Meningioma is a neoplasm derived from meningothelial cells. Grade1 meningiomas consist 9 different subtypes. One of the rare subtypes is metaplastic meningioma. Metaplastic meningioma could be defined as ''xanthomatous meningioma'' in the presence of prevalent xanthomatous changes. A 32 years old male patient had admitted to outpatient clinics with complaints of vertigo and tinnitus. Magnetic resonance imaging revealed a large mass of 7.4 cm in the right frontal region with an extra axial localization. Resection material demonstrated a neoplasm composed of classic meningothelial meningioma areas accompanied with areas of xanthomatous changes, containing cells with clear, vacuolated cytoplasm. EMA, Vimentin, and progesterone expression were evident in both xanthomatous and meningothelial meningioma areas. Additionally, CD68 positivity was also observed in xanthomatous areas. EMA positivity is a neoplastic marker for xanthomatous cells and is a critic marker to differentiate these cells from macrophages which is crucial for pathologists in differential diagnosis. Xanthomatous meningiomas are quite rare and our case presentation is the 7th one in the current literature.
Objectives: Odontogenic keratocyst (OKC) and ameloblastoma are slowly growing and locally invasive tumors with high recurrence rate. The aim of this study was to investigate the clinicopathologic features of recurrent ameloblastoma and OKC cases, and evaluate outcomes of our treatments in terms of recurrence. Material and Methods: A total of 23 patients with confirmed recurrent ameloblastoma or OKC and treated in our clinic within eleven years period were reviewed retrospectively. Results: Eleven recurrent OKC cases and twelve recurrent ameloblastoma cases were included. Most recurrences occurred within five years after the initial treatment (69.6%). Enucleation had the highest recurrence rate among the first treatments (18/23). All recurrences were located in the mandible, with one exception (22/23). All recurrent OKCs were multilocular. Different histopathologic subtypes of ameloblastoma were seen in our study, follicular ameloblastoma was the most common (8/12). The mean diameter of the lesions was 4.3 cm (ranging from 2 cm to 7 cm). Statically significant relation was found between location and diameter of lesion and year of recurrence onset (p=0.004; p=0.026). We performed radical treatments in these cases (ten patients underwent marginal resections, and thirteen patients underwent segmental resection), and no recurrence was observed during the follow-up period. Conclusion: Previous inadequate surgical procedures were the most important cause of recurrence. Marginal or segmental resection with safety margins is the best method to treat recurrences of OKC or ameloblastoma cases.
Micropapillary carcinoma is an entity defined histologically in many organs. It is associated with lymph node metastasis and poor prognosis. The main mechanism for its histopathologic appearance is reverse polarization. Although the studies on this subject are limited, carcinomas with micropapillary morphology observed in different organs are examined by immunohistochemical and molecular methods. Differences are shown in these tumors compared with conventional carcinomas regarding the rate of somatic mutations, mRNA and miRNA expressions, and protein expression levels. TP53, PIK3CA, TERT, KRAS, EGFR, MYC, FGFR1, BRAF, AKT1, HER2/ERBB2, CCND1, and APC mutations, which genes frequently detected in solid tumors, have also been detected in invasive micropapillary carcinoma (IMPC) in various organs. 6q chromosome loss, DNAH9, FOXO3, SEC. 63, and FMN2 gene mutations associated with cell polarity or cell structure and skeleton have also been detected in IMPCs. Among the proteins that affect cell polarity, RAC1, placoglobin, as well as CLDNs, LIN7A, ZEB1, CLDN1, DLG1, CDH1 (E-cadherin), OCLN, AFDN/AF6, ZEB1, SNAI2, ITGA1 (integrin alpha 1), ITGB1 (integrin beta 1), RHOA, Jagged-1 (JAG1) mRNAs differentially express between IMPC and conventional carcinomas. Prediction of prognosis and targeted therapy may benefit from the understanding of molecular mechanisms of micropapillary morphology. This review describes the molecular pathologic mechanisms underlying the micropapillary changes of cancers in various organs in a cell polarity-related dimension.
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