Microglandular adenosis (MGA) is a rare breast lesion, which has long been considered to be hyperplastic. However, atypical forms of MGA (AMGA) and invasive carcinomas arising in the background of MGA are recorded. Recent studies have suggested that MGA may be a non-obligate precursor of invasive carcinomas that are negative for hormone receptors and lack HER-2 overexpression (triple-negative phenotype). The aim of this study was to determine whether MGA is clonal and whether it harbours chromosomal aberrations similar to those found in matched invasive ductal carcinoma of no special type (IDC-NST).
We report on a case comprising MGA, AMGA and a high-grade IDC-NST. The three components were separately microdissected and subjected to genetic analysis with high-resolution microarray comparative genomic hybridisation. Identical genetic changes were detected in all components with subsequent acquisition of additional genetic aberrations in the invasive component, suggesting that MGA was the substrate for the development of the invasive carcinoma. Immunohistochemistry revealed concordant profiles across all components, characterized by triple-negative phenotype and variable positivity for basal markers.
Similar to adenomas, MGA is, at least in some cases, a clonal lesion and may be a non-obligate precursor of a subgroup of high-grade triple-negative and basal-like breast carcinomas.
"Histologically, MGA is characterized by a haphazard infiltration of small, uniformly open, and round glands in dense, hypocellular, and fibrous tissue, or fatty mammary stroma [3,4]. The glands are lined by a monolayer of flat to cuboidal epithelial cells that lack a myoepithelial layer (Figure 3) , which can be verified by immunohistochemistry. MGA immunohistochemistry is positive for pancytokeratin and negative for smooth muscle actin (Figures 5, 6), so the lesion is often confused with a tubular carcinoma. "
[Show abstract][Hide abstract] ABSTRACT: Microglandular adenosis (MGA) of the breast is a very rare and benign proliferative lesion. Most patients complain of a palpable breast mass that may arouse a clinical suspicion of breast cancer. Histopathologically, it is hard to distinguish MGA from breast cancer because of the lack of a myoepithelial layer and infiltrative proliferation. Several studies have reported a strong relationship between MGA and carcinoma arising in MGA, so the mass should be excised completely in cases of MGA determined from a core needle biopsy rather than observation. A 72-years-old woman presented with a palpable breast mass. On physical examination, a mass was palpable in the right upper outer quadrant area and somewhat fixed to the surrounding tissues and pectoralis major muscle. We could not detect any mass or dense lesion on mammography because of a grade 4 dense breast. Ultrasonographic findings revealed a low echoic lesion with indistinct margins. The result of a core needle biopsy was MGA, which was confirmed by excision. We report one case of MGA, which was believed to breast cancer clinically.
[Show abstract][Hide abstract] ABSTRACT: DNA copy number changes in cancer cells, in particular, amplifications, occur frequently, have prognostic impact and are associated with subtypes of breast cancer. Some amplicons contain well-characterized oncogenes, including 11q13 (CCND1) and 17q12 (HER2). HER2 amplification and overexpression defines the HER2+ subgroup of breast cancer patients and is both a prognostic marker for poor outcome and a predictive marker for response to anti-HER2 targeted therapies. Therefore, there is considerable interest in documenting the locations of other recurring amplifications in breast cancers as they may also provide a rich source of new biomarkers and novel therapeutic targets for these subgroups. This article focuses on the genomic profiling of breast cancer, with an emphasis on the characteristics of the amplifications found in subtypes of breast cancer, including luminal (ER+)/HER2(-)), HER2+ and basal-like (ER(-)/HER2(-)), and discusses their known or potential roles in cancer biology and their clinical implications.
[Show abstract][Hide abstract] ABSTRACT: Lopez-Garcia M A, Geyer F C, Lacroix-Triki M, Marchió C & Reis-Filho J S (2010) Histopathology 57, 171–192 Breast cancer precursors revisited: molecular features and progression pathways
Increasingly more coherent data on the molecular characteristics of benign breast lesions and breast cancer precursors have led to the delineation of new multistep pathways of breast cancer progression through genotypic–phenotypic correlations. It has become apparent that oestrogen receptor (ER)-positive and -negative breast lesions are fundamentally distinct diseases. Within the ER-positive group, histological grade is strongly associated with the number and complexity of genetic abnormalities in breast cancer cells. Genomic analyses of high-grade ER-positive breast cancers have revealed that a substantial proportion of these tumours harbour the characteristic genetic aberrations found in low-grade ER-positive disease, suggesting that at least a subgroup of high-grade ER-positive breast cancers may originate from low-grade lesions. The ER-negative group is more complex and heterogeneous, comprising distinct molecular entities, including basal-like, HER2 and molecular apocrine lesions. Importantly, the type and pattern of genetic aberrations found in ER-negative cancers differ from those of ER-positive disease. Here, we review the available molecular data on breast cancer risk indicator and precursor lesions, the putative mechanisms of progression from in situ to invasive disease, and propose a revised model of breast cancer evolution based on the molecular characteristics of distinct subtypes of in situ and invasive breast cancers.
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