Head and Neck: Squamous cell carcinoma: an overview
Written | 2011-09 | Audrey Rousseau, Cécile Badoual |
Universite d'Angers, Departement de Pathologie Cellulaire et Tissulaire, CHU Angers, 4 rue Larrey, 49100 Angers, France (AR); Universite Rene Descartes Paris 5, Service d'Anatomie Pathologique, Hopital Europeen Georges Pompidou, 20 rue Leblanc, 75015 Paris, France (CB) |
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1. Identity
ICD-Topo | C301,C310-C313,C318-C319,C030-C031,C039-C041,C048-C052,C058-C062,C068-C069,C129-C132,C138-C139,C320-C323,C328-C329,C000-C006,C008-C009,C300,C110-C113,C118-C119,C690-C691,C693,C695-C698,C090-C091,C098-C104,C108-C109,C140,C142,C148,C079-C081,C088-C089,C019-C024,C028-C029,C339 ACCESSORY, SINUSES, MIDDLE & INNER EAR / GUM, FLOOR OF MOUTH, & OTHER MOUTH / HYPOPHARYNX / LARYNX / LIP / NASAL CAVITY (INCLUDING NASAL CARTILAGE) / NASOPHARYNX / ORBIT & LACRIMAL GLAND, (EXCL. RETINA, EYE, NOS) / OROPHARNYX / PHARYNX / SALIVARY GLAND / TONGUE / TRACHEA |
ICD-Morpho | 8070/3 Squamous cell carcinoma, NOS |
Atlas_Id | 5078 |
Phylum | Head and Neck::Squamous cell carcinoma |
WHO/OMS Classification | Head and Neck |
Note | Head and neck squamous cell carcinoma (HNSCC) develops from the mucosal linings of the upper aerodigestive tract, comprising 1) the nasal cavity and paranasal sinuses, 2) the nasopharynx, 3) the hypopharynx, larynx, and trachea, and 4) the oral cavity and oropharynx. Squamous cell carcinoma (SCC) is the most frequent malignant tumor of the head and neck region. HNSCC is the sixth leading cancer by incidence worldwide. There are 500000 new cases a year worldwide. Two thirds occur in industrialized nations. HNSCC usually develops in males in the 6th and 7th decade. It is caused by tobacco and alcohol consumption and infection with high-risk types of human papillomavirus (HPV). SCC often develops from preexisting dysplastic lesions. The five-year survival rate of patients with HNSCC is about 40-50%. |
2. Classification
SCC can occur either in 1) the nasal cavity and paranasal sinuses, 2) the nasopharynx, 3) the hypopharynx, larynx, and trachea, or 4) the oral cavity and oropharynx. The 2005 World Health Organization (WHO) classification of Head and Neck Tumors (Barnes et al., 2005) distinguishes different types of SCC: - Conventional - Verrucous - Basaloid - Papillary - Spindle cell (sarcomatoid) - Acantholytic - Adenosquamous - Cuniculatum Each variant can arise in any one of the 4 above mentioned head and neck regions, except for the cuniculatum type which only develops from the oral mucosa. |
3. Clinics and Pathology
Etiology | The most important risk factors for developing HNSCC are tobacco smoking and alcohol consumption, which have a synergistic effect. Smoking habits that increase the risk of developing HNSCC are smoking black tobacco (compared to blond tobacco), smoking at a young age, long duration, high number of cigarettes per day, and deep smoke inhalation (Benhamou et al., 1992). Avoiding cigarettes and alcohol could prevent about 90% of HNSCCs, especially laryngeal and hypopharyngeal tumors. Tobacco chewing is a major cause of oral and oropharyngeal SCC in the Indian subcontinent, parts of South-East Asia, China and Taiwan, especially when consumed in betel quids containing areca nut (Znaor et al., 2003). In India, chewing accounts for nearly 50% of oral and oropharyngeal tumors in men and over 90% in women (Barnes et al., 2005). Significant risk increases of developing HNSCC have also been reported among non-drinking smokers and, to a lesser extent, non-smoking heavy drinkers. Heavy consumption of all types of alcoholic beverages (wine, beer, hard liquors) confers an increased risk (La Vecchia et al., 1999). Conversely, protective effects of diets rich in fresh fruits and vegetables have been described (Pelucchi et al., 2003). Some occupational exposures may be associated with a higher risk of developing HNSCC, especially of the larynx: polycyclic aromatic hydrocarbons, metal dust, cement dust, varnish, lacquer, etc... Significant associations were also found with ionizing radiation, diesel exhausts, sulphuric acid mists, and mustard gas (Barnes et al., 2005). The incidence of HNSCC in specific sites has been slowly declining during the past decade, due to a decrease in the prevalence of the more traditional risk factors, most notably smoking. However, in the Western World, HNSCCs, notably of the oral cavity and oropharynx, are becoming more prevalent, which may be related to an increase in oral and oropharyngeal HPV infections (Leeman et al., 2011). Indeed, recent studies have shown that infection with high-risk types of HPV (e.g. HPV-16 and -18) is responsible for a subgroup of HNSCCs. HPV-positive tumors represent a different clinicopathological and molecular entity compared to HPV-negative cases (see below). HPV infection is now recognized as one of the primary causes of oropharyngeal SCC (especially SCC of the tonsils and the base of the tongue). In the USA, about 40-80% of oropharyngeal cancers are caused by HPV, whereas in Europe the proportion varies from around 90% in Sweden to less than 20% in communities with the highest tobacco use (Marur et al., 2010). Patients tend to be younger, with no prior history of tobacco and/or heavy alcohol consumption. There is evidence that HPV-positive HNSCC is a sexually transmitted disease. A strong association between sexual behavior (oral sex) and risk of oropharyngeal cancer as well as HPV-16-positive HNSCC has been demonstrated (Smith et al., 2004; Gillison et al., 2008). Finally, certain inherited disorders, such as Fanconi anemia or Bloom syndrome, predispose to HNSCC (Kutler et al., 2003; Barnes et al., 2005). | ||||||||||||||||||
Epidemiology | SCC is the most frequent malignant tumor of the head and neck region. HNSCC represents the sixth leading cancer by incidence and there are 500000 new cases a year worldwide (Kamangar et al., 2006). Two thirds occur in industrialized nations. Most HNSCCs arise in the hypopharynx, larynx, and trachea, and in the oral cavity and oropharynx. The majority of laryngeal SCCs originate from the supraglottic and glottic regions. Tracheal SCCs are rare compared to laryngeal ones. The most common oropharyngeal site of involvement is the base of the tongue. Within the oral cavity, most tumors arise from the floor of the mouth, the ventrolateral tongue or the soft palate complex. HNSCCs occur most frequently in the sixth and seventh decades. They typically develop in men though women are more and more affected because of increased prevalence of smoking over the last two decades (Barnes et al., 2005). For laryngeal, hypopharyngeal and tracheal SCCs, the incidence in men is high in Southern and Central Europe, some parts of South America, and among Blacks in the United States. The lowest rates are recorded in South-East Asia and Central Africa. The disease is slightly more common in urban than in rural areas. For oral and oropharyngeal SCCs, the disease usually affects adults in the 5th and 6th decades of life. Extremely elevated rates are observed in France, parts of Switzerland, Northern Italy, Central and Eastern Europe, and parts of Latin America. Rates are high among both men and women throughout South Asia. In the US, incidence rates are two-fold higher in Blacks compared to Whites (Barnes et al., 2005). | ||||||||||||||||||
Clinics | Clinical features of HNSCC depend on the localization of the tumor. Nasal and paranasal sinuses Nasopharynx Hypopharynx, larynx, and trachea Oral cavity and oropharynx | ||||||||||||||||||
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Figure 1: Endoscopy. Exophytic and ulcerative SCC of the left vocal cord. Figure 2: Large exophytic and ulcerative SCC of the left amygdala. Fig. 1-2 were kindly provided by Dr S. Hans (Georges Pompidou European Hospital, Paris, France). | |||||||||||||||||||
Pathology | Precursor lesions The 2005 WHO classification of precursor lesions (Barnes et al., 2005) is as follows: - Squamous cell hyperplasia Hyperplasia describes increased cell numbers. This may be in the spinous layer (acanthosis) and/or in the basal/parabasal cell layers (progenitor compartment), termed basal cell hyperplasia. The architecture shows regular stratification without cellular atypia. - Mild dysplasia (Squamous Intraepithelial Neoplasia (SIN) 1) - Moderate dysplasia (SIN 2) - Severe dysplasia (SIN 3) - Carcinoma in situ (SIN 3) The Ljubljana classification of squamous intraepithelial lesions has also been proposed (see below) (Barnes et al., 2005).
The clinical picture of precursor lesions depends on the location and severity of the disease. In case of dysplastic lesions of the hypopharynx, larynx or trachea, patients may present with fluctuating hoarseness, sore throat, and/or chronic cough of a few months' duration. However, some individuals may be asymptomatic. Endoscopically, the lesions may be discrete or diffuse, smooth or irregular, flat or exophytic. Precursor lesions may present as a small flat patch or as a large warty plaque. The surface may be brown to red (erythroplakia) or present with circumscribed whitish plaques (leukoplakia). White patches may be ulcerated. Leukoplakia, in contrast to erythroplakia, tends to be well demarcated and seems to have a lower risk of malignant transformation. The lesions are commonly diffuse, with a thickened appearance. However, in a minority of cases, patchy atrophy may be present. In the larynx, the precursor lesions appear mainly along the anterior true vocal cords. Two thirds of vocal cord lesions are bilateral. Occasionally, precursor lesions may present macroscopically as normal mucosa (Barnes et al., 2005; Thompson, 2006). Microscopically, dysplasia is defined as architectural and cytological changes of the epithelium, without evidence of invasion. The diagnostic features of dysplasia are not uniformly accepted or interpreted. In dysplastic lesions, the epithelium presents with irregular stratification, loss of polarity of basal cells, drop-shaped rete ridges, increased number of mitotic figures, abnormal superficial mitoses, premature keratinization in single cells (dyskeratosis) and keratin pearls within rete pegs. Cytological changes include abnormal variation in nuclear or cell size and shape, increased nuclear to cytoplasmic ratio, increased nuclear size, atypical mitotic figures, increased number and size of nucleoli, and hyperchromasia. The spectrum of dysplasia is divided for practical reasons into mild, moderate and severe. In mild dysplasia, architectural disturbances and cytological atypia are limited to the lower third of the epithelium. In moderate dysplasia, architectural and cytological changes extend into the middle third of the epithelium. Up-grading from moderate to severe dysplasia may be considered when there is marked cytological atypia. Severe dysplasia displays greater than two thirds altered epithelium. Carcinoma in situ presents with full thickness or almost full thickness architectural abnormalities accompanied by cytological atypia (Fig.3). Superficial and atypical mitotic figures are commonly seen. By definition, invasion has not yet occurred. Differential diagnosis of dysplastic lesions includes reactive or regenerative squamous epithelium (Barnes et al., 2005; Thompson, 2006). Conventional type squamous cell carcinoma Verrucous carcinoma Basaloid squamous cell carcinoma Papillary squamous cell carcinoma Spindle cell carcinoma Acantholytic squamous cell carcinoma Adenosquamous carcinoma Carcinoma cuniculatum is a rare variant of oral cancer displaying similarities with lesions more commonly described in the foot in which the tumor infiltrates deeply into the bone. There is proliferation of stratified squamous epithelium in broad processes with keratin cores and keratin-filled crypts which seem to burrow into bone tissue, but lack obvious cytological features of malignancy. Clinical-pathological correlation is often needed to make the diagnosis (Barnes et al., 2005). Nasopharyngeal carcinoma and lymphoepithelial carcinoma are rare entities distinct from conventional squamous cell carcinomas. Lymphoepithelial carcinoma (LEC) may develop in the nasal cavity and paranasal sinuses, the hypopharynx, larynx and trachea, and in the oral cavity and oropharynx. It is a poorly differentiated squamous cell carcinoma or histologically undifferentiated carcinoma accompanied by a prominent reactive lymphoplasmacytic infiltrate, morphologically similar to nasopharyngeal carcinoma. Most sinonasal LECs are associated with Epstein-Barr virus (EBV) infection (Barnes et al., 2005). Histogenesis | ||||||||||||||||||
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Figure 3: Carcinoma in situ. Full thickness architectural abnormalities and cytological atypia Hematoxylin and eosin staining (original magnification x200). Figure 4: Invasive SCC. Invasive growth with disruption of the basement membrane and extension into the underlying tissue. Hematoxylin and eosin staining (original magnification Fig. 4A: x20, Fig. 4B: x100). Figure 5: Invasive SCC. Mitoses (at 9 o' clock) and nuclear atypia. Hematoxylin and eosin staining (original magnification x400). Figure 6: Invasive SCC. Focal keratinization (left hand side). Hematoxylin and eosin staining (original magnification x400). Figure 7: Verrucous carcinoma. Thickened, club-shaped, projections of well-differentiated squamous epithelium and abundant surface keratosis (church-spire keratosis). Hematoxylin and eosin staining (original magnification x20). Figure 8: Basaloid SCC. Solid pattern of growth and central comedo-type necrosis. Hematoxylin and eosin staining (original magnification x100). Figure 9: p16 immunostaining in basaloid SCC (original magnification x200). | |||||||||||||||||||
Cytogenetics | Precursor lesions Malignant transformation of the mucosal lining is a genetic process resulting from accumulation of multiple genetic alterations that dictates the frequency and pace of progression to invasive carcinoma. LOH studies indicate that the earliest alterations appear to target specific genes located on chromosomes 3p, 9p21 (CDKN2A), and 17p13 (TP53). Alterations that tend to occur in association with higher grades of dysplasia and SCC include cyclin D1 amplification, PTEN inactivation, and LOH at 13q21, 14q32, 6p, 8, 4q27, and 10q23 (Barnes et al., 2005). There are no individual markers that reliably predict malignant transformation of dysplastic lesions. Ploidy studies of dysplastic leukoplakias showed that the great majority of aneuploid lesions developed SCC in the follow-up period, by contrast with 60% of tetraploid lesions and only about 3% of diploid lesions (Sudbo et al., 2001). Similar studies on erythroplakias confirmed the higher predictive potential of aneuploidy in identifying cases which progressed to SCC (Sudbo et al., 2002). Invasive squamous cell carcinoma | ||||||||||||||||||
Prognosis | Precursor lesions Some precursor lesions are self-limiting and reversible (particularly if apparent etiologic factors are removed), others persist and some progress to SCC. The likelihood of malignant change directly relates to the severity of dysplasia. However, it is clear that malignancy can develop from any grade of dysplasia or even from morphologically normal epithelium. Dysplastic lesions classified as moderate to severe have an 11% rate of malignant transformation. Diagnosis of precursor lesions implies a need for close follow-up and complete excision. Patients with carcinoma in situ require more extensive management (Thompson, 2006). Dysplastic lesions are frequently found in the surgical margins of invasive SCC, meaning such lesions can remain in the patient. These unresected fields act as an important source of local recurrences and second primary tumors that often occur in patients treated for HNSCC. Invasive squamous cell carcinoma |
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5. Citation
This paper should be referenced as such : |
Rousseau A, Badoual C |
Head and Neck: Squamous cell carcinoma: an overvie |
Atlas Genet Cytogenet Oncol Haematol. in press |
On line version : http://atlasgeneticsoncology.usal.es/classic/Tumors/HeadNeckSCCID5078.html |
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