title: Oncoprotein HCCR-1 expression in breast cancer is well correlated with known breast cancer prognostic factors including the HER2 overexpression, p53 mutation, and ER/PR status.
abstract: BACKGROUND
  Oncoprotein HCCR-1 functions as a negative regulator of the p53 and contributes breast tumorigenesis. The serum HCCR-1 assay is useful in diagnosing breast cancer and mice transgenic for HCCR developed breast cancers. But it is unknown how HCCR-1 contributes to human breast tumorigenesis.
  
  
  METHODS
  Oncogene HCCR-1 expression levels were determined in normal breast tissues, breast cancer tissues and cancer cell lines. We examined whether HCCR-1 protein expression in breast cancer is related to different biological characteristics, including ER, PR, p53 genotype, and HER2 status in 104 primary breast cancer tissues using immunohistochemical analyses.
  
  
  RESULTS
  HCCR-1 was upregulated in breast cancer cells and tissues compared with normal breast tissues. In this study, overexpression of HCCR-1 was well correlated with known breast cancer prognostic markers including the presence of steroid receptors (ER and PR), p53 mutation and high HER2 overexpression. HCCR-1 was not detected in the ER-negative, PR-negative, p53 negative and low HER2 breast cancer tissues. These data indicate that the level of HCCR-1 in breast cancer tissues is relatively well correlated with known breast cancer factors, including the HER2 overexpression, p53 mutation, and ER/PR status.
  
  
  CONCLUSIONS
  Determination of HCCR-1 levels as options for HER2 testing is promising although it needs further evaluation.
authors.affiliation: Department of Molecular Genetic Laboratory, College of Medicine, The Catholic University of Korea, Seoul, Korea. hsa387@hanmail.net
authors.forename: Seon-Ah
authors.initials: SA
authors.lastname: Ha
authors.forename: Youn Soo
authors.initials: YS
authors.lastname: Lee
authors.forename: Seung Min
authors.initials: SM
authors.lastname: Shin
authors.forename: Hyun Kee
authors.initials: HK
authors.lastname: Kim
authors.forename: Sanghee
authors.initials: S
authors.lastname: Kim
authors.forename: Hong
authors.initials: H
authors.lastname: Namkoong
authors.forename: Hae Joo
authors.initials: HJ
authors.lastname: Kim
authors.forename: Sang Min
authors.initials: SM
authors.lastname: Jung
authors.forename: Yu Sun
authors.initials: YS
authors.lastname: Lee
authors.forename: Yeun Jun
authors.initials: YJ
authors.lastname: Chung
authors.forename: Sang Seol
authors.initials: SS
authors.lastname: Jung
authors.forename: Jin Woo
authors.initials: JW
authors.lastname: Kim
mesh_terms: D015152:Blotting, Northern; D045744:Cell Line, Tumor; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D005838:Genotype; D006801:Humans; D007150:Immunohistochemistry; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000378:metabolism*; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000235:genetics / Q000378:metabolism*; D011960:Receptors, Estrogen / Q000235:genetics / Q000378:metabolism*; D011980:Receptors, Progesterone / Q000235:genetics / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism*
chemical_list: D011518:Proto-Oncogene Proteins; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D016159:Tumor Suppressor Protein p53; C476732:LETMD1 protein, human