title: [High-grade transformation in adenoid cystic carcinoma: a clinicopathologic study].
abstract: OBJECTIVE
  To study the clinicopathologic features and possible molecular mechanisms of adenoid cystic carcinoma with high-grade transformation.
  
  
  METHODS
  Four cases of adenoid cystic carcinoma with high-grade transformation were enrolled into the study. Immunohistochemical study for smooth muscle actin, p63, p53 and Ki-67 was carried out. C-myc gene status was analyzed by fluorescence in-situ hybridization.
  
  
  RESULTS
  There were altogether 3 males and 1 female. The mean age of the patients was 55.5 years. Two patients died 17 months and 29 months after operation, respectively. One patient had distant metastasis 23 months after operation and was still alive at 26-month follow up. The remaining patient remained tumor free at 3-month follow up. High-grade transformation in adenoid cystic carcinoma presented either as poorly differentiated adenocarcinoma or undifferentiated carcinoma. Histologic examination showed sheets of pleomorphic tumor cells occupying more than one low-power field. The high-grade carcinoma cells showed increased nuclear-cytoplasmic ratio, prominent eosinophilic nucleoli and active mitosis (ranging from 8 to 25 per high-power field). Comedo necrosis was observed in 2 cases and multiple foci of calcifications in 3 cases. Immunohistochemical study demonstrated loss of myoepithelial differentiation, overexpression of p53 and high proliferative index by Ki-67. No c-myc translocation or copy-number changes were observed.
  
  
  CONCLUSIONS
  High-grade transformation in adenoid cystic carcinoma is rare. The histopathologic features are rather distinctive and the biologic behavior is aggressive. C-myc gene mutation does not seem to play a key role in the pathogenesis.
authors.forename: Quan
authors.initials: Q
authors.lastname: Zhou
authors.forename: Hong
authors.initials: H
authors.lastname: Chang
authors.forename: Yi-ding
authors.initials: YD
authors.lastname: Han
authors.forename: Ying
authors.initials: Y
authors.lastname: Gao
authors.forename: Hong-gang
authors.initials: HG
authors.lastname: Liu
mesh_terms: D000199:Actins / Q000378:metabolism; D000230:Adenocarcinoma / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D000328:Adult; D000368:Aged; D002277:Carcinoma / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D003528:Carcinoma, Adenoid Cystic / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D002471:Cell Transformation, Neoplastic; D005134:Eye Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D005260:Female; D005500:Follow-Up Studies; D016259:Genes, myc; D006801:Humans; D019394:Ki-67 Antigen / Q000378:metabolism; D007765:Lacrimal Apparatus; D007766:Lacrimal Apparatus Diseases / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D008175:Lung Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D008297:Male; D008444:Maxillary Sinus Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D008565:Membrane Proteins / Q000378:metabolism; D008875:Middle Aged; D009154:Mutation; D010307:Parotid Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D015996:Survival Rate; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: C541116:ACTA2 protein, human; D000199:Actins; C081876:CKAP4 protein, human; D019394:Ki-67 Antigen; D008565:Membrane Proteins; D016159:Tumor Suppressor Protein p53