title: Neovascularization in mucinous ductal carcinoma in situ suggests an alternative pathway for invasion.
abstract: OBJECTIVE
  Ductal carcinoma in situ (DCIS) associated with invasive mucinous carcinoma (IMC) has not been well characterized. The aim was to characterize mucinous DCIS (mDCIS) of the breast and to describe, to our knowledge for the first time, neovascularization in mucin.
  
  
  RESULTS
  The pathology reports and slides were reviewed from 44 patients treated between 2003 and 2006 at The University of Texas M. D. Anderson Cancer Center, whose diagnosis fulfilled the criteria of IMC or DCIS with mucin production. The patients, all female, had a mean age of 62 years. DCIS was present in 93% of cases and the predominant histological types were solid, cribriform and micropapillary. The DCIS was grade 1 in 12 of 41 cases (29.3%), grade 2 in 25 of 41 cases (61%) and grade 3 in four of 41 cases (9.8%). Mucin was seen in the lumen of the ducts involved by DCIS in 88% of cases, mucin and vessels in 63.4% of cases and neither mucin nor vessels in 12.2%. The DCIS was vascular endothelial growth factor-positive, platelet-derived growth factor receptor-beta-positive and CDX-2-negative (100%). Occasional luminal cells within the DCIS were immunopositive for CD68.
  
  
  CONCLUSIONS
  A significant number of mDCIS showed neovascularization in intraluminal mucin. When identified on core needle biopsy, the presence of vascularized mucin should not be used alone to discriminate between invasive and in situ carcinoma. A hypothesis proposed for the source of recruitment of vessels in the mucin is that mucin can promote neovascularization and that tumour cells invade not into the adjacent fibroconnective tissue, but rather into the mucinous, richly vascularized stroma that they have induced. Alternatively, it is possible that both cells and their secretory product invade together. To our knowledge, this is the first study to characterize neovascularization within the mucinous component of DCIS associated with and without IMC.
authors.affiliation: Department of Pathology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA.
authors.forename: S A
authors.initials: SA
authors.lastname: Gadre
authors.forename: G H
authors.initials: GH
authors.lastname: Perkins
authors.forename: A A
authors.initials: AA
authors.lastname: Sahin
authors.forename: N
authors.initials: N
authors.lastname: Sneige
authors.forename: M T
authors.initials: MT
authors.lastname: Deavers
authors.forename: L P
authors.initials: LP
authors.lastname: Middleton
mesh_terms: D002288:Adenocarcinoma, Mucinous / Q000473:pathology*; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001943:Breast Neoplasms / Q000473:pathology*; D000071616:CDX2 Transcription Factor; D018270:Carcinoma, Ductal, Breast / Q000098:blood supply / Q000473:pathology*; D002285:Carcinoma, Intraductal, Noninfiltrating / Q000098:blood supply* / Q000473:pathology*; D018450:Disease Progression; D005260:Female; D018398:Homeodomain Proteins / Q000378:metabolism; D006801:Humans; D008875:Middle Aged; D009077:Mucins / Q000378:metabolism; D009389:Neovascularization, Pathologic; D015534:Trans-Activators / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D000071616:CDX2 Transcription Factor; D018398:Homeodomain Proteins; D009077:Mucins; D015534:Trans-Activators; D042461:Vascular Endothelial Growth Factor A