title: Expression of Her2/neu, steroid receptors (ER and PR), Ki67 and p53 in invasive mammary ductal carcinoma associated with ductal carcinoma In Situ (DCIS) Versus invasive breast cancer alone.
abstract: OBJECTIVE
  (a) To assess the expression patterns of HER2/neu, steroid receptors (ER and PR), Ki67 and p53 in invasive ductal cancer (IDC) and IDC associated with carcinoma in situ (IDC/DCIS) and (b) to determine if there is a differential expression of these molecular markers between IDC and IDC/DCIS.
  
  
  METHODS
  Paraffin-fixed breast cancer samples, diagnosed with only one histological invasive tumor (IDC (n=130), and IDC/DCIS (n=36) were analyzed by immunohistochemical means. The non-parametric Mann-Whitney and chi2 tests were used to evaluate any statistical differences between different groups. Significance was assumed at p<0.05.
  
  
  RESULTS
  A significant increase of the tumor grading was observed between IDC and IDC/DCIS (p<0.05). Her2/neu amplification was demonstrated in 49.6% of IDC compared to 31% of IDC/DCIS (p<0.05). ER expression showed no statistical differences between IDC and IDC/DCIS. The PR expression was demonstrated in 71% of IDC with significantly lower intensity than IDC/DCIS (p<0.05). The Ki67 expression was significantly higher (p<0.05) in IDC cases (64%) versus IDC/DCIS (49.7%). No differences were observed between IDC and IDC/DCIS for p53 expression.
  
  
  CONCLUSIONS
  We demonstrated significantly different expression patterns of Her2/neu, PR and Ki67 in IDC versus IDC/DCIS. Since these molecular markers play important roles in carcinogenesis and tumor progression, IDC/DCIS could be an important subtype of mammary invasive ductal cancer. Differences in expression of the evaluated markers might suggest a higher malignant potential of invasive carcinomas alone. The lower expression of Her2/neu and Ki67 in IDC/DCIS could implicate a less malignant behavior compared to a differentiated IDC. Additionally, these results might suggest that DCIS might be a malignant preform and the interaction with neoplastic tissue could result in an aggressive type of invasive tumor.
authors: Ludwig-Maximilians University Munich, 1st Department of Obstetrics and Gynecology, 80337 Munich, Germany. Ioannis.mylonas@med.uni-muenchen.de
authors: Ioannis
authors: I
authors: Mylonas
authors: Josef
authors: J
authors: Makovitzky
authors: Udo
authors: U
authors: Jeschke
authors: Volker
authors: V
authors: Briese
authors: Klaus
authors: K
authors: Friese
authors: Bernd
authors: B
authors: Gerber
mesh_terms: D001943:Breast Neoplasms / Q000378:metabolism* / Q000473:pathology; D002278:Carcinoma in Situ / Q000378:metabolism* / Q000473:pathology; D044584:Carcinoma, Ductal / Q000378:metabolism* / Q000473:pathology; D005260:Female; D018734:Genes, erbB-2; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000378:metabolism*; D009361:Neoplasm Invasiveness; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000378:metabolism*; D011960:Receptors, Estrogen / Q000378:metabolism*; D011980:Receptors, Progesterone / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
chemical_list: D019394:Ki-67 Antigen; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D016159:Tumor Suppressor Protein p53