title: Up-regulation of human arrest-defective 1 protein is correlated with metastatic phenotype and poor prognosis in breast cancer.
abstract: BACKGROUND
  Human arrest defective 1 protein (ARD1), as a N-terminal acetyltransferase, has been reported to play a crucial role in tumorigenesis, but the results are somewhat controversial. To explore the clinical and pathological significance of ARD1 in breast tumorigenesis, we analyzed ARD1 status in multiple types of breast disease.
  
  
  METHODS
  The expression of ARD1 protein was assessed by immunohistochemistry in 356 cases including 82 invasive ductal carcinomas (IDC), 159 fibroadenomas, 66 hyperplasia of mammary glands, 19 inflammatory breast disease, 30 breast cysts, and in 29 postoperative treatment patients. We assessed the relationship of ARD1 protein with clinical and pathological characteristics using χ2 test.
  
  
  RESULTS
  ARD1 protein was observed at 61.0% (50/82), 54.7% (87/159), 37.9% (25/66), 36.8% (7/19) in IDC, fibroadenoma, hyperplasia, and inflammation, respectively, and less than 30.0% for breast cyst. Thus, high ARD1 expression correlated with breast cancer (relative risk = 1.32, P < 0.005). Moreover, the level of ARD1 protein in carcinoma patients was distinctly related to lymph node metastasis and ER status, with 94.0% (47/50) as copmpared to 6.0% (3/50) in metastatic and non-metastatic (P < 0.001), and 84.0% (42/50) and 16.0% (8/50) for ER + and ER - (P < 0.01), respectively. In addition, the level of ARD1 appeared to have potential for evaluation of prognosis in breast cancer patients after postoperative therapy.
  
  
  CONCLUSIONS
  These results suggest that ARD1 expression may be as a potential target for exploring the mechanism of breast cancer metastasic to lymph nodes and hormone-responsive regulation.
authors.affiliation: Laboratory of Biochemistry and Molecular Biology, School of Life Science, Yunnan University, Kunming, China.
authors.forename: Ze-Hua
authors.initials: ZH
authors.lastname: Wang
authors.forename: Jun-Li
authors.initials: JL
authors.lastname: Gong
authors.forename: M
authors.initials: M
authors.lastname: Yu
authors.forename: H
authors.initials: H
authors.lastname: Yang
authors.forename: J H
authors.initials: JH
authors.lastname: Lai
authors.forename: M X
authors.initials: MX
authors.lastname: Ma
authors.forename: H
authors.initials: H
authors.lastname: Wu
authors.forename: L
authors.initials: L
authors.lastname: Li
authors.forename: D Y
authors.initials: DY
authors.lastname: Tan
mesh_terms: D000123:Acetyltransferases / Q000096:biosynthesis / Q000235:genetics* / Q000378:metabolism; D000328:Adult; D047688:Breast Cyst / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D001943:Breast Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology* / Q000556:secondary; D018270:Carcinoma, Ductal, Breast / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D005260:Female; D018226:Fibroadenoma / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D006801:Humans; D006965:Hyperplasia / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D007150:Immunohistochemistry; D007249:Inflammation / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D008207:Lymphatic Metastasis; D008875:Middle Aged; D063209:N-Terminal Acetyltransferase A; D063213:N-Terminal Acetyltransferase E; D010641:Phenotype; D011184:Postoperative Period; D011379:Prognosis; D015854:Up-Regulation
chemical_list: D000123:Acetyltransferases; D063209:N-Terminal Acetyltransferase A; C504824:NAA10 protein, human; D063213:N-Terminal Acetyltransferase E