View the Disease Management Project
Table of Contents

Published May 30, 2002

Rebecca C.
Tung, MD

Department of
Dermatology

Allison T.
Vidimos, RPh, MD

Department of
Dermatology

Print Chapter

Copyright 2002
The Cleveland Clinic
Foundation

INTRODUCTION

     Definition

     Incidence and          Prevalence   

     Pathophysiology

     Signs and      Symptoms   

     Diagnosis

     Therapy

     Outcomes

     Follow-up and      Prognosis

     Definition

     Incidence and      Prevalence   

     Pathophysiology

     Signs and      Symptoms   

     Diagnosis

     Therapy

     Outcomes

     References

National Guidelines Basal Cell Carcinoma-(AAD) Squamous Cell Carcinoma-(AAD)

 

 

More than one million cases of skin cancer will be diagnosed in the United States this year. About 80% of these new skin cancer cases will be basal cell carcinoma (BCC), 16% will be squamous cell carcinoma, and 4% will be melanoma. On a preventive health note, it has been estimated that regular application of sunscreen with sun protection factor of 15 or greater for the first 18 years of life would reduce the lifetime incidence of non-melanoma skin cancers by 78%. While non-melanoma skin cancers (basal and squamous cell carcinoma) are the most common types of malignancies in humans, melanoma ranks as the 6th and 7th most common cancer in men and women, respectively. Although the number of non-melanoma skin cancers is staggering, both basal cell and squamous cell carcinomas have a better than 95% cure rate if detected and treated early.

Basal cell carcinoma is the most common cutaneous malignancy in humans. This tumor is believed to arise from the pluripotential primordial cells in the basal layer of the epidermis and less often from the outer root sheath of the hair follicle or sebaceous gland or other cutaneous appendages.¹ While BCCs are slow growing and rarely metastasize, they can cause extensive tissue destruction through direct extension, leading to significant patient morbidity if untreated.

It is estimated that over 800,000 cases of BCC will occur in the United States this year. The annual incidence in Americans is 146 cases per 100,000 people.² Although the incidence of BCC increases with advancing age, it is becoming more common in younger adults. An Australian study showed that while there is a higher incidence of BCC in men, the incidence in women has also been steadily increasing.³

Factors such as excessive, chronic sun exposure, indoor tanning, fair-skin complexion, prior ionizing radiation exposure, chemical co-carcinogens such as arsenic, and genetic determinants are significant risks factors. The most common etiologic factor in the induction of BCC is ultraviolet light, specifically ultraviolet B (UVB, 290-320 nm). It has been shown that UVB induces characteristic DNA mutations in the skin called pyrimidine dimers. The p53 tumor suppressor gene is responsible for arresting the cell cycle so that any induced mutations can be repaired by the cell. In BCC, the same ultraviolet light induced pyrimidine dimer mutations have also been found in the p53 tumor suppressor gene. This mutated p53 gene is non-functional and leads to disregulation of the cell cycle, with resultant unlimited cell proliferation (cancer). While the exact mechanism of BCC propagation is unknown, it is believed that basal cell carcinomas arise when mutations, which control cell growth, via the hedgehog pathway, activate immature pluripotential cells in the epidermis. This most often occurs through inactivation of the tumor suppressor gene, patched, located on chromosome 9. Other mutations in smoothened and hedgehog have also been seen RAS and p53 mutations may also play a role in oncogenesis. Additionally, the distinctive biologic behavior of BCC, characterized by local invasiveness but rare metastatic spread, may be related to alterations in certain basement membrane components.⁴

Basal cell carcinomas are most frequently found on the head and neck, with the nose being the most common site. The typical lesion is a small pearly (waxy) nodule with a central depression and rolled border containing dilated blood vessels, which may have a history of ulceration, crusting, and/or bleeding. Basal cell carcinoma has 5 clinicopathologic subtypes: nodular-ulcerative, superficial, pigmented, morpheaform (sclerosing) and basosquamous.

Nodular-ulcerative (Figure 1)
The nodular-ulcerative variant is the most common type of BCC, which presents as a small, pearly dome-shaped papule with surface telangiectasias and a typical rolled border. Over time, central ulceration with bleeding or crusting is often seen. Differential diagnosis of this lesion includes sebaceous hyperplasia, squamous cell carcinoma, verruca vulgaris virus, molluscum contagiosum, intradermal nevus, appendageal tumors, amelanotic melanoma, and stasis ulcers when located on the shins.

Superficial (Figure 2)
Superficial basal cell carcinomas are the least aggressive form. They frequently present as several scaly, dry, round-to-oval, erythematous plaques with a thread-like, raised border on the trunk and extremities. If untreated, superficial BCCs may enlarge to 10-15 cm in diameter without ulceration. Differential diagnosis of superficial basal cell carcinoma includes eczema, psoriasis, and Bowen's disease.

Pigmented (Figure 3)
Pigmented BCCs are seen more often in darker skinned individuals such as Hispanics and Asians. This subtype has all the characteristics of the nodular-ulcerative variety plus brown or black pigmentation due to melanin. A history of arsenic ingestion has been seen with pigmented and superficial types of BCCs.

Morpheaform (sclerosing) (Figure 4)
An indurated yellow-to-white plaque with an indistinct border and an atrophic surface characterizes morpheaform or sclerosing BCC. Ulceration and crusting are usually absent. This variety has an aggressive growth pattern and invasion of muscle, nerve, and bone may be seen. Morpheaform BCC is particularly insidious because of its benign scar-like appearance. Differential diagnosis of morpheaform BCC includes scar and localized superficial scleroderma (morphea).

Basosquamous
The basosquamous or metatypical variant of BCC is diagnosed on a histologic basis. This tumor possesses features of both BCC and SCC. It is mentioned because it is associated with a higher rate of metastasis.

Two syndromes that have multiple BCCs as a feature include nevoid basal cell carcinoma syndrome (Gorlin's syndrome) and Basex's syndrome. Gorlin's syndrome is characterized by BCCs, odontogenic jaw cysts, pitted depression of the hands and feet, osseous anomalies of the ribs, spine, and skull, and characteristic facies (frontal bossing, hypoplastic maxilla, a broad nasal root, and true ocular hypertelorism).⁵ This genetic disorder presents in an autosomal dominant pattern. There is a mutation of the patched tumor suppressor gene located on chromosome 9.⁵ Basex's syndrome is another autosomally dominant inherited disorder. It is characterized by multiple BCCs of the face, follicular atrophoderma of the extremities, localized or generalized hypohidrosis, and hypotrichosis.

Clinical diagnosis of BCC is confirmed by performing a biopsy of the suspected lesion for histopathologic interpretation. For the majority of BCC subtypes, a shave biopsy will suffice. However, when the lesion is believed to be a morpheaform BCC, a deep shave, punch biopsy, or incisional biopsy is recommendation to obtain a sufficient tissue samples for correct interpretation.

Basal cell carcinoma may be effectively treated by a variety of therapeutic modalities. Among the clinical subtypes of BCC, small nodular or superficial BCCs respond to most treatment options; whereas, large nodular ulcerative or morpheaform lesions may require more aggressive therapy. No single treatment method is ideal for all lesions. The treating physician should carefully evaluate each BCC on an individual basis in order to choose the modality which is most appropriate for the lesion's size, site, and histologic type, as well as the patient's age and functional status.¹

Electrodesiccation and Curettage (ED and C)
According to the American Academy of Dermatology (AAD) Guidelines of Care, ED and C is best suited for primary lesions, but may be useful in some recurrent lesions. It is less effective in the cure of recurrent lesions that are in scar tissue.¹ Superficial and nodular BCC respond especially well to ED and C. It is less effective in the cure of recurrent lesions or in the morpheaform subtype because of indistinct margins. Selected low risk lesions (small, well-defined primary lesions with nonaggressive histology usually in non-critical sites) can achieve 5-year cure rates of up to 97% when treated with ED and C.⁷ Primary, non-morpheaform basal cell carcinomas are more friable than surrounding normal skin and are initially debulked with a curette. The stroma and surrounding dermis are then electrodesiccated. This process is usually repeated 2 more times. The resulting wound heals with a hypopigmented scar over 2 to 6 weeks. The main disadvantage of this treatment is the absence of histologic margin control. Treatment of facial lesions with this modality is not advocated because of the risk of deep invasion in embryonal fusion planes, the difficulty of adequate curettage in the sebaceous skin of the nose, and poor cosmetic appearance.

Cryosurgery
According to the AAD Guidelines of Care, cryosurgery is useful in treating primary lesions and in some recurrent lesions. It is especially useful in certain areas of the body and in patients with multiple lesions.¹ Superficial and small nodular BCCs respond well to liquid nitrogen cryosurgery. Liquid nitrogen (temperature -196°C ) produces tissue destruction by reducing the temperature of the skin cancer to tumoricidal levels. It is not indicated for tumors deeper than 3 mm or those with indistinct margins. The main disadvantages include a hypopigmented scar, prolonged healing, pain during the procedure, and risk of recurrence.

Surgical Excision
According to the AAD Guidelines, excision is useful in both primary and recurrent tumors. The main goal of any excisional surgery is to remove the tumor entirely. Postoperatively, the surgical margins of the specimen are examined histologically for assessment of adequate tumor removal. The wound defect can be closed primarily with side-to-side closures, flaps, grafts, or can be allowed to heal by secondary intention.¹ For small (< 20 mm) primary, well-defined BCCs, 3 mm peripheral surgical margins will clear the tumor in 85% of cases, and a 4-5 mm margin will increase the peripheral clearance rate to approximately 95%.⁷ Larger and morpheaform lesions require wider and potentially deeper surgical margins for complete histological resection. The main disadvantage for surgical excision is incomplete margin control,⁷ as the routine vertical sectioning technique (breadloafing and quartering methods of margin checking) only assess 1% of the margin.

Mohs Micrographic Surgery (MMS)
According to the AAD Guidelines, MMS is particularly efficacious in dealing with recurrent tumors displaying one or more of the following risk factors such as, but not limited to, tumors in certain anatomic locations and/or tumors that have been present for long periods of time and have become relatively large, and certain subtypes including large, nodular, and morpheaform BCCs.¹ Mohs micrographic surgery consists of the removal of the tumor by scalpel in sequential horizontal layers. Each tissue specimen is mapped, frozen, stained, and microscopically examined. This procedure is especially suited for the treatment of recurrent lesions and those primary tumors displaying one or more of the following risk factors:

• ill-defined clinical borders,
• anatomic sites with a high risk of local recurrence in areas of important tissue conservation on the face including, but not limited to, the central third of the face, nose, nasolabial folds, periorbital, perioral, and periauricular regions, hands, feet, genitalia,
• history of incomplete removal,
• history of prior irradiation therapy,
• history of recurrence,
• large size,
• specific histologic patterns including morpheaform, keratinizing, metatypical, infiltrating, contiguous tumors (ie, BCC and SCC), multicentric,
• deep tissue or bone involvement, or perineural or perivascular involvement,
• rapidly growing or aggressive BCCs, or
• tumors in immunocompromised patients.⁶

The procedure is predicated on histologically inspecting the entire perimeter and undersurface of the excised specimen to ensure a tumor-free margin. The Mohs micrographic procedure has an extremely high cure rate: 99% for primary BCCs and more than 96% for recurrent lesions. Defects after Mohs surgery can be closed immediately or a delayed repair may be done in select cases. Repair can be achieved with primary linear closure, adjacent tissue transfer (flap), skin grafting, or healing by secondary intention.¹

Radiation
The AAD Guidelines state that radiation is useful for definitive treatment of primary tumors and some recurrent cancers and for palliation of inoperable tumors.² This modality is useful in the treatment of elderly patients who are not suitable candidates for surgical procedures. Superficial x-rays are administered in multiple, divided doses over several weeks. In general, a total of 10 treatments are needed. Radiation therapy is contraindicated in the treatment of morpheaform BCC, or recurrent BCC tumors regardless of pathologic subtype.

Evolving Therapies
According to the AAD Guidelines, laser surgery is a recognized and evolving therapy that may be used to vaporize superficial and multiple basal cell carcinomas. The laser can also be used in lieu of a scalpel for excisional surgery to provide for improved hemostasis.¹ Other modalities such as retinoids, imiquimod, 5-fluorouracil, immunotherapy (IL-1, IL-2 interferon alpha-2b, and interferon gamma) and photodynamic therapy have been used with variable success. Chemotherapy used in the treatment of metastatic disease may have a role in treating patients with multiple lesions or as adjunctive therapy in patients being treated with radiation.¹

The natural progression of untreated BCC is slow growth with progressive invasion and destruction of adjacent tissues. Metastasis is very rare in basal cell carcinoma with a relative rate of 0.0028% to 0.1%. When metastasis occurs, the site of the primary lesion has most often been on the head and neck. The sites of BCC metastasis in order of frequency are the regional lymph nodes, lung, bone, skin, liver, and pleura. The average interval for metastasis is 9 years. Metastatic BCC has a poor prognosis with a median survival of 8 months. Basal cell carcinoma metastasis has usually been observed in men with large, neglected ulcerated tumors.

Five-year recurrence rates after treatment of primary BCC with the following modalities are: Mohs micrographic surgery (1%), cryotherapy (7.5%), radiation therapy (8.7%), electrodesiccation and curettage (7.7%), and surgical excision (10.1%).⁸ The main goal in the treatment of BCC should be complete removal of the malignancy with the highest cure rate and minimal amount of cosmetic disfigurement or functional impairment.

Self-examination and long-term follow-up in patients who have had a BCC is essential because of the possibility of recurrence and because these patients have a much higher propensity toward the development of new cutaneous malignancies.¹ Studies show that patients who have had one BCC are at significantly higher risk (50%) of developing new primary lesions, which may go undetected by patients.⁷ Early detection and appropriate retreatment of either recurrent BCCs or new primary BCCs may increase the chances of a permanent cure and ultimately to minimize morbidity. Prevention and education are also integral parts of the total care of a patient with basal cell carcinoma.⁷

Squamous cell carcinoma (SCC) is a malignant tumor arising from the keratinocytes in the epidermis or its dermal appendages.⁹ SCC is the second most common cutaneous malignancy after BCC. Unlike BCC, cutaneous squamous cell carcinoma is associated with a greater risk of metastasis.¹⁰

It is estimated that greater than 160,000 cases of cutaneous squamous cell carcinoma will occur in 2001. The age-adjusted incidence of SCC among whites is 100-150/100,000 persons/year and the age-specific incidence among persons over the age of 75 is approximately 10 times that rate. The most recent data reports that the lifetime risk of SCC was 9% to 14% among men and 4% to 9% among women.5 The incidence of SCC doubles with each 8-10 degrees decline in latitude (proximity to the equator). Over the past 10 to 30 years, the age-adjusted incidence of SCC has increased by 50% to 200%.¹¹

SIGNS AND SYMPTOMS

Actinic Keratosis (potential precursor to SCC) (Figure 5) Actinic keratoses (AK) are premalignant skin lesions that result from chronic sun exposure and are found chiefly on the face, ears, dorsal hands, and forearms. They are usually multiple, discrete, flat or raised, verrucous or keratotic, pigmented, erythematous or skin-colored. The surface is usually scaly. The annual transformation rate into SCC is 0.24% for each actinic keratosis.¹¹ However, approximately 5% to 20% of AKs may develop into invasive squamous cell carcinoma over 10-25 years.¹¹ The transformation may be heralded by the development of erosion, induration, inflammation, or enlargement. Options for treatment include cryosurgery, ED and C, topical fluorouracil, photodynamic therapy, dermabrasion, chemical peel, and laser resurfacing. It has been calculated that there is a 10.2% chance of at least one AK on a given patient transforming into a SCC within a 10-year period. However, this rate may actually be much higher, especially in immunocompromised patients such as organ transplant recipients.

Bowen's Disease (squamous cell carcinoma-in-situ) (Figure 6)
Well-demarcated erythematous, scaly, slowly enlarging plaques that may occur on any part of the body characterize Bowen's disease or squamous cell carcinoma in-situ. When it occurs on the glans penis, it is referred to as erythroplasia of Queyrat. The development of ulceration or induration may portend transformation into invasive squamous cell carcinoma, which occurs in up to 5% of cases. Bowen's disease affects mostly older white males. Chronic sun damage and arsenicism have been implicated in the cause of Bowen's disease. Treatment options include excision, ED and C, photodynamic therapy, imiquimod, cryosurgery, 5-fluorouracil, and Mohs surgery.

Keratoacanthoma (KA) (Figure 7)
This rapidly growing tumor is believed to be a low grade SCC. KAs usually start out as a 1 millimeter, flesh-colored macule or papule and enlarge to as much as a 2.5 cm nodule with a keratin-filled crater in only 3-8 weeks. In the majority of cases, solitary KAs will involute over 2-6 months, frequently healing with scarring. KAs are generally found on sun-exposed areas such as the central face, dorsal hands, arms, and legs, although they can occur anywhere on the body including the mucosa. While KAs may ultimately involute, the duration of regression is unpredictable. Furthermore, KAs can also mimic invasive SCC with regard to rapid growth pattern and clinical characteristics.¹⁰ Therefore, a method of removal that ensures adequate depth for histopathologic review is important. Options for therapy include observation, surgical excision, ED and C, topical or intralesional 5-fluorouracil, cryosurgery, radiation, and Mohs surgery.

Squamous Cell Carcinoma (SCC) (Figure 8)
Squamous cell carcinoma can occur on the skin or mucous membranes. It generally occurs in middle-aged and elderly adults with more lesions occurring in males. The most common sites affected are the scalp, dorsal hands, ears, lower lip, neck, forearms, and legs. Clinically SCC presents as an enlarging indurated erythematous papule, nodule, or plaque with scale. Ulceration and crusting occur later followed by possible invasion of underlying structures and development of regional lymphadenopathy. On the lower lip, SCC arises on the chronically sun-damaged skin of the vermilion border. Patients usually note the presence of a firm nodule growing either inward or outward with ulceration. Squamous cell carcinomas of the lip metastasize approximately 10% to 15% of the time.

Verrucous Carcinoma (Figure 9)
Verrucous carcinoma is a variant of well-differentiated invasive SCC. They present as indolent cauliflower-shaped nodules that resemble warts. They are locally aggressive, but less likely to metastasize.¹⁰ Verrucous carcinoma can occur on the soles, glans penis, scrotum, vulva, scalp, face, back, nail bed, or larynx. The most effective treatment is excision, with Mohs micrographic surgery being required in some cases.¹⁰

Invasive squamous cell carcinoma has the potential to recur and metastasize. The 5-year recurrence of primary cutaneous lesions is 8% and the 5-year metastasis rate is 5%.¹⁰ Risk factors for metastasis include: size > 2 cm, site (lip, ear), immunosuppression, history of prior treatment, and aggressive histologic features (depth > 4 mm, poorly differentiated appearance, and perineural invasion).¹⁰ Additional variables which put SCC in the high-risk category include: etiology (scar, chronic ulcer, sinus tract, radiation dermatitis) and rapid growth pattern.¹¹

DIAGNOSIS

As with BCC, a total body examination of the skin is the only screening test available for cutaneous SCC. A physical examination of a patient with SCC should always include a thorough examination of the areas of lymphatic drainage.⁹ The clinical presence of lymphadenopathy necessitates exclusion of metastatic disease. Suspicious cutaneous lesions for SCC should be promptly biopsied. Since even the most astute physicians can make incorrect clinical diagnoses, most biopsies of all suspected non-melanoma skin cancers should be adequate to allow proper diagnosis and treatment. This sample can be obtained as a shave or punch biopsy. The tissue is then sent for histopathologic review.

THERAPY

Fortunately, the majority of SCCs are small, low-risk tumors.¹¹ A variety of surgical and non-surgical therapeutic modalities provide effective treatment of SCC.

Electrodesiccation and Curettage (ED and C)
According to the American Academy of Dermatology (AAD) Guidelines, ED and C may be suitable for small primary lesions on sun-exposed skin. In selected patients, curettage used alone or in conjunction with cryosurgery or ionizing radiation is an acceptable treatment method. ED and C is less effective in the cure of recurrent lesions that have associated scar tissue. Tumors that extend into the subcutaneous tissues histologically or are found to have clinically invaded the subcutaneous fat at the time of treatment are less likely to result in cure when treated with this method.⁹ As previously discussed, ED and C is a process used to sequentially scrape the tumor away followed by destruction of an extra margin of normal skin by electrodesiccation performed up to 3 times to maximize the possibility of complete removal. Five-year cure rates with small primary SCCs treated with ED and C may be as high as 96%.¹⁰ The main drawbacks with ED and C are that there is no tissue available for histological evaluation to ensure tumor-free resection. ED and C may also result in poor cosmetic outcome. ED and C is not advisable for the treatment of tumors on the face because there may be extension along the hair follicles beyond the reach of the curette.

Cryosurgery
According to the AAD Guidelines, this modality uses liquid nitrogen to destroy the tumor by lowering the temperature to tumoricidal levels. It is especially useful in patients with bleeding disorders and in those in which other forms of surgery are contraindicated or refused by the patient.⁹ During treatment, it is important to include a rim of 3-4 mm of normal tissue beyond clinically visible margins of the tumor.

Excision
According to AAD Guidelines, this surgical procedure is useful for both primary and recurrent tumors. The advantages are that tissue can be assessed microscopically, there is rapid healing of the wound, and improved cosmesis.⁹ The wound is closed primarily with side-to-side closure, flaps, grafts, or allowed to heal by second intention.⁹ SCCs which are well-differentiated; smaller than 2 cm; not occurring on the scalp, ears, eyelids, lips, or nose; not involving the subcutaneous fat, a margin of 4 mm around the clinical border of the lesion can result in a 95% chance of clearance. For tumors that have a high risk of recurrence and are larger than 2 cm, a 6 mm margin is recommended.¹⁰

Mohs Micrographic Surgery (MMS)
According to AAD Guidelines, MMS is particularly efficacious in dealing with some recurrent and some primary tumors that display one or more of the following risk factors associated with aggressive biologic behavior: size > 1 cm; rapid growth; ulceration; growth into deeper tissues including subcutaneous fat, fascia, muscle, bone, or cartilage; immunocompromised host; occurrence in a previously inflammatory or degenerative process or scar; recurrent SCC; anatomic locations (mucous membranes, ear, temple, scalp, eyelid, or other); perineural invasion which may be indicated by pain or paresthesia; histologic features (undifferentiated histologic pattern, depth beyond the subcutaneous fat, perineural invasion, and lymphatic invasion).⁹ The Mohs procedure offers the highest cure rates for patients with high-risk, primary, or recurrent SCC. Mohs micrographic surgery uses horizontal frozen sectioning of the tumor to provide a view of 100% of the peripheral and deep margins of the specimen to ensure tumor-free planes.¹⁰ The 5-year rates of local control for primary SCC at any site, except for the lips and ears, for Mohs micrographic surgery is 96.9% in contrast to 92.1% with other forms of treatment.¹⁰ In patients with recurrent SCC, MMS is associated with 5-year cure rates of 90% to 93.3% in comparison to a rate of 76.7% for recurrent tumors treated with standard excision.¹⁰ Squamous cell carcinoma cases that have lymph node involvement are additionally treated with radiation and lymph node dissection. This combination therapy offers the 5-year cure rate of 30% to 40%.¹⁰ Cases involving distant metastases may be treated with systemic chemotherapy or other biologic response modifiers.¹⁰

Laser Surgery
According to AAD Guidelines, the carbon dioxide laser may be used to excise or destroy SCC. Use of the laser allows for excision of tissue in a bloodless fashion because the laser seals small blood vessels during the treatment, while also allowing for margin control by histopathologic evaluation.⁹

Ionizing Radiation
According to AAD Guidelines, this modality is useful for definitive treatment of primary tumors in selected patients and some recurrent cancers. It is also used for palliation of inoperable tumors. Radiation is not used for treatment of verrucous carcinoma because there is some evidence to suggest that the metastatic potential may be enhanced.⁹

Evolving Therapies
Photodynamic therapy employs a photoactive compound applied to the SCC lesion followed by photoirradiation. Intralesional interferon and other agents may also prove useful in the future. Additionally, oral and topical retinoids are being evaluated for therapeutic and chemoprophylaxis management.⁹

Most patients with primary cutaneous SCC have a very good prognosis.¹⁰ Conversely, those with metastatic disease have a poor long-term prognosis. Patients with regional lymphadenopathy have a < 20% 10-year survival rate, and patients with distant metastases have < 10% 10-year survival rate.¹⁰ When metastasis does occur, it mainly involves the regional lymph nodes.¹⁰ Distant sites including lungs, liver, brain, skin, and bone are less often affected.¹⁰ Patients with squamous cell carcinoma are at risk for developing other malignancies such as cancers of the respiratory organs, buccal cavity, pharynx, small intestines (in men), non-Hodgkin's lymphoma, and leukemia.

To review, the natural course of invasive SCCs in the skin is variable. The incidence of metastases from cutaneous SCC ranges from 1% to 20% in most surveys. In reference to metastatic disease, the metastatic rates result from SCCs arising in scars (37.9%), the lip (13.7%), and the external ear (8.8%). Five-year cure rates after treatment for primary SCC were 96.9% with Mohs micrographic surgery compared to 92.1% with all other forms of treatment (excision, ED and C, cryosurgery, etc.). As with all skin cancer treatment, therapy should be carefully tailored to the specific lesion and influenced by the medical status of the patient. Since there is a 30% risk of having a second primary SCC within 5 years after therapy for the first malignancy, skin cancer patients should have a total body examination once or twice yearly.¹⁰ Patients with squamous cell carcinoma should also follow sun-safety tips. (See AAD Sun Safety Tips).

Return to Medicine Index

1. Drake LA, Ceilley RI, Cornelison RL, et al, for the Committee on Guidelines of Care, Task Force on Basal Cell Carcinoma. Guidelines of Care for Basal Cell Carcinoma. J Am Acad Dermatol. 1992; 26:117-120.
   
   
2. Miller DL, Weinstock MA. Non-melanoma skin cancer in the United States: Incidence. J Am Acad Dermatol. 1994;30:774-778.
   
   
3. Czarnecki D, Meehan C, O'Brien T, Leahy S, Nash C. The changing face of skin cancer in Australia. Int J Dermatol. 1991; 30:715-717.
   
   
4. Korman NJ, Hrabovsky SL. Basal cell carcinomas display extensive abnormalities in the hemidesmosome anchoring fibril complex. Exp Dermatol. 1993;2:139-144.
   
   
5. Tsao H. Update on familial cancer syndromes and the skin. J Am Acad Dermatol. 2000; 42:939-969.
   
   
6. Drake LA, Dinehart SM, Goltz R, et al, for the Guidelines/Outcomes Committee, Task Force on Mohs Micrographic Surgery. Guidelines of care for Mohs micrographic surgery. J Am Acad Dermatol. 1995; 33:271-278.
   
   
7. Telfer NR, Colver GB, Bowers PW. Guidelines for the management of basal cell carcinoma. Br J Dermatol.1999;141:415-423.
   
   
8. Rowe DE, Carroll RJ, Day CL. Long-term recurrence rates in previously untreated (primary) basal cell carcinomas: implications for patient follow-up. Journal of Dermatologic Surgery & Oncology.1989;15:315-328.
   
   
9. Committee on Guidelines of Care, Task Force on Cutaneous Squamous Cell Carcinoma. Guidelines of Care for Cutaneous Squamous Cell Carcinoma. J Am Acad Dermatol. 1993;28:628-631.
   
   
10. Alam M, Ratner D. Cutaneous squamous cell carcinoma. N Engl J Med. 2001:344:975-983.
    
    
11. Johnson TM, Rowe DE, Nelson BR, Swanson NA. Squamous cell carcinoma of the skin (excluding the lip and oral mucosa). J Am Acad Dermatol. 1992;26:467-484.

Disclaimer