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Immunohistochemistry of basal cell adenoma (monomorphic type) and canalicular adenoma of minor salivary glands
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Abstracts,AAOP
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY October 1995
particular the sebaceous glands m a y be a target for androgen actions as well. IMMUNOHISTOCHEMISTRY OF BASAL CELL ADENOMA (MONOMORPHIC TYPE) AND CANALICULAR ADENOMA OF MINOR SALIVARY GLANDS. S.O.M. Sousa. R.M. Melhado. N.S. Araujo, V.C. Araujo. University of S~o Paulo. Brazil. The latest classification of the W H O considers basal cell aden o m a and canalicular adenoma as two distinct entities based on histologic, ultrastructural, and histochemical aspects. To compare the immunohistochemical profile of these two tumors, the expression of vimentin and cytokeratins (CKs) 7, 8. 13, 14. 18 and 19 were investigated in three basal cell adenomas (monomorphic type) and three canalicular adenomas. Immnnostaining was carried out in formalin-fixed tissue sections (3 jam), by the streptavidin-biotin technique. Before the C K s reaction, the sections in citric acid (10 mM, pH 6.0) were treated in a microwave oven. Most of the cells of the studied basal cell adenomas revealed positivity for vimentin and C K s 8 and 18. Both antibodies exhibited the same pattern of staining, a thin ring around the nucleus. In the canalicular adenoma m o s t of the cells expressed CKs 7. 13. and 19, whereas only groups of cells, uniformly distributed, were positive for C K 14. C K s 8 and 18 were expressed focally. Vimentin was negative. These results showed different immunohistochemica] profiles for these tumors and pointed out an intercalated duct origin for basal cell adenoma (monomorphic type) and an excretory duct origin for canalicular adenoma, as had been suggested by previous ultrastrucmral studies. A CASE OF RET PROTOONCOGENE (RET) MUTATION IN MULTIPLE ENDOCRINE NEOPLASIA SYNDROME TYPE 2B (MEN 2B). M. Kahn. R. Gagel, and E. Kaufman University of Tennessee. Memphis. University of Texas M.D. Anderson Center. Houston. and Lovelace Clinic. Albuquerque. N.M.
M E N 2B is one clinical variant of a group of autosomal dominant neurocristopathies. In M E N 2B there is an association of medullary thyroid carcinoma (MTC) and pheochromocytoma with oral, ocular, and alimentary submucosal neuromas and Marfanoid body features; approximately 50% of cases are spontaneous mutations. The RET protooncogene is a 21 exon gene encoding a tyrosine kinase receptor, Recently, a codon 918 germline mutation of R E T has been identified in 95% of M E N 2B patients, which converts a highly conserved methionine to a threonme in the intracellular tyrosine kinase portion of this receptor. This mutation is easily detected by a direct D N A sequencing or restriction enzyme (FOK 1) analysis of amplified products, replacing earlier techniques for detecting M T C by calcitonin measurement after pentagastrin injection. The R E T protooncogene is normally expressed in the oral and gastrointestinal submucosal neural.ganglia and the codon 918 mutation is thought to cause neuromas by virtue of its transforming activity in these ganglia. The identification of clinical features of M E N 2B in a 10-yearold boy by an oral pathologist led to confirmation by mutational analysis. Before genetic testing, the patient, and at a later date, his mother underwent thyroidectomies based solely on biochemical testing. The patient had the codon 918 mutation whereas his phenotypically normal mother, father, and older brother had normal RET analyses. Studies in families have demonstrated the mutant allele is derived from the father, with possible acquisition during spermatogenesis. W e believe the mother of our patient to be normal; the absence of phenotypic features of M E N 213 and a normal genotype suggest her calcitonin abnormalities and minimal evidence for C cell hyperplasia were inconsequential. Molecular analysis for R E T protooncogene abnormalities will likely supplant biochemical methods of diagnosis in M E N 2B patients.
Abstracts,AAOP
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY October 1995
particular the sebaceous glands m a y be a target for androgen actions as well. IMMUNOHISTOCHEMISTRY OF BASAL CELL ADENOMA (MONOMORPHIC TYPE) AND CANALICULAR ADENOMA OF MINOR SALIVARY GLANDS. S.O.M. Sousa. R.M. Melhado. N.S. Araujo, V.C. Araujo. University of S~o Paulo. Brazil. The latest classification of the W H O considers basal cell aden o m a and canalicular adenoma as two distinct entities based on histologic, ultrastructural, and histochemical aspects. To compare the immunohistochemical profile of these two tumors, the expression of vimentin and cytokeratins (CKs) 7, 8. 13, 14. 18 and 19 were investigated in three basal cell adenomas (monomorphic type) and three canalicular adenomas. Immnnostaining was carried out in formalin-fixed tissue sections (3 jam), by the streptavidin-biotin technique. Before the C K s reaction, the sections in citric acid (10 mM, pH 6.0) were treated in a microwave oven. Most of the cells of the studied basal cell adenomas revealed positivity for vimentin and C K s 8 and 18. Both antibodies exhibited the same pattern of staining, a thin ring around the nucleus. In the canalicular adenoma m o s t of the cells expressed CKs 7. 13. and 19, whereas only groups of cells, uniformly distributed, were positive for C K 14. C K s 8 and 18 were expressed focally. Vimentin was negative. These results showed different immunohistochemica] profiles for these tumors and pointed out an intercalated duct origin for basal cell adenoma (monomorphic type) and an excretory duct origin for canalicular adenoma, as had been suggested by previous ultrastrucmral studies. A CASE OF RET PROTOONCOGENE (RET) MUTATION IN MULTIPLE ENDOCRINE NEOPLASIA SYNDROME TYPE 2B (MEN 2B). M. Kahn. R. Gagel, and E. Kaufman University of Tennessee. Memphis. University of Texas M.D. Anderson Center. Houston. and Lovelace Clinic. Albuquerque. N.M.
M E N 2B is one clinical variant of a group of autosomal dominant neurocristopathies. In M E N 2B there is an association of medullary thyroid carcinoma (MTC) and pheochromocytoma with oral, ocular, and alimentary submucosal neuromas and Marfanoid body features; approximately 50% of cases are spontaneous mutations. The RET protooncogene is a 21 exon gene encoding a tyrosine kinase receptor, Recently, a codon 918 germline mutation of R E T has been identified in 95% of M E N 2B patients, which converts a highly conserved methionine to a threonme in the intracellular tyrosine kinase portion of this receptor. This mutation is easily detected by a direct D N A sequencing or restriction enzyme (FOK 1) analysis of amplified products, replacing earlier techniques for detecting M T C by calcitonin measurement after pentagastrin injection. The R E T protooncogene is normally expressed in the oral and gastrointestinal submucosal neural.ganglia and the codon 918 mutation is thought to cause neuromas by virtue of its transforming activity in these ganglia. The identification of clinical features of M E N 2B in a 10-yearold boy by an oral pathologist led to confirmation by mutational analysis. Before genetic testing, the patient, and at a later date, his mother underwent thyroidectomies based solely on biochemical testing. The patient had the codon 918 mutation whereas his phenotypically normal mother, father, and older brother had normal RET analyses. Studies in families have demonstrated the mutant allele is derived from the father, with possible acquisition during spermatogenesis. W e believe the mother of our patient to be normal; the absence of phenotypic features of M E N 213 and a normal genotype suggest her calcitonin abnormalities and minimal evidence for C cell hyperplasia were inconsequential. Molecular analysis for R E T protooncogene abnormalities will likely supplant biochemical methods of diagnosis in M E N 2B patients.