose.

Mark T Duffy, MD, PhD Consulting Staff, Division of Oculoplastic, Orbito-facial, Lacrimal and Reconstructive Surgery, Green Bay Eye Clinic, BayCare Clinic; Medical Director, Advanced Cosmetic Solutions, A BayCare Clinic

Mark T Duffy, MD, PhD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, American Society of Ophthalmic Plastic and Reconstructive Surgery, Sigma Xi, and Society for Neuroscience

Disclosure: Allergan - Botox Cosmetic Honoraria Speaking and teaching

Hon-Vu Q Duong, MD Clinical Instructor of Ophthalmology and Ophthalmic Pathology, Westfield-Nevada Eye and Ear; Senior Lecturer of Neurosciences:Anatomy and Physiology, Nevada State College

Hon-Vu Q Duong, MD is a member of the following medical societies: American Academy of Ophthalmology

Disclosure: Nothing to disclose.

Dirk M Elston, MD Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Jaime R Garza, MD, DDS, FACS Consulting Staff, Private Practice

Jaime R Garza, MD, DDS, FACS is a member of the following medical societies: Alpha Omega Alpha, American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Society for Aesthetic Plastic Surgery, American Society of Maxillofacial Surgeons, Texas Medical Association, and Texas Society of Plastic Surgeons

Disclosure: Allergan None Speaking and teaching; LifeCell None Consulting; GID, Inc. Grant/research funds Other

Shahin Javaheri, MD Chief, Department of Plastic Surgery, Martinez Veterans Affairs Outpatient Clinic; Consulting Staff, Advanced Aesthetic Plastic & Reconstructive Surgery

Shahin Javaheri, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery and American Society of Plastic Surgeons

Disclosure: Nothing to disclose.

Shang I Brian Jiang, MD Associate Clinical Professor of Medicine and Dermatology, Director, Dermatologic and Mohs Micrographic Surgery, Program Director, UCSD Dermatologic and Mohs Surgery Fellowship, University of California School of Medicine, San Diego

Shang I Brian Jiang, MD, is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Surgery, American Society for Dermatologic Surgery, and Association of Professors of Dermatology

Disclosure: DUSA Corporation Grant/research funds PI for Industry Sponsored Clincal Trial

Klaus-Dieter Lessnau, MD, FCCP Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory; Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital

Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Arlen D Meyers, MD, MBA Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine

Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Head and Neck Society

Disclosure: Covidien Corp Consulting fee Consulting; US Tobacco Corporation Unrestricted gift Unknown; Axis Three Corporation Ownership interest Consulting; Omni Biosciences Ownership interest Consulting; Sentegra Ownership interest Board membership; Medvoy Ownership interest Management position; Cerescan Imaging Consulting; Headwatersmb Consulting fee Consulting; Venturequest Royalty Consulting

Maurice Y Nahabedian, MD, FACS Associate Professor, Department of Plastic Surgery, Georgetown University Hospital

Maurice Y Nahabedian, MD, FACS is a member of the following medical societies: American Association of Plastic Surgeons, American College of Surgeons, American Society for Reconstructive Microsurgery, American Society of Plastic Surgeons, Johns Hopkins Medical and Surgical Association, and Northeastern Society of Plastic Surgeons

Disclosure: Lifecell corp Honoraria Speaking and teaching

Samia Nawaz, MBBS, MD Associate Professor, Department of Pathology, University of Colorado Health Science Center

Samia Nawaz, MBBS, MD is a member of the following medical societies: American Society for Clinical Pathology, American Society of Cytopathology, and International Academy of Pathology

Disclosure: Nothing to disclose.

Ron W Pelton, MD, PhD Private Practice, Colorado Springs, Colorado

Ron W Pelton, MD, PhD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, American Society of Ophthalmic Plastic and Reconstructive Surgery, AO Foundation, and Colorado Medical Society

Disclosure: Nothing to disclose.

Michael L Ramsey, MD Director, Mohs Surgery Fellowship, Co-Director, Procedural Dermatology Fellowship, Department of Dermatology, Geisinger Medical Center

Michael L Ramsey, MD is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Micrographic Surgery and Cutaneous Oncology, and Pennsylvania Academy of Dermatology

Disclosure: Nothing to disclose.

Rana Rofagha Sajjadian, MD Clinical Instructor, Department of Dermatology, University of Irvine, California; Division of Mohs Surgery, Department of Dermatology, Southern California Permanente Medical Group

Rana Rofagha Sajjadian, MD is a member of the following medical societies: American Academy of Dermatology, American Society for Dermatologic Surgery, and American Society for MOHS Surgery

Disclosure: Nothing to disclose.

Thomas M Roy, MD Chief, Division of Pulmonary Diseases and Critical Care Medicine, Quillen Mountain Home Veterans Affairs Medical Center; Professor, Department of Internal Medicine, Division of Pulmonary Medicine, Fellowship Program Director, East Tennessee State University, James H Quillen College of Medicine

Thomas M Roy, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, Southern Medical Association, and Wilderness Medical Society

Disclosure: Nothing to disclose.

M Sherif Said, MD, PhD Associate Professor of Pathology, Director of Head and Neck Pathology, Department of Pathology, University of Colorado School of Medicine

M Sherif Said, MD, PhD is a member of the following medical societies: American Society for Clinical Pathology and College of American Pathologists

Disclosure: Nothing to disclose.

Ali Sajjadian, MD, FACS Private Practice, Newport Beach, California; Former Assistant Professor of Plastic Surgery, Former Director of Aesthetic Plastic Surgery Satellite Centers, University of Pittsburgh Medical Center

Ali Sajjadian, MD, FACS is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Medical Association, American Society of Plastic Surgeons, American Society of Plastic Surgeons, American Society of Plastic Surgeons, California Medical Association, Northeastern Society of Plastic Surgeons, and PennsylvaniaMedical Society

Disclosure: Nothing to disclose.

Negar Sajjadian, MD Assistant Professor of Pediatrics, Tehran University of Medical Sciences, Shariati Hospital

Disclosure: Nothing to disclose.

Wayne Karl Stadelmann, MD Stadelmann Plastic Surgery, PC

Wayne Karl Stadelmann, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Society of Plastic Surgeons, New Hampshire Medical Society, Northeastern Society of Plastic Surgeons, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Katherine Szyfelbein, MD Staff Physician, Department of Dermatology, Boston University, Boston Medical Center

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

R Stan Taylor, MD The JB Howell Professor in Melanoma Education and Detection, Departments of Dermatology and Plastic Surgery, Director, Skin Surgery and Oncology Clinic, University of Texas Southwestern Medical Center

R Stan Taylor, MD is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Surgery, American Dermatological Association, American Medical Association, American Society for Dermatologic Surgery, Christian Medical & Dental Society, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Can basal cell carcinoma return after surgery?

Can basal cells return same spot?

Does basal cell carcinoma recur after complete conventional surgery excision?

What happens if basal cell carcinoma returns?