title: Estrogen receptor expression is high but is of lower intensity in tubular carcinoma than in well-differentiated invasive ductal carcinoma.
abstract: BACKGROUND
  Tubular carcinoma (TC) is a rare, luminal A subtype of breast carcinoma with excellent prognosis, for which adjuvant chemotherapy is usually contraindicated.
  
  
  OBJECTIVE
  To examine the levels of estrogen receptor (ER) and progesterone receptor expression in cases of TC and well-differentiated invasive ductal carcinoma as compared to normal breast glands and to determine if any significant differences could be detected via molecular testing.
  
  
  METHODS
  We examined ER and progesterone receptor via immunohistochemistry in tubular (N = 27), mixed ductal/tubular (N = 16), and well-differentiated ductal (N = 27) carcinomas with comparison to surrounding normal breast tissue. We additionally performed molecular subtyping of 10 TCs and 10 ductal carcinomas via the PAM50 assay.
  
  
  RESULTS
  Although ER expression was high for all groups, TC had statistically significantly lower ER staining percentage (ER%) (P = .003) and difference in ER expression between tumor and accompanying normal tissue (P = .02) than well-differentiated ductal carcinomas, with mixed ductal/tubular carcinomas falling between these 2 groups. Mean ER% was 79%, 87%, and 94%, and mean tumor-normal ER% differences were 13.6%, 25.9%, and 32.6% in tubular, mixed, and ductal carcinomas, respectively. Most tumors that had molecular subtyping were luminal A (9 of 10 tubular and 8 of 10 ductal), and no significant differences in specific gene expression between the 2 groups were identified.
  
  
  CONCLUSIONS
  Tubular carcinoma exhibited decreased intensity in ER expression, closer to that of normal breast parenchyma, likely as a consequence of a high degree of differentiation. Lower ER% expression by TC may represent a potential pitfall when performing commercially available breast carcinoma prognostic assays that rely heavily on ER-related gene expression.
authors.affiliation: From the Department of Pathology (Drs Jorns and Thomas) and Comprehensive Cancer Center (Mr Healy and Ms Daignault), University of Michigan, Ann Arbor; the Genome Institute (Ms Vickery and Dr Mardis) and Division of Oncology (Ms Snider and Drs Davies and Ellis), Washington University School of Medicine, St Louis, Missouri; and the Department of Laboratory Medicine and Pathology (Dr Visscher), Mayo Medical Laboratories, Rochester, Minnesota.
authors.forename: Julie M
authors.initials: JM
authors.lastname: Jorns
authors.forename: Dafydd G
authors.initials: DG
authors.lastname: Thomas
authors.forename: Patrick N
authors.initials: PN
authors.lastname: Healy
authors.forename: Stephanie
authors.initials: S
authors.lastname: Daignault
authors.forename: Tammi L
authors.initials: TL
authors.lastname: Vickery
authors.forename: Jacqueline E
authors.initials: JE
authors.lastname: Snider
authors.forename: Elaine R
authors.initials: ER
authors.lastname: Mardis
authors.forename: Sherri R
authors.initials: SR
authors.lastname: Davies
authors.forename: Matthew J
authors.initials: MJ
authors.lastname: Ellis
authors.forename: Daniel W
authors.initials: DW
authors.lastname: Visscher
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D000328:Adult; D000368:Aged; D001943:Breast Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D018270:Carcinoma, Ductal, Breast / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D002454:Cell Differentiation; D005260:Female; D020869:Gene Expression Profiling; D006801:Humans; D007150:Immunohistochemistry; D008875:Middle Aged; D058889:Molecular Typing; D011960:Receptors, Estrogen / Q000378:metabolism*; D011980:Receptors, Progesterone / Q000378:metabolism
chemical_list: D011960:Receptors, Estrogen; D011980:Receptors, Progesterone