eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Pathology

Skin Cancer: Basal Cell Carcinoma

Author: M Abraham Kuriakose, MD, DDS, FRCS, Chairman, Head and Neck Institute, Amrita Institute of Medical Sciences
Contributor Information and Disclosures

Updated: Dec 11, 2006

Introduction

Background

Basal cell carcinoma (BCC) constitutes approximately 80% of all nonmelanoma skin cancers. The tumors most often appear in individuals aged 40-60 years. BCC's predilection for the head and neck is notable and is related to its primary etiology—solar exposure. Approximately 75-86% of primary BCCs are found on the head or neck. The most common location on the head is the nose, specifically the nasal tip and alae. Australia has the highest incidence of basal cell carcinoma in the world.

Sun exposure is the primary etiologic agent for the development of BCC. Risk is related to skin type and the degree of exposure to sunlight, particularly UV-B radiation. The tumors are more frequent in individuals with fair complexions. Fitzpatrick skin-type scale, which ranges from very fair (skin type I) to very dark (skin type VI), categorizes cutaneous sensitivity to UV radiation. It is based on the individual's tendency to burn and tan and is a good predictor of relative risk among whites. The prevalence of BCC increases in areas of higher altitude and in areas of lower latitude. The incidence of BCC is rising, partly because of atmospheric changes and the increased popularity of sunbathing.

Pathophysiology

BCC primarily affects sun-exposed skin, particularly the upper two thirds of the face.

Frequency

United States

For statistical purposes, BCC and squamous cell carcinomas (SCCs) are grouped as nonmelanoma skin cancer. Incidence of non-melanoma skin cancer varies depending on geographic location. These cancers cause about 300 cases per 100,000 population in Texas and Arizona. The incidence is about half that figure in New York and Maine.

International

Australia has the highest incidence of BCC, ranging from 650-1560 cases per 100,000 population.

Mortality/Morbidity

The estimated annual death rate from this tumor is 0.44 per 100,000 persons. Most of these deaths are due to SCC. BCC rarely causes death. Morbidity is associated with uncontrolled advanced disease.

Race

Whites of Celtic ancestry have the highest risk for BCC. Incidence is low in blacks, Asians, and Hispanics.

Sex

BCC has a male predilection, with a 2:1 male-to-female ratio.

Age

Incidence peaks in persons aged 55-75 years.

Clinical

History

BCC appears as insidious, painless, nonhealing ulcers or nodules on the sun-exposed parts of the body. BCC has a particular predilection for the upper two thirds of the face and is common among white men who are elderly. Because of changing sun-exposing lifestyle patterns among the sexes, the male sex predilection is gradually decreasing. During the clinical evaluation, the patient's social and occupational history of sun exposure, family history of skin cancer, and geographic area of origin are determined to estimate the likelihood that a second primary tumor will develop. Obtain a past history of treatment of the index tumor or other skin tumors. In patients with recurrent tumors, deeper invasion should be expected. Recurrence following radiation therapy is often biologically more aggressive.

Physical

Physical examination should attempt to elicit the subtype of BCC, extent of the tumor, and involvement of important cosmetic and functional structures. Palpation should be used to attempt to estimate the depth of invasion and fixation to the underlying structures. In patients with recurrent or deeply infiltrative tumors, involvement of the facial nerve or branches of the trigeminal nerve should be tested. Facial nerve function can be monitored by comparing facial symmetry during voluntary facial movements with that at rest. Sensory nerve function can be tested and compared to the nonaffected side by means of light touch and pinprick. Orbital invasion can cause diplopia, proptosis, and ophthalmoplegia. Any limitation in ocular movements and/or diplopia should be tested.

BCC seldom causes regional or distant metastasis, with the exception of the metatypical basosquamous type. To evaluate for lymph node metastasis, particular attention should be taken to examine the parotid posterior auricular, suboccipital, and upper cervical groups of lymph nodes. Four different clinicopathologic types of BCC exist, each with distinct biologic behavior.

• Undifferentiated BCC
• Nodular or noduloulcerative BCC
  • More than 60% of BCCs belong to this subtype.
  • These lesions appear as well-circumscribed, dome-shaped, pearly nodules with or without ulceration.
• Superficial BCC
  • This BCC subtype appears as a red scaly patch that resembles the chronic dermatitis predominantly seen in the extremities.
  • These tumors spread superficially and can involve a large surface area.
  • Although satellite islands appear multifocal on standard histopathologic examination, 3-dimensional reconstruction shows that they are interconnected.
• Morpheaform or sclerosing BCC
  • This form accounts for 10% of lesions.
  • Lesions appear as flat or slightly depressed, fibrotic, and firm.
  • The tumor has a deeply infiltrative character, which may extend beyond the clinically obvious tumor. This feature increases the recurrence potential of morpheaform or sclerosing BCC.
• Micronodular BCC
  • This type manifests as a plaquelike indurated lesion with poorly demarcated contours.
  • They have increase incidence of recurrence and an aggressive behavior.
• Other BCCs
  • Aggressive-growth BCC
  • Infiltrative-growth BCC
  • Metatypical BCC
• Differentiated BCCs
  • Keratotic BCC
  • Infundibulocystic BCC
  • Follicular BCC
  • Pleomorphic BCC

Causes

Incidence of BCC correlates with the amount of accumulated sun exposure. Epidemiologic and molecular studies have confirmed that the UV radiation (UVR) spectrum of sunlight, in synergy with genetic susceptibility, is responsible for BCCs.

• UV radiation
  • The UVR spectrum of sunlight is divided into 3 parts: long wave UV-A (320-400 nm), intermediate wave UV-B (290-320 nm), and shortwave UV-C (200-290 nm).
    • UV-B and UV-C can modify unsaturated chemical bonds of nucleic acids, which may lead to mutations.
    • UV-C does not penetrate the atmospheric ozone layer; therefore, UV-B is the primary agent responsible for most skin cancers.
    • The UV-A spectrum is absorbed by melanin and, through free-radical transfer, affects cellular deoxyribonucleic acid (DNA).
  • Mutations caused by UVR 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.
• Host factors
  • In addition to environmental factors, host factors play a critical role in the pathogenesis of BCC. Host factors include racial predilections, genetic syndromes, predisposing syndromes, and immunologic factors.
  • Racial and ethnic factors
    • White race with Celtic ancestry (eg, Irish, Scottish, Welsh) has the highest predilection for BCC.
    • Predilection is primarily related to the pigmentary characteristics of the skin and sun sensitivity.
    • Ability to tan is the most important protective factor.
    • Light eye color; red, blonde, or light-brown hair color; and freckling are strong predictors of BCC.
  • Genetic syndromes
    • Xeroderma pigmentosa is a rare autosomal recessive disorder characterized by hypersensitivity to UVR. It causes defects in DNA repair and synthesis, resulting in cutaneous cancers (eg, BCC, SCC, melanoma).
    • Nevoid basal cell syndrome is an autosomal dominant disorder associated with multiple BCCs, odontogenic keratocysts, calcification of falx cerebri, and rib abnormalities.
    • Epidermodysplastic verruciformis is an autosomal recessive disorder characterized by the development of BCC and SCC from warts.
• Molecular alterations
  • Inappropriate activation of the hedgehog (HH) 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 SHH, SMO, and GLI.
  • Mutations in TP53 are found in about 50% of sporadic cases. Most show signature mutations that indicate exposure to UV-B radiation.

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