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Molecular evidence in support of the neoplastic and precursor nature of microglandular adenosis
Author(s) -
Geyer Felipe C,
LacroixTriki Magali,
Colombo PierreEmmanuel,
Patani Neill,
Gauthier Arnaud,
Natrajan Rachael,
Lambros Maryou B K,
Khalifeh Ibrahim,
Albarracin Constance,
Orru Sandra,
Marchiò Caterina,
Sapino Anna,
Mackay Alan,
Weigelt Britta,
Schmitt Fernando C,
Wesseling Jelle,
Sneige Nour,
ReisFilho Jorge S
Publication year - 2012
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/j.1365-2559.2012.04207.x
Subject(s) - biology , pathology , immunohistochemistry , tissue microarray , comparative genomic hybridization , carcinoma , medicine , gene , genetics , genome
Geyer F C, Lacroix‐Triki M, Colombo P‐E, Patani N, Gauthier A, Natrajan R, Lambros M B K, Khalifeh I, Albarracin C, Orru S, Marchiò C, Sapino A, Mackay A, Weigelt B, Schmitt F C, Wesseling J, Sneige N & Reis‐Filho J S (2012) Histopathology   60, E115–E130 Molecular evidence in support of the neoplastic and precursor nature of microglandular adenosis Aims:  Microglandular adenosis (MGA) is a proliferative breast lesion, which has been proposed to be a potential precursor of triple‐negative breast cancers. The aims of this study were to determine whether MGAs harbour genetic alterations and if any such genetic aberrations found in MGAs are similar to those found in matched invasive carcinomas. Methods and results:  Twelve cases of MGA and/or atypical MGA (AMGA), 10 of which were associated with invasive carcinoma, were evaluated. Immunohistochemical profiling revealed that all invasive carcinomas were of triple‐negative phenotype and expressed S100, cytokeratins 8/18 and ‘basal’ markers. The morphologically distinct components of each case (MGA, AMGA and/or invasive carcinoma) were microdissected and subjected to microarray comparative genomic hybridization. Apart from three typical MGAs, all samples harboured genetic alterations. The percentage of the genome affected by copy number aberrations in MGA/AMGA ranged from 0.5 to 61.9%, indicating varying levels of genetic instability. In three cases, MGA/AMGA displayed copy number aberrations similar to those found in matched invasive components, providing strong circumstantial evidence that MGA may constitute the substrate for the invasive carcinoma development. Conclusions:  Our results support the contention that MGA can be a clonal lesion and non‐obligate precursor of triple‐negative breast cancer.

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