title: Intraductal spread of invasive breast carcinoma has a positive correlation with c-erb B-2 overexpression and vascular invasion.
abstract: BACKGROUND
  Studies of the histologic characteristics and biologic behavior of the intraductal spread of breast carcinoma are critically important in that they may lead to the identification of a unique spread pattern rather than a noninvasive lesion.
  
  
  METHODS
  Paraffin embedded specimens of 187 primary invasive breast carcinomas and 4 noninvasive ductal carcinomas, obtained by wide excision, quadrantectomy, total glandectomy, or mastectomy, were studied immunohistochemically. The overexpression of c-erb B-2, p53, bcl-2, and MIB-1, as well as the histologic characteristics of intraductal spread (such as histologic features and histologic grade), were assessed. Chi-square and Fisher exact tests were conducted to evaluate significant differences; the Macintosh for Expert StatView 4.0 system was used to conduct these tests.
  
  
  RESULTS
  The histologic characteristics of intraductal spread were similar to those of noninvasive ductal carcinoma. However, the expressions of c-erb B-2, p53, and other biologic markers of intraductal spread were similar to those of the main invasive tumor. The overexpression of c-erb B-2 protein was found more often in the group that was positive for intraductal spread than in the group that was negative (P < 0.01). Intraductal spread was found more often in the group that was positive for lymphatic and venous invasion than in the group that was negative (P < 0.005). Subnipple margin positive status was related closely to intraductal spread (P < 0.0001).
  
  
  CONCLUSIONS
  The positive correlation between intraductal spread and c-erb B-2 overexpression as well as lymphatic, venous invasion was recognized, and it was determined that intraductal spread of invasive breast carcinoma possesses an invasive and metastatic potential that is distinct from noninvasive ductal carcinoma.
authors.affiliation: Second Department of Pathology, Wakayama Medical College, Wakayama City, Japan.
authors.forename: X
authors.initials: X
authors.lastname: Jing
authors.forename: K
authors.initials: K
authors.lastname: Kakudo
authors.forename: M
authors.initials: M
authors.lastname: Murakami
authors.forename: Y
authors.initials: Y
authors.lastname: Nakamura
authors.forename: M
authors.initials: M
authors.lastname: Nakamura
authors.forename: T
authors.initials: T
authors.lastname: Yokoi
authors.forename: Q
authors.initials: Q
authors.lastname: Yang
authors.forename: S
authors.initials: S
authors.lastname: Oura
authors.forename: T
authors.initials: T
authors.lastname: Sakurai
mesh_terms: D034961:Antigens, Nuclear; D014408:Biomarkers, Tumor / Q000378:metabolism; D001940:Breast / Q000473:pathology*; D001943:Breast Neoplasms / Q000098:blood supply / Q000378:metabolism* / Q000473:pathology*; D018270:Carcinoma, Ductal, Breast / Q000098:blood supply / Q000378:metabolism* / Q000473:pathology*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen; D015999:Multivariate Analysis; D009361:Neoplasm Invasiveness; D009363:Neoplasm Proteins / Q000378:metabolism*; D009687:Nuclear Proteins / Q000378:metabolism; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000378:metabolism*; D012044:Regression Analysis; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D019043:Vascular Neoplasms / Q000473:pathology*
chemical_list: D034961:Antigens, Nuclear; D014408:Biomarkers, Tumor; D019394:Ki-67 Antigen; D009363:Neoplasm Proteins; D009687:Nuclear Proteins; D018719:Erb-b2 Receptor Tyrosine Kinases; D016159:Tumor Suppressor Protein p53