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53% (9/17) for CIS and 3/17 (18%) for moderate-severe dysplasia [75], The progression rate of CIS to invasive carcinoma was found to be 63% in a group of 27 patients managed conservatively, after a mean follow-up time of 9 months [90], In the series of Gillis et al. [91] progression to CIS or invasive carcinoma was observed in 3/7 patients with keratosis and in 5/12 cases of atypia with or without keratosis; progression to invasive SCC was observed in 3/8 cases of CIS. Norris and Peale [73] used the same terminology and found that the incidence of progression was related to the presence of atypia: only 1/30 keratosis without atypia progressed to SCC after 32 months. Of 86 cases of keratosis with atypia, 11 progressed, after an average of 22 months: 5 to SCC, 4 to CIS, and 2 to CIS with equivocal evidence of invasion. Hellquist et al. [78] found an overall incidence of progression to SCC of 8.7% («=161). SCC developed in 2/98 (2%) of patients with slight dysplasia, 3/24 (12%) with moderate dysplasia, and 9/39 (23%) with severe dysplasia/CIS. Additionally, 5/98 cases with hyperplasia or mild dysplasia progressed to moderate or severe dysplasia; 3/24 moderate dysplasia progressed to severe dysplasia. The mean follow-up time was not indicated, but more than 86% of patients had more than 2 years follow-up and 57% more than 5 years. Crissman et al. [14] stressed that 36% of 25 patients with CIS had microinvasive carcinoma (Figs. 4.26 and 4.27) and another three developed invasive carcinoma in 6 to 8 years (data summarized in Table 4.9). In a large series of patients followed from 1.5 to 12 years and classified according to the Ljubjana classification scheme, 0.7% of simple (« = 380), 1% of abnormal («=414), and 9.5% of atypical hyperplasia («=105) progressed to invasive carcinoma [18],

Other investigators have stressed the importance of specific histological parameters in predicting progression into invasive SCC. The occurrence of single cell intraepithelial keratinization (Figs. 4.17, 4.18, and 4.22) [14] pleomorphism, mitotic activity, and mucosa-associated

FIGURE 4.26 Microinvasive carcinoma at low power.

FIGURE 4.27 Microinvasive carcinoma at high power. Dysplastic cells, from a layer of basal cells showing marked pleomorphism, encroach upon the underlying submucosa. The basement membrane in this area has become blurred. Further down, a detached nest of pleomorphic cells, with individual cell keratinization, is present. These findings are compatible with early microscopic invasion.

FIGURE 4.27 Microinvasive carcinoma at high power. Dysplastic cells, from a layer of basal cells showing marked pleomorphism, encroach upon the underlying submucosa. The basement membrane in this area has become blurred. Further down, a detached nest of pleomorphic cells, with individual cell keratinization, is present. These findings are compatible with early microscopic invasion.

inflammation [15] has been found to confer an increased likelihood for progression to SCC. In the series of Crissman et al. [14], dyskeratosis was further associated with an increased likelihood of recurrence.

Follow-up studies of dysplasia highlight that these lesions may recur not only in the same site, but also in anatomically separate foci, as either CIS or invasive carcinoma. Thus in the series of Gillis et al. [91], 13 of 57 patients treated by radiotherapy or surgery recurred or developed de novo as CIS or invasive SCC. In 2/42 patients, a second primary occurred. These data highlight the presence of multiple foci of transformed cells within the upper aerodigestive tract, stressing that the entire field is prone to develop cancer, as first described by Slaughter et al. [92],

References

1. Coltrera, M„ Zarbo, R. J., Sakr, W„ and Gown, A. M. (1992). Markers for dysplasia of the upper aerodigestive tract. Am. J. Pathol. 141, 817-825.

2. Yashima, K., Maitra, A., Rogers, B. B., Timmons, C. F., Rathi, A., Pinar, H„ Wright, W. E., Shay, J. W., and Gazdar, A. (1998). Expression of the RNA component of telomerase during human development and differentiation. Cell Growth Differ. 805-813.

3. Zidar, N., Cor, and Kambic, V. (1996). Expression of Ki-67 antigen and proliferative cell nuclear antigen in benign and malignant epithelial lesions of the larynx. J. Laryngol. Otol. 110, 440-445.

4. World Health Organization Collaborating Centre for Oral Precancerous Lesions. (1978). Definition of leukoplakia and related lesions: An aid to studies on oral precancer. Oral Surg. 46(4), 518-539.

5. Browne, R. M., and Potts, A. J. C. (1986). Dysplasia in salivary gland ducts in sublingual leukoplakia and erythroplakia. Oral Surg. Oral Med. Oral Pathol. 62, 44-48.

TABLE 4.9 Incidence of Progression to SCC in Relation to Histology in Laryngeal Dysplasia
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