Browsing by Subject "adenoid cystic carcinoma"

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    Assessment of p63 expression in the salivary gland neoplasms adenoid cystic carcinoma, polymorphous low-grade adenocarcinoma, and basal cell and canalicular adenomas
    (2004-05) Edwards, Paul C.; Bhuiya, Tawfiqul; Kelsch, Robert D
    Purpose The purpose of this study was to determine the extent of p63 immunoreactivity in the malignant salivary gland neoplasms adenoid cystic carcinoma (ACC) and polymorphous low-grade adenocarcinoma (PLGA) and to compare this to the expression of this marker in the benign salivary gland tumors canalicular adenoma and basal cell adenoma. Few studies on the expression of p63 in head and neck salivary gland tumors have been published to date. P63, a selective immunohistochemical marker of basal/stem cells of stratified epithelium and of myoepithelial cells, is a p53 homologue that plays an essential role in both morphogenesis of epidermis and limb development. P63 immunoreactivity has been demonstrated in squamous cell and urothelial carcinomas. It is generally absent in most nonsquamous cell carcinomas. Study design Formalin-fixed paraffin-embedded sections from 49 salivary gland neoplasms, representing 6 canalicular adenomas, 11 basal cell adenomas, 17 PLGA and 15 ACC accessioned from 1989 to 2002 by the Department of Pathology, Long Island Jewish Medical Center, New Hyde Park, NY, were stained with an anti-p63 monoclonal antibody. Results Nuclear p63 reactivity was uniformly positive in PLGA (17/17, 100%). Positive reactivity was also identified in the majority of cases of ACC (13/15, 87%), primarily in the nonluminal myoepithelial-like cells surrounding luminal cells. Canalicular adenoma did not exhibit any p63 immunoreactivity. All basal cell adenomas of parotid origin stained strongly for p63, with staining localized to the peripheral tumor cells situated adjacent to the connective tissue stroma. None of the basal cell adenomas originating in the upper lip stained with p63. In native adjacent salivary gland tissue, p63 reactivity was identified focally in the nuclei of myoepithelial and basal duct cells. Conclusions P63 is strongly expressed in basal cell adenoma of parotid origin, and in ACC and PLGA. Canalicular adenoma did not demonstrate p63 staining, consistent with this tumor's putative luminal ductal cell differentiation. Our results suggest that the neoplastic cells in PLGA may represent either a population of p63-positive epithelial stem/reserve cells similar to the basal cells of stratified epithelium, or modified myoepithelial cells. Given the staining pattern of the tumors examined, p63 does not appear to be an ideal marker for distinguishing between ACC, PLGA, and basal cell adenoma.
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    The Birth of an Adenoid Cystic Carcinoma
    (Sage, 2015-02) Fusco, Nicola; Guerini-Rocco, Elena; Schultheis, Anne M.; Badve, Sunil S.; Reis-Filho, Jorge S.; Weigelt, Britta; Department of Pathology and Laboratory Medicine, IU School of Medicine
    Adenoid cystic carcinoma is a rare malignancy of exocrine glands defined by the presence of a dual population of cells (epithelial and myoepithelial cells) organized in varying combinations of cribriform, tubular, and solid patterns.1,2 This neoplasm most frequently originates in the salivary glands; however, it can also occur in other anatomical sites, including the breast.1,3 More than 90% of adenoid cystic carcinomas of the breast harbor the recurrent translocation t(6;9), resulting in the MYB-NFIB fusion gene, which leads to MYB overexpression.4 Adenoid cystic carcinoma in situ has been described in the breast; however, its identifica-tion is not trivial.3 Here, we illustrate an in situ adenoid cystic carcinoma partially involving a mammary duct in a 68-year-old woman with primary adenoid cystic carci-noma of the right breast. The double population of cells composing this intraductal lesion can be appreciated by its immunohistochemical profile (Figure 1). Given that the neoplastic cells of the in situ lesion already express MYB, our findings are consistent with the notion that MYB overexpression is an early event in the tumorigen-esis of adenoid cystic carcinomas.4,5
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    Proton Therapy for Head and Neck Adenoid Cystic Carcinoma: Initial Clinical Outcomes
    (Wiley, 2015-01) Linton, Okechukwu R.; Moore, Michael G.; Brigance, Joseph S.; Summerlin, Don-John; McDonald, Mark W.; Department of Otolaryngology Head & Neck Surgery, IU School of Medicine
    Background The purpose of this study was to report outcomes of proton therapy in head and neck adenoid cystic carcinoma. Methods We conducted a retrospective analysis of 26 patients treated between 2004 and 2012. Twenty patients (77%) had base of skull involvement; 19 (73%) were treated for initial disease and 7 (27%) for recurrent disease. Twenty patients were treated postoperatively, 6 after biopsy alone and 24 had positive margins or gross residual disease. Median dose delivered was 72 Gy (relative biological effectiveness [RBE]). Results Median follow-up was 25 months (range, 7–50 months). The 2-year overall survival was 93% for initial disease course and 57% for recurrent disease (p = .19). The 2-year local control was 95% for initial disease and 86% for recurrent disease (p = .48). The 2-year distant metastatic rate was 25%. Late toxicity of grade 0 or 1 was seen in 17 patients, grade 2 in 5, grade 3 in 2, grade 4 in 1, and grade 5 in 1. Conclusion Initial outcomes of proton therapy are encouraging. Longer follow-up is required.