eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Pathology
Skin Cancer: Squamous Cell Carcinoma
Updated: Jan 15, 2009
Introduction and Epidemiology
Skin cancers are the most frequently diagnosed cancers in the United States. More than a million estimated new nonmelanoma skin cancers were diagnosed in the United States in 2005. This is nearly equivalent to the number of all other cancers diagnosed in the United States the same year. Of these, approximately 80% are basal cell carcinoma (BCC) and 20% are squamous cell carcinoma (SCC), making cutaneous squamous cell carcinoma (cSCC) the second most common skin cancer and one of the most common cancers overall in the United States. In Australia, nonmelanoma skin cancer incidences as high as 1.17 per 100 have been reported, a rate 5 times greater than all other cancers combined.
Despite increased knowledge and public education regarding the causes of skin cancer and modes of prevention, the incidence of cSCC continues to rise worldwide. This increasing incidence is likely multifactorial. Speculated causes for the increased incidence of skin cancer include an aging population, improved detection, an increased use of tanning beds, and environmental factors such as depletion of the ozone layer. Although patients infrequently die from cSCC, these tumors can cause significant morbidity. Most cSCCs are located in the head and neck region, where surgery for advance stage disease can be disfiguring. Furthermore, the cost of treatment has been shown to pose a significant public health burden. In a study of the Medicare population, the treatment of nonmelanoma skin cancers ranked fifth among the most expensive cancers to treat.
For excellent patient education resources, visit eMedicine's Cancer and Tumors Center. Also, see eMedicine's patient education articles Skin Cancer and Skin Biopsy.
Risk Factors and Pathogenesis
Risk factors
Exposure to cancer-promoting stressors and the response of the body to those exposures (host response) combine to determine the risk of developing cutaneous squamous cell carcinoma (cSCC). Well-known factors that have been shown to promote the development of cSCC include ultraviolet radiation (UVR), immunosuppression, exposure to ionizing radiation or chemical carcinogens, and infection with human papillomavirus (HPV).
Chronic UVR exposure is the most important risk factor for the development of cSCC. UVR is a known mutagen capable of inducing DNA damage that can lead to keratinocyte transformation. UVR has also been shown to alter the cutaneous immune response, leaving the skin susceptible to tumor formation. A number of surrogate indices of chronic UVR exposure from the sun are well known. Specifically, epidemiologic evidence suggests that geographic proximity to the equator, a history of precancerous lesions or prior skin cancers, older age, and male sex predispose an individual to the development of cSCC.
Immunosuppression is also increasingly recognized as a risk factor for the development of skin cancer. For organ transplant recipients on chronic immunosuppression agents, skin cancers account for 90% of all diagnosed malignancies. In this group of patients, cSCC is more common than other keratinocyte-derived neoplasms, including BCC. The risk of developing cSCC is 65-250 times greater among transplant patients than in the general population. Patients immunosuppressed secondary to human immunodeficiency virus (HIV) infection have a more modestly elevated risk of developing a nonmelanoma skin cancer, 3-5 times that of the general population, but do not have the altered SCC-to-BCC ratio typical of transplant recipients. Regardless of etiology, cSCC that arises in the setting of immunosuppression exhibits a more aggressive course, with a higher rate of local recurrence, metastasis, and death.
Host responses that influence cSCCs development include chronic inflammation, genetic predispositions to DNA damage, and, in particular, susceptibility to UVR damage. Fair skin (or a history of repeated sunburns), hazel or blue eyes, blonde or red hair, and albinism are all well-known markers for UVR vulnerability. At the genetic level, only one abnormality has been causally linked to UVR-induced cSCC. Xeroderma pigmentosum is a rare genetic defect in UVR-induced DNA repair characterized by severe sensitivity of UVR and premature development of cSCC. Otherwise, the genetic influences that contribute to the development of cSCC from UVR are still poorly described.
The following are exposure-related risk factors in the development of cSCC:- UVR exposure
- Immunosuppression
- HIV
- Iatrogenic (transplant recipients)
- Ionizing radiation
- Infections (human papillomavirus [HPV])
- Chemical carcinogens
- Arsenic
- Polyaromatic hydrocarbons
The following are host responses that influence cSCC development:
- Genetic susceptibility (xeroderma pigmentosum)
- Susceptibility to UVR
- Fair skin
- Blonde or red hair
- Light-colored eyes
- Chronic inflammation (eg, nonhealing burns or scars [eg, Marjolin ulcer])
Pathogenesis
Malignant transformation of normal epidermal keratinocytes is the hallmark of cSCC. One critical pathogenic event is the development of apoptotic resistance through functional loss of TP53, a well-studied tumor suppressor gene. UVR causes DNA damage through the creation of pyrimidine dimers, a process known to result in genetic mutation of TP53. TP53 mutations are seen in over 90% of skin cancers diagnosed in the United States, as well as most precursor skin lesions, suggesting that loss of TP53 is an early event in the development of cSCC.1
Upon subsequent UVR exposure, keratinocytes undergo clonal expansion, acquiring further genetic defects, and ultimately leading to invasive cSCC. Many other genetic abnormalities are believed to contribute to the pathogenesis of cSCC, including mutations of BCL2 and RAS. Likewise, alterations in intracellular signal transduction pathways, including epidermal growth factor receptor (EGFR) and cyclooxygenase (COX), have been shown to play a role in the development of cSCC.
Pathology
Histopathologic features of cutaneous squamous cell carcinoma (cSCC) remain important for the clinician, as they carry prognostic value and help to define the most appropriate treatment for patients.
Squamous cell carcinoma in situ (CIS), sometimes referred to as Bowen disease, is a precursor to invasive cSCC. This lesion is characterized by nuclear atypia, frequent mitoses, cellular pleomorphism, parakeratosis and hyperkeratosis, and a disorganized progression of cells from the basal to apical layers of the epidermis. CIS is differentiated from actinic keratosis (AK), a similar precancerous skin lesion, by full thickness involvement of the epidermis.
Invasive cSCC is differentiated from CIS and AK by the invasion of the basement membrane by malignant-appearing cells. With invasive cSCC, nests of atypical cells are found within the dermis, surrounded by an inflammatory infiltrate. Conventional cSCC can be divided into 3 histologic grades based the degree of nuclear atypia and keratinization found. Well-differentiated cSCC is characterized by more normal-appearing nuclei with abundant cytoplasm and extracellular keratin pearls. In contrast, poorly differentiated cSCC shows a high degree of nuclear atypia with frequent mitoses, a greater nuclear-cytoplasmic ratio, and less keratinization. Poorly differentiated cSCC carries an increased rate of metastasis and an overall worse prognosis. Moderately differentiated cSCC shares exhibits features of both well-differentiated and poorly differentiated lesions.
Other histologic variants include acantholytic (adenoid) SCC, which is characterized by a pseudoglandular appearance and spindle cell SCC, which has atypical spindle-shaped cells, both of which exhibit a more aggressive clinical course.
Clinical Presentation and Assessment
Clinical presentation
The initial presentation of cutaneous squamous cell carcinoma (cSCC) typically includes a history of a nonhealing ulcer or abnormal growth in a sun-exposed area (see Image 1).
Large sun-induced squamous cell carcinoma on the forehead/temple. Image courtesy of Glenn Goldman, MD.
Approximately 70% of all cSCCs occur on the head and neck, most frequently involving the lower lip, external ear, and periauricular region or the forehead and scalp. Frequently, the presentation of cSCC is preceded by the presence of actinic keratosis (AK). These precancerous lesions appear as scaly plaques or papules, often with an erythematous base. AK is usually only several millimeters in size and ranges from normal skin color to pink or brown. Patients with multiple AKs have an estimated 6-10% lifetime risk of developing skin cancer.
Assessment
Clinical examination should begin with a thorough review of the risk factors for cSCC development. An assessment of the rate of tumor growth is important, as this often reflects the aggressiveness of the lesion. Any history of pain, numbness, visual change, facial muscle weakness, or twitching should be elicited to assess potential peripheral nerve involvement by the tumor.
Every patient should undergo a comprehensive head and neck examination. The overall appearance of any skin lesion must be detailed. The classic presentation of a cSCC is that of a shallow ulcer with heaped-up edges, often covered by a plaque. Of course, the presenting appearance of each cSCC varies according to the site and extent of disease.
In addition to general appearance, the size and location of the lesion should be recorded, as both have prognostic and therapeutic importance. For instance, lesions larger than 2 cm and those located on the external ear and lip have been shown to have a higher rate of metastatic spread. Additionally, tumor size and location affect the cosmetic and functional outcome of surgical excision. Therefore, reconstructive options should be carefully considered in the assessment of every head and neck cSCC. Lesions located near critical areas, such as around the eyes, may require additional evaluation by a dedicated reconstructive surgeon before excision.
Up to 14% of cSCCs exhibit perineural invasion. Evidence of cranial nerve dysfunction on examination should raise concern of significant perineural invasion. The most frequently involved cranial nerves are the facial and trigeminal nerves, underscoring the importance of assessment of facial movement and sensation. Therefore, every patient with head and neck cSCC should undergo systematic evaluation of cranial nerve function.
Finally, regional lymphatics should be assessed for metastatic spread. Regional metastasis of cSCC occurs in 2-6% of cases. The risk of metastasis correlates roughly with tumor size and differentiation. The most frequently involved lymphatics include those located within the parotid gland and upper cervical lymph node levels. Rarely, cSCC presents as a parotid or neck mass because of lymphatic spread from an occult cutaneous lesion or remotely treated skin cancer (see Image 2). The median time from initial treatment to presentation with a parotid or neck mass ranges 10-13 months. Fine-needle aspiration (FNA) biopsy can be of assistance in the evaluation of any mass suspected to represent occult metastasis.
In advanced-stage cSCC, anatomic imaging using computed tomography (CT) or magnetic resonance imaging (MRI) can be helpful in defining the extent of disease. CT is useful for determining the presence of bone or soft tissue invasion (see Image 3) and for evaluating cervical lymph nodes at risk for metastasis. For evaluation of perineural invasion and orbital or intracranial extension, MRI is the preferred imaging modality.
Identifying High-Risk Lesions
Advanced-stage cutaneous squamous cell carcinoma (cSCC) exhibits an aggressive clinical course with a greater likelihood of recurrence and cervical metastasis. Therefore, recognition of these higher risk lesions and subsequent treatment by a qualified specialist is critical.
Lesions found on or around the ear have a 5-18% rate of metastatic spread, roughly 3 times the average rate. Those located in the preauricular region are particularly troublesome given their propensity to invade the parotid gland (see Image 3). cSCC of the lip also shows a high rate of nodal involvement. Therefore, prophylactic neck dissection for select cSCC located at these sites may be warranted.
Size is the most important determinant of outcome for patients with cSCC. Both the depth and width of the lesion influence the potential for recurrence and metastasis. Lesions larger than 2 cm have a higher rate of recurrence (15.2% vs 7.4%) and metastasis (30.3% vs 9.1%) than those smaller than 2 cm. Similarly, lesions that extend to a depth greater than 4 mm have a 45.7% rate of metastatic spread versus 6.7% for those less than 3 mm.
Pathologic features, including poor differentiation, perineural invasion, and lymphovascular involvement, are more likely to be seen with regional lymph node involvement. Poorly differentiated cSCC demonstrates rates of metastatic spread significantly higher than those of other grades (17% vs 4%). Those exhibiting perineural and lymphovascular invasion also exhibit higher rates of metastasis.
cSCC that arises in immunocompromised patients can also exhibit an aggressive course, particularly when the immunosuppression is secondary to solid organ transplantation. This population has a high incidence of both initial and recurrent lesions with the potential for rapid growth and early metastatic spread. Some evidence suggests that these lesions metastasize at a more shallow depth and smaller width than those in nonimmunocompromised patients.
The following are features of high-risk cSCC:
- Size
- Width greater than 2 cm
- Depth greater than 4 mm
- Location
- Ear
- Lip
- Histologic features
- Perineural invasion
- Lymphovascular invasion
- Poorly differentiated grade
- Recurrence
- Immunosuppression
Diagnosis
A biopsy should be performed for any lesion suspected of being a cutaneous neoplasm. For most lesions, the biopsy can be readily accomplished in the clinic under local anesthesia. The type of biopsy performed depends on the size of the lesion. Small skin lesions in noncritical areas may be amenable to excisional biopsy, where the entire area of concern is removed. This method has the benefit of being diagnostic as well as potentially therapeutic without the need for a second procedure. For larger lesions or those located in cosmetic or functionally critical areas, confirming the diagnosis before embarking on surgical excision that may be extensive and require reconstruction is often preferable. In these cases, an incisional or punch biopsy should be performed initially with further treatment based on the pathology results.
Whatever biopsy method chosen, several principles should be followed. The biopsy should contain the full thickness of the skin in order to evaluate the depth of the lesion. Therefore, a shave biopsy is generally not recommended when malignancy is suspected. The biopsy should be centered over the transition point between normal and involved skin, thereby providing a reference for comparison by the pathologist. When possible, incisions should be made parallel to the natural lines of skin tension (Langer lines) for optimal cosmetic outcome. For punch biopsies, stretching the skin perpendicular to the Langer lines creates an ellipse oriented in this optimal direction and facilitates closure.
Prevention and Treatment
Prevention
Given the central role that ultraviolet radiation (UVR) plays in the pathogenesis of cutaneous squamous cell carcinoma (cSCC), methods aimed at decreasing UVR exposure form the cornerstone of cSCC prevention. Several randomized controlled clinical trials have shown a protective role for the daily application of sunscreen in the prevention new AKs and new cSCC. In addition, sun-avoiding behaviors aimed at limiting overall UVR exposure are believed to be beneficial.
The evidence behind other measures to prevent cSCC is lacking. Large well-controlled studies failed to show a beneficial role for dietary supplements in the prevention of skin cancers, including selenium, beta-carotene, retinal, and isotretinoin.
Current recommendations for screening skin examinations from the American Cancer Society call for a skin examination every 3 years for persons aged 20-39 years and annually after age 40 years. The American Academy of Dermatology recommends annual screening for all patients.
Treatment of precancerous lesions
Several effective treatment modalities exist for precancerous skin lesions, including carcinoma in situ (CIS) and actinic keratosis (AK). Most of these treatments are easily performed in an outpatient setting. Topical application of 5-flourouracil (Efudex) or imiquimod is effective in treating precancerous lesions of the head and neck. Similarly, the application of liquid nitrogen cryotherapy or electrocautery and curettage is used, with cure rates reported at greater than 95%. Although efficacious in the treatment of CIS and AK, these methods should not be used on confirmed or suspected invasive cSCC because they fail to provide a diagnostic tissue sample or a way to assess the adequacy of treatment. For confirmed or suspected cSCC, surgical excision with microscopic assessment of tissue margins is the treatment of choice.
Treatment of cutaneous squamous cell carcinoma
Primary surgical excision and Mohs micrographic surgery are the 2 primary treatment options for invasive cSCC. With appropriate patient selection, these techniques have comparable cure rates. Mohs surgery was developed by Frederic E. Mohs in the 1930s and is a method of tumor excision in which the surgeon first excises the visible tumor with a small margin of normal tissue. Horizontal frozen sections are then prepared, and the entire margin is evaluated under the microscope. Areas that demonstrate residual microscopic tumor involvement are re-excised, and the margins are reexamined. This cycle is completed until no further tumor is visualized.
This technique has a high reported cure rate for early-stage cSCC and is considered ideal for removing small lesions on the face. However, Mohs surgery is time consuming and highly dependent on technique. Mohs surgery is ill suited for large, aggressive, or recurrent cSCC, in which the risk of recurrence or regional metastasis is high (see Image 3). In these cases, en bloc surgical excision is the standard method of treatment.
Unlike melanoma, no large randomized studies have addressed the issue of appropriate margin size in cSCC. Margins of 4 mm and 6 mm have been suggested for lesions less than and greater than 2 cm, respectively, providing a clearance rate of 95% or greater. However, these should be taken only as rough guidelines with the understanding that large aggressive lesions frequently have substantial extension beyond the apparent superficial boundary. Therefore, surgeon experience and judgment in planning surgical margins is paramount to the successful treatment of cSCC.
For patients at risk for metastatic spread to lymph nodes, the standard treatment is surgical excision of the primary lesion along with the involved lymph node basins. Skin cancers located in the periauricular region, frontotemporal scalp, and mid face often drain via lymph nodes in the parotid gland. Consequently, the parotid is the most frequently involved site of metastatic spread. In cases that involve parotid involvement, a parotidectomy with or without a simultaneous neck dissection is the procedure of choice.
Radiation therapy as a primary form of treatment is typically reserved for patients who are unable to undergo surgical excision. More frequently, radiation therapy is used as an adjuvant to surgery for improved locoregional control. Postoperative radiotherapy is considered for tumors that exhibit perineural invasion or other high-risk features and for those that involve regional metastasis. Chemotherapy has not been found to be effective for the treatment of cSCC. However, emerging evidence suggests that epidermal growth factor receptor (EGFR) inhibitors may be useful adjuncts to surgical treatment.
Staging and Prognosis
Like many cancers, cutaneous squamous cell carcinoma (cSCC) is classified according to the American Joint Committee on Cancer (AJCC)/International Union against Cancer (UICC) tumor-node-metastasis (TNM) staging system. This anatomy-based staging system is designed to stratify patients into general prognostic cohorts based on the size and extent of disease (see TNM Staging system for nonmelanoma skin cancers [NMSC]). Although TNM staging is useful for estimating the outcome for a group of cSCC patients with similar tumor characteristics, it cannot estimate the risk for an individual patient. It does not take into consideration other tumor and patient factors, such as ultraviolet radiation (UVR) exposure, age, and comorbidity, that may also affect prognosis. Therefore, current methods for estimating the outcome of a patient with head and neck cSCC depend heavily on the experience of the treating physician and can vary significantly between surgeons.
Despite the inherent limitations of TNM staging, the outcomes of patients with head and neck cSCC follow a predictable pattern. In general, most patients with early-stage tumors fare well (overall 5-yr survival rate >90%) when the tumors are adequately treated. Most patients present with early-stage tumors. The outcome of patients with advanced-stage cSCC is considerably worse. For patients with lymph node metastases, the 5-year survival is even lower, estimated at 28-45%.
TNM staging system for NMSC
- Primary tumor (T)
- TX - Primary tumor cannot be assessed.
- T0 - No evidence of primary tumor
- Tis - Carcinoma in situ
- T1 - Tumor 2 cm or less
- T2 - Tumor larger than 2 cm but smaller than 5 cm
- T3 - Tumor larger than 5 cm
- T4 - Tumor invades deep extradermal structures (bone, muscle, cartilage).
- Regional lymph nodes (N)
- NX - Regional lymph nodes cannot be assessed.
- N0 - No regional lymph node metastasis
- N1 - Regional lymph node metastases
- Distant metastasis (M)
- MX - Distant metastasis cannot be assessed.
- M0 - No distant metastasis
- M1 - Distant metastasis
Table 1. Stage Grouping
Open table in new window
Table
| Stage | Primary Tumor | Regional Lymph Nodes | Distant Metastasis |
| Stage 0 | Tis | N0 | M0 |
| Stage I | T1 | N0 | M0 |
| Stage II | T2 | N0 | M0 |
| T3 | N0 | M0 | |
| Stage III | T4 | N0 | M0 |
| Any T | N1 | M0 | |
| Stage IV | Any T | Any N | M1 |
| Stage | Primary Tumor | Regional Lymph Nodes | Distant Metastasis |
| Stage 0 | Tis | N0 | M0 |
| Stage I | T1 | N0 | M0 |
| Stage II | T2 | N0 | M0 |
| T3 | N0 | M0 | |
| Stage III | T4 | N0 | M0 |
| Any T | N1 | M0 | |
| Stage IV | Any T | Any N | M1 |
Multimedia
 | Media file 1: Large sun-induced squamous cell carcinoma on the forehead/temple. Image courtesy of Glenn Goldman, MD. |
 | Media file 2: Preauricular and helical scars (black arrows) from prior excisions are noted in a patient who presented with cervical metastases (white arrow) from an occult cutaneous squamous cell carcinoma (cSCC). |
 | Media file 3: Contrast-enhanced, axial computed tomography (CT) of a patient with soft tissue invasion of the right parotid gland (arrow) by an ulcerative cutaneous squamous cell carcinoma (cSCC). |
 | Media file 4: Large, neglected cutaneous squamous cell carcinoma (cSCC) of the right ear that requires wide local excision via auriculectomy and reconstruction. The risk of lymph node metastasis with this deeply ulcerative tumor is sufficient enough to warrant elective neck dissection. |
Keywords
skin cancer, squamous cell carcinoma, SCC, SCCa, SCCA, cSCC, squamous cell carcinoma of the skin, basal cell cancers, squamous cell cancers, tumors, cancer, skin trauma, actinic keratosis, carcinoma in situ, squamous cell carcinoma in situ, in situ skin carcinomas, recurrent lesions, Mohs surgery, Mohs micrographic surgery, metastatic disease, basal cell carcinoma, Bowen disease, abnormal masses, malignant squamous neoplasm
More on Skin Cancer: Squamous Cell Carcinoma |
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Further Reading
Keywords
skin cancer, squamous cell carcinoma, SCC, SCCa, SCCA, cSCC, squamous cell carcinoma of the skin, basal cell cancers, squamous cell cancers, tumors, cancer, skin trauma, actinic keratosis, carcinoma in situ, squamous cell carcinoma in situ, in situ skin carcinomas, recurrent lesions, Mohs surgery, Mohs micrographic surgery, metastatic disease, basal cell carcinoma, Bowen disease, abnormal masses, malignant squamous neoplasm
