A comparative analysis of LEF-1 in odontogenic and salivary tumors.

LEF-1 is a nuclear transcription factor of the Wnt pathway that regulates multipotent skin stem cell differentiation. ß-Catenin is considered a transcriptional coactivator that interacts with LEF-1.This study evaluates LEF-1 in a variety of odontogenic and salivary tumors and determines the prevalence of ß-catenin coexpression. Ninety-eight salivary gland tumors and 51 odontogenic tumors were evaluated for LEF-1 and ß-catenin immunohistochemical staining. Positivity was defined as at least 2+ intensity in more than 50% of tumor cells, which required a composite score of 6 or more. LEF-1 was positive in 64% (7/11) of calcifying cystic odontogenic tumors (CCOT). Nuclear ß-catenin was present in 82% (9/11) of CCOT. Coexpression of LEF-1 and nuclear ß-catenin was noted in all LEF-1-positive CCOT. Strong and diffuse LEF-1 expression was seen in 69% (11/16) of basal cell adenocarcinomas (BCAC) and 63% (5/8) of basal cell adenomas (BA). Nuclear ß-catenin was present in 50% (4/8) of BA and 43% (6/14) of BCAC. For BA, 4 of 5 LEF-1-positive tumors showed coexpression of ß-catenin, and for BCAC, 5 of 9 LEF-1-positive tumors showed coexpression. In conclusion, this study documents for the first time the presence of LEF-1 expression and nuclear ß-catenin coexpression in select basaloid salivary gland tumors and various odontogenic tumors. We demonstrate LEF-1 expression in both BA and BCAC preferentially over other salivary gland tumors suggesting some utility as a diagnostic marker.

Squamous cell carcinoma metastatic to neck from an unknown primary: the potential impact of modern pathologic evaluation on perceived incidence of human papillomavirus-positive oropharyngeal carcinoma prior to 1970.

OBJECTIVES/HYPOTHESIS: From the 1950s through the 1960s, an unknown number of oropharyngeal squamous cell carcinomas (SCCs) presented with metastases to cervical lymph nodes from an unknown primary (SCCUP) and were not recognized as oropharyngeal in origin. At present, pathologic evaluation of SCCUP for human papillomavirus (HPV) improves discovery of occult oropharyngeal SCC and may partially explain increased incidence of HPV-positive oropharyngeal SCC. STUDY DESIGN: Retrospective cohort study. METHODS: A retrospective study of 13 cases of SCCUP diagnosed from 1956 to 1969 was performed. The probability of these cases of metastatic SCC to originate from the oropharynx was assessed by characterizing their morphology (keratinizing vs. nonkeratinizing) and HPV status by in situ hybridization and p16 immunostaining. RESULTS: Two cases of nonkeratinizing SCC positive for HPV by in situ hybridization and p16 immunohistochemistry were identified. These cases were most likely of oropharyngeal origin. CONCLUSIONS: These two cases can be added to the other 15 cases of HPV-positive primary oropharyngeal SCC identified in our department from 1956 to 1969. When determining the incidence of HPV-positive oropharyngeal SCC before the 1970s, a correction factor of about +13% (2/15) accounting for modern pathologic workup of SCCUP during the last couple of decades may be appropriate.

Lymphadenoma of the salivary gland: clinicopathological and immunohistochemical analysis of 33 tumors.

Lymphadenomas (LADs) are rare salivary gland tumors. Their clinicopathologic characteristics and etiopathogenesis are poorly understood. We examined 33 LADs in 31 patients (17 women and 14 men) aged 11-79 years (median 65 years). There were 22 sebaceous LADs in 21 patients (9 women and 12 men) and 11 non-sebaceous LADs in 10 patients (8 women and 2 men). Two patients had synchronous double tumors. Twenty-six tumors (79%) arose in parotid, three in the neck, and two each in submandibular gland and oral cavity. Extraparotid tumors were seen in 2 of 21 (10%) patients with sebaceous and 4 of 10 (40%) patients with non-sebaceous LADs. Seven of twenty-three (30%) patients had immunosuppressive therapy for unrelated diseases. The tumors were well circumscribed, encapsulated (n=28, 84%) painless masses, varying in size from 0.6 to 6 cm (median 2.2). The cut surfaces were gray-tan to yellow, homogeneous and multicystic (n=24, 72%). The epithelial cells were basaloid, squamous and glandular, forming solid nests, cords, tubules, and cysts. Sebaceous differentiation was restricted to sebaceous lymphadenoma. The epithelial cells expressed basal cell markers (p63, 34BE12, and/or CK5/6, 18/18, 100%) and the luminal glandular cells expressed CK7 (12/12, 100%). Myoepithelial cells were absent (n=10/16, 63%) or focal. The lymphoid stroma was reactive, with germinal centers in 28 (84%). There was no evidence of HPV (0/11), EBV (0/7), and HHV-8 (0/8). Malignant transformation to sebaceous and basal cell adenocarcinoma was seen in one patient each. None of the 11 patients with follow-up (1-8 years) recurred. In summary, sebaceous and non-sebaceous LADs are benign, encapsulated, solid and cystic tumors affecting older adults. Non-sebaceous LADs affect women and extraparotid sites more frequently than sebaceous LADs. Altered immune status may have a role in their etiopathogenesis. Multiple synchronous tumors, origin in buccal mucosa, and malignant transformation may rarely occur.

Fluorescence in situ hybridization for detection of MAML2 rearrangements in oncocytic mucoepidermoid carcinomas: utility as a diagnostic test.

Oncocytic mucoepidermoid carcinoma poses diagnostic challenge because of its histologic overlap with other oncocytic salivary gland lesions, including Warthin tumor. Although the prognostic value of the t(11;19) MECT1-MAML2 fusion gene has been established in mucoepidermoid carcinoma, its diagnostic use in discriminating oncocytic mucoepidermoid carcinoma from histologic mimics is unexplored. We evaluated the translocation status in 14 cases of oncocytic mucoepidermoid carcinoma using a MAML2-11q21 break-apart probe spanning the entire chromosome region of the MAML2 gene and correlated these findings with clinicopathologic parameters including age, sex, stage, predominant growth pattern, grade, and p63 immunostaining pattern. All oncocytic mucoepidermoid carcinomas were parotid tumors with a mean patient age of 54.6 years (range, 9-85) and a female to male ratio of 5:2. Grade distribution was as follows: low grade, 9; intermediate grade, 2; and high grade, 3. The histologic patterns observed were as follows: solid, 4; cystic, 8 (of these, 5 had Warthin-like lymphoid stroma); and mixed, 2. Solid oncocytic mucoepidermoid carcinomas showed a diffuse p63 staining pattern, whereas cystic oncocytic mucoepidermoid carcinomas showed staining of the outer layer of intermediate cells ranging from a bilayer to areas of complex multilayering and plaque-like proliferation. Ten (71%) of the 14 cases showed a MAML2 rearrangement by fluorescence in situ hybridization. No correlation was seen between rearrangement status and histologic grade, growth pattern, or p63 staining pattern. However, we demonstrate that the presence of MAML2 rearrangement can be used as supportive evidence to distinguish oncocytic mucoepidermoid carcinoma from other oncocytic lesions.

Pathology archive: evaluation of integrity, regulatory compliance, and construction of searchable database from print reports.

Tissue repositories maintained by pathology departments represent an abundant resource of clinically annotated human specimens. The storage expenses associated with pathology archives are known to administrators of most pathology departments. However, such basic repository characteristics as the quality of stored materials, ease of access, and search and retrieval rates are often unclear. The aims of our work were to design a framework to assess the quality of a historic pathology archive, to propose the definition of "archive integrity," and to provide benchmarks for tissue block retrieval rates and DNA integrity. We share our experience with scanning approximately 120,000 pathology reports from 1956 to 1979 into an electronically searchable archive, with a $9,000 budget, completed in 6 weeks. Several ethical and legal considerations that shaped the technical side of this project are discussed.

Clear cell carcinoma and clear cell odontogenic carcinoma: a comparative clinicopathologic and immunohistochemical study.

Clear cell carcinoma or hyalinizing clear cell carcinoma (CCC) and clear cell odontogenic carcinoma (CCOC) are rare, low-grade and typically indolent malignancies that can be diagnostically challenging. In this study the clinicopathologic, histologic, and immunohistochemical features of 17 CCCs and 12 CCOCs are examined. The differential diagnosis of clear cell malignancies in the head and neck is discussed. The relationship of CCCs and CCOCs to other clear cell tumors on the basis of their immunohistochemical staining patterns is postulated.

Progressive genetic alterations of adenoid cystic carcinoma with high-grade transformation.

CONTEXT: Although genome-wide imbalances have been characterized in conventional adenoid cystic carcinoma, other than p53 mutational status, the molecular profile of adenoid cystic carcinoma with high-grade transformation has not been explored. OBJECTIVE: To evaluate progressive genetic alterations in adenoid cystic carcinoma with high-grade transformation using array comparative genomic hybridization. DESIGN: Five adenoid cystic carcinomas with high-grade transformation (4 primary tumors and 1 paired metastasis) were selected and characterized at the DNA level by array comparative genomic hybridization on formalin-fixed paraffin-embedded tissue. Select alterations were validated by fluorescence in situ hybridization. RESULTS: Chromosomal gains were mostly confined to the areas of high-grade transformation while losses were seen only in the conventional areas. Chromosomal regions with significant gains included 8q24, 17q11.2-q12, 17q23, and 15q11-13. Regions that showed the significant losses included 9q34, 4p16, 1p36.1, and 11q22. Fluorescence in situ hybridization analysis demonstrated increases in C-MYC (8q24.12-q24.13) and a low level increases in ERBB2 ( formerly HER2/neu ) (17q11.2-q12) in cases showing gains by array comparative genomic hybridization in these regions. However, no tumor showed HER2/ neu immunopositivity. CONCLUSIONS: High-grade transformation in adenoid cystic carcinoma is a complex process that is reflected by several chromosomal alterations. Our findings implicate C-MYC amplification in this progression, although the role of HER2/neu is still unclear. Other candidate oncogenes, particularly on chromosome 17q23, warrant investigation in this rare tumor.

Common Malignant Salivary Gland Epithelial Tumors.

Malignant salivary gland epithelial tumors are histologically diverse with at least 24 recognized distinct entities. In general, malignant tumors account for 15% to 30% of parotid tumors, 40% to 45% of submandibular tumors, 70% to 90% of sublingual tumors, and 50% of minor salivary tumors. Common malignancies include mucoepidermoid carcinoma, adenoid cystic carcinoma, acinic cell carcinoma, salivary duct carcinoma, carcinoma ex pleomorphic adenoma, polymorphous lowgrade adenocarcinoma, and myoepithelial carcinoma. Each tumor type has its own unique histologic variants and prognostic pathologic features, and only mucoepidermoid carcinomas have a formalized grading system. The molecular pathogenesis of certain tumors, such as mucoepidermoid carcinoma and adenoid cystic carcinoma, has recently begun to be elucidated.

Rare Malignant and Benign Salivary Gland Epithelial Tumors.

Although at least 24 distinct histologic salivary gland carcinomas exist, many of them are rare, comprising only 1% to 2% of all salivary gland tumors. These include epithelial-myoepithelial carcinoma, (hyalinizing) clear cell carcinoma, basal cell adenocarcinoma, cystadenocarcinoma, low-grade salivary duct carcinoma (low-grade cribriform cystadenocarcinoma), oncocytic carcinoma, and adenocarcinoma not otherwise specified. Few tumors (clear cell carcinoma and basal cell adenocarcinoma) have unique molecular correlates. Benign tumors, although histologically less diverse, are far more common, with pleomorphic adenoma and Warthin tumor the most common salivary gland tumors. Many benign tumors have malignant counterparts for which histologic distinction can pose diagnostic challenge.

Large cell neuroendocrine carcinoma of the larynx: definition of an entity.

Laryngeal atypical carcinoids (AC/moderately-differentiated neuroendocrine carcinoma) are associated with moderately aggressive clinical behavior; however, a subset of tumors classified as AC have much greater aggressive potential. These tumors fulfill the proposed diagnostic criteria for pulmonary large cell neuroendocrine carcinoma, albeit in the larynx. In the current WHO classification, laryngeal large cell neuroendocrine carcinomas (LCNEC) are classified as variants of AC, whereas pulmonary LCNEC are classified as poorly-differentiated neuroendocrine carcinomas. Reported outcomes for pulmonary tumors support the separate classification of LCNEC. Five and ten year survival rates for pulmonary AC are 61-73, and 35-59%, respectively, while the 5-year survival rate for pulmonary LCNEC is as low as 30%. By extension, we postulate that the biologic potential of laryngeal LCNEC is similar to that of small-cell carcinoma (poorly-differentiated neuroendocrine carcinoma), and as such, warrants reclassification. The files of Barnes Jewish Hospital/Washington University were searched for the term "neuroendocrine" and the anatomic subsite larynx. Neuroendocrine carcinoma cases were evaluated using the WHO definitions for pulmonary AC and LCNEC; small cell carcinoma was excluded. Cases were also solicited from the larger head and neck pathology community. A literature search was also performed for cases of laryngeal neuroendocrine carcinoma, and cases which could be clearly classified as LCNEC by this scheme were captured as well. Six new cases plus four reported cases were identified which fulfill the WHO criteria for pulmonary LCNEC (eight men and two women). Nine patients presented at stage IV and 88% died of disease (DOD), 75 and 100% of these at 2 and 3 years, respectively. Laryngeal LCNEC is a rare entity, distinct from AC. We recommend that laryngeal tumors fulfilling WHO criteria for pulmonary LCNEC not be classified as variants of AC, but as variants of small cell carcinoma (poorly-differentiated neuroendocrine carcinoma) as they are associated with poorer outcome.

Polymorphous low-grade adenocarcinoma: the University of Pittsburgh experience.

OBJECTIVE: To reappraise the clinical and histologic variables associated with a more aggressive outcome in polymorphous low-grade adenocarcinoma (PLGA). DESIGN: Retrospective cohort. SETTING: University hospital. PATIENTS: Twenty-four patients with PLGA treated from January 1, 1973, through December 31, 2005. MAIN OUTCOME MEASURE: Analysis of clinical and pathologic variables in 30 biopsy or resection specimens from 24 patients. RESULTS: Only 4 PLGAs were not initially diagnosed as such. However, 8 non-PLGAs (thus excluded) were incorrectly diagnosed as PLGA. Most carcinomas (14 of 24 [58%]) were palatal. Recurrent carcinomas had a significantly higher mitotic rate (2.7 mitoses per 10 high-power fields) compared with primary tumors (1.2 mitoses per high-power fields, P = .046), and 3 of 7 (43%) recurrences showed progression to an intermediate-grade histologic type. No patient died of disease. Median disease-free survival was 12.8 years. Four of 24 patients (17%) had regional lymph node metastases, 3 with carcinomas of the base of the tongue. One PLGA metastasized to the subcutaneous tissue of the face, orbit, and lungs at 19.6 years. An extrapalatal site was the only significant determinant of disease-free survival (P = .03). CONCLUSIONS: Diagnosis of PLGA remains a challenge. Extrapalatal carcinomas appear to behave in a more aggressive fashion than those of the palate, and cancer arising from the base of the tongue frequently metastasizes to the cervical lymph nodes, suggesting a role for neck dissection in these patients. Recurrent cancers show evidence of histologic progression, justifying an aggressive approach to achieving initial complete excision.

Basal cell adenocarcinoma of a hard palate minor salivary gland: case report and review of the literature.

OBJECTIVE: Basal cell adenocarcinoma of a minor salivary gland is extremely rare. The goal of this report is to increase awareness of this rare disease and to review and discuss the differential diagnosis and important considerations in treatment. STUDY DESIGN: Case report and review of the literature. METHODS: Case report of a basal cell adenocarcinoma of a hard palate minor salivary gland and review of the literature of basal cell adenocarcinoma. RESULTS: Basal cell adenocarcinomas are slow-growing tumours that most commonly involve the parotid gland and very rarely involve minor salivary glands. Although recurrence rates for these tumours are high, mortality rates are low. Histological diagnosis is important to distinguish this tumour from adenoid cystic carcinoma given the significant difference in disease prognosis. CONCLUSIONS: Diagnosis of these tumours must be made histologically. Recommended treatment options include wide local excision with radiotherapy reserved for close surgical margins or for local recurrence.

Update on selected salivary gland neoplasms.

CONTEXT: Malignancies of the salivary gland are uncommon and account for 0.3% of all malignancies. In addition to their rarity, diagnosing these tumors can be challenging given the histologic overlap among various subtypes, their morphologic heterogeneity, and the recent recognition of new entities. OBJECTIVE: To provide an overview of 4 salivary gland malignancies that we often see in consultation, with a focus on essential diagnostic features and the importance of reporting pertinent diagnostic information to ensure appropriate clinical management. DATA SOURCES: Review of the literature, supplemented by the personal experience of the authors, which is based on their respective institutional experiences and consultation services. CONCLUSIONS: When diagnosing carcinoma ex pleomorphic adenoma, pathologists must report several important pieces of information to allow for optimal clinical management. In addition to histologic subtype, the degree of differentiation as well as the degree of invasion, if any, must be reported because all have prognostic relevance. Polymorphous low-grade adenocarcinoma can be a challenging diagnosis on biopsy specimens. Evaluation of the tumor periphery and nuclear features should lead to the correct diagnosis in most cases. Salivary duct carcinoma is an aggressive malignancy characterized by histologic resemblance to breast carcinoma, high-grade cytologic features, and expression of androgen receptor. Benign and malignant myoepithelial neoplasms have a broad morphologic spectrum, and immunohistochemistry is important in reaching the correct diagnosis.

New variants of epithelial-myoepithelial carcinoma: oncocytic-sebaceous and apocrine.

CONTEXT: Recently described variants of epithelial-myoepithelial carcinoma have not been well characterized but raise a distinct set of differential diagnostic considerations than the classic type. OBJECTIVE: To report a detailed analysis of oncocytic-sebaceous epithelial-myoepithelial carcinoma (OEMCa) and a similar, but novel, variant, apocrine epithelial-myoepithelial carcinoma (ApEMCa). DESIGN: Clinical, histologic, and immunophenotypic features of 5 OEMCas and 5 ApEMCas were analyzed. Ultrastructural examination was also performed on 3 OEMCa and 1 ApEMCa tumors. RESULTS: The mean age for OEMCa (74.4 years; range, 58-82 years) was slightly higher than for ApEMCa (61.6; range, 46-79 years). All tumors arose in the parotid glands and demonstrated a multinodular pattern of growth with an average size of 3.3 cm (range, 2.3-6.5 cm). Available follow-up (n = 6; 3 OEMCas, 3 ApEMCas) shows a favorable course (no evidence of disease; mean, 17.4 months). Both were morphologically similar, but only OEMCa had sebaceous elements. Phosphotungstic acid hematoxylin staining, antimitochondrial antibody immunohistochemistry, and ultrastructural examination confirm the abundance of mitochondria in OEMCa but not in ApEMCa. The ductal component in ApEMCa was distinguished from that of OEMCa by apical snouts, intracytoplasmic vacuoles, nuclear pleomorphism, prominent nucleoli, and androgen receptor immunoreactivity. CONCLUSIONS: Oncocytic-sebaceous epithelial-myoepithelial carcinoma and ApEMCa should be considered in the differential diagnosis of oncocytic/oncocytoid salivary gland tumors. Oncocytic-sebaceous epithelial-myoepithelial carcinoma morphology may reflect a senescent phenotype, similar to other oncocytic lesions. The ductal component of ApEMCa shares some similarities with salivary duct carcinoma and supports the notion that epithelial-myoepithelial carcinoma can serve as the progenitor tumor for hybrid tumors.

Salivary type tumors seen in consultation.

The aim of this study is to characterize personal consultation practice in salivary pathology and to identify most common diagnostic challenges. Seven hundred sixty consultation requests were prospectively indexed over 12 months, and 205 cases of salivary type tumors were identified. The following data were recorded: anatomic site, patients' age and gender, geographic origin of cases, diagnoses by submitting pathologist and consultant, and turn-around time. Final diagnosis was offered by submitting pathologist in 77 of 205 cases (37.5%). The definitive diagnosis was provided to contributors in 188 of 205 cases (91.7%); diagnostic limitations and potential adequacy issues were addressed in 17 remaining cases. The average turn-around time was 4.4 days. The three most common diagnostic problems were acinic cell carcinoma, epithelial myoepithelial carcinoma, and adenoid cystic carcinoma. Pathologists' adherence to recommendations by Association of Directors of Anatomic and Surgical Pathology regarding consultation practice is described.

Seromucinous hamartomas: a clinicopathological study of a sinonasal glandular lesion lacking myoepithelial cells.

AIMS: To describe seven cases of sinonasal seromucinous hamartoma. MATERIALS AND RESULTS: The clinicopathological and immunohistochemical features of seven seromucinous hamartomas were analysed. There were four men and three women. Six lesions involved the posterior nasal septum and one the lateral wall. Size ranged from 6 to 40 mm. Four patients had no recurrences. One patient had local recurrences 24 and 60 months after diagnosis. The masses were covered by respiratory epithelium. Their stroma was oedematous to fibrous and contained invaginated respiratory epithelium forming glands and cysts, cysts with cuboidal to flat epithelium, and small serous glands, ducts and tubules with lobular and irregular haphazard patterns. One case had numerous glands surrounded by hyalinized basement membrane with features of respiratory epithelial adenomatoid hamartoma (REAH). One case had focal REAH-like changes. Both respiratory and serous components were positive for cytokeratin (CK) 7 and CK19. The serous component lacked myoepithelial cells when stained for CK14, p63, calponin and muscle-specific antigen in five cases. CONCLUSIONS: Seromucinous hamartomas show a broader histopathological appearance than previously reported. The serous proliferation in these lesions lacks myoepithelial cells. The presence of occasional REAH-like features and common location in the posterior nasal septum suggest a spectrum from pure seromucinous hamartoma to REAH.

Ceruminous gland carcinomas: a clinicopathologic and immunophenotypic study of 17 cases.

BACKGROUND: Ceruminal gland carcinomas are rare neoplasms confined to the skin lining the cartilaginous part of the external auditory canal. DESIGN: Retrospective. RESULTS: The patients included 11 men and 6 women, aged 33-82 years (mean, 59.5 years). Patients presented clinically with a mass of the outer half of the external auditory canal (n = 14), hearing changes (n = 5), drainage (n = 4), or paralysis of the facial nerve (n = 3). The polypoid masses ranged in size from 0.5 to 3 cm in greatest dimension (mean, 1.8 cm). Histologically, the tumors demonstrated a solid to cystic pattern, composed of an infiltrating glandular to cribriform arrangement of epithelial cells. Histologic features included a dual cell population (although not the dominant histology), increased cellularity, moderate to severe nuclear pleomorphism, irregular nucleoli, increased mitotic figures (mean, 3/10 HPF), including atypical forms, and tumor necrosis (n = 2). Tumors were divided into three types of adenocarcinoma based on pattern of growth and cell type (ceruminous, NOS [n = 12], adenoid cystic [n = 4], mucoepidermoid [n = 1]). CK7 and CD117 highlighted the luminal cells, while S1-00 protein showed a predilection for the basal cells of ceruminous and adenoid cystic carcinomas. Metastatic adenocarcinoma or direct extension from salivary gland neoplasms are the principle differential considerations. Surgical resection was used in all patients with radiation used in four patients. Eleven patients were alive or had died of unrelated causes without evidence of disease (mean, 11.2 years); six patients had died with disease (mean, 4.9 years), all of whom had developed local recurrence. CONCLUSION: Ceruminous-type carcinomas, with the exception of ceruminous mucoepidermoid carcinoma, all demonstrated a dual cell population of basal myoepithelial-type cells and luminal apocrine cells. The specific histologic sub-type does not influence the long-term patient outcome.

Parathyroid lipoadenomas and lipohyperplasias: clinicopathologic correlations.

Parathyroid lipoadenomas and lipohyperplasias are rare histologic variants with both an increase in stromal fat and parenchyma. We report the most comprehensive single institution series of lipoadenomas and lipohyperplasias to date and review the literature. Eight lipoadenomas and 3 lipohyperplasias (27 y period) were reviewed. The mean age was 60.3 years (range: 50 to 77 y) with a female predilection (1.75:1). The most common symptoms on presentation were fatigue (55.6%) and bone/joint pain (44.4%). Only 1 patient was euparathyroid. Ultrasound localized lipoadenomas in 50% of tested cases whereas sestamibi was successful in 71.4%. Despite increased stromal fat (median: 50%), the weight and the appearance of large, occasionally nodular expansions of parathyroid parenchyma within the fatty stroma distinguished lipoadenomas and lipohyperplasias from normal parathyroid tissue; none of the cases were misclassified as normal on frozen section. Mean weight for lipoadenomas was 1553 mg (range: 173 to 4587 mg), whereas the mean weight for lipohyperplasia glands was 389.1 mg. Variant morphologies included follicular patterned, oxyphil predominant, and thymic elements (thymolipoadenoma). In 1 lipohyperplasia case, not all glands were involved. Oil Red O stains showed decreased intracytoplasmic lipid in most cases. Median follow-up was 9.2 months (range: <1 to 51 mo). Only 1 lipohyperplasia patient had persistent hypercalcemia, but was asymptomatic. Lipoadenomas and lipohyperplasias are clinically similar and as histologically diverse as their conventional counterparts. Lipoadenomas are more difficult to localize preoperatively by imaging. Despite the potential difficulty at frozen section, accurate weight documentation and recognition of key histologic features diminish this challenge.

Basal/myoepithelial cells in chronic sinusitis, respiratory epithelial adenomatoid hamartoma, inverted papilloma, and intestinal-type and nonintestinal-type sinonasal adenocarcinoma: an immunohistochemical study.

CONTEXT: The pathogenesis of respiratory epithelial adenomatoid hamartoma (REAH) and inverted papilloma (IP) is poorly understood, especially compared with sinonasal adenocarcinoma (SNAC). One feature of malignant glandular lesions is loss of the basal/myoepithelial layer. The immunophenotype of the basal/myoepithelial layer has not been fully examined in benign glandular lesions of the sinonasal tract. OBJECTIVE: To examine benign and malignant glandular lesions in the sinonasal tract for the immunophenotype of basal/myoepithelial cells, proliferation index, and cytokeratin and intestinal differentiation profiles. DESIGN: Sinonasal adenocarcinoma (intestinal-type adenocarcinoma [ITAC] and nonintestinal type adenocarcinoma [non-ITAC]), REAH, IP, and chronic sinusitis (CS) were stained for cytokeratin (CK) 7, CK20, 34betaE12, CDX-2, p63, Ki-67, smooth muscle actin (SMA), S100 protein, and calponin. RESULTS: Basal/myoepithelial cells in CS and REAH were positive for p63 and 34betaE12 but negative for SMA, S100 protein, and calponin. Proliferative activity was localized to the compartment containing p63-positive cells. Inverted papilloma demonstrated broad areas staining for p63 and 34betaE12, with intermediate proliferative activity in these areas. Sinonasal adenocarcinoma had the highest Ki-67 labeling index, and p63-positive SNACs had higher proliferation indices than p63-negative SNACs. REAH, IP, CS, and most SNACs expressed CK7. Only SNAC expressed CK20. Sixty percent of morphologic ITACs expressed CDX-2. CONCLUSIONS: Basal/myoepithelial cells in CS and REAH should be considered basal and not myoepithelial cells. In benign lesions, proliferative activity is limited to the compartments with p63 staining. In SNAC and IP, p63 expression correlates with proliferation index. REAH, IP, and CS share similar immunoprofiles (CK7+, CK20-, and CDX-2-), contrasting with SNAC (CK7+, CK20+/-, CDX-2-/+).