J Breast Cancer.  2020 Feb;23(1):93-99. 10.4048/jbc.2020.23.e2.

Malignant transformation in a Breast Adenomyoepithelioma Caused by Amplification of c-MYC: A Common pathway to Cancer in a Rare Entity

Affiliations
  • 1Arkadi M. Rywlin Department of Pathology and Laboratory Medicine, Mount Sinai Medical Center, Miami Beach, FL, USA. christopher.febres@msmc.com
  • 2Section of Surgical Oncology, Mount Sinai Medical Center, Miami Beach, FL, USA.
  • 3Department of Pathology, Herbert Wertheim College of Medicine, Florida International University, Miami, FL, USA.

Abstract

Breast adenomyoepitheliomas are composed of a biphasic proliferation of myoepithelial cells around small epithelial-lined spaces. Due to the rarity of adenomyoepitheliomas, the molecular data describing them are limited. Adenomyoepitheliomas are considered to be benign or have low malignant potential, and be prone to local recurrence. Malignant transformation has been associated with homozygous deletion of CDKN2A or somatic mutations in TERT, but remains unexplained in many cases. Here, we describe a case of carcinomatous transformation of both epithelial and myoepithelial cells in an estrogen receptor-negative adenomyoepithelioma caused by amplification of MYC. Break-apart fluorescence in situ hybridization revealed an increase in the MYC gene copy number (3-4 copies/cell in 37%, > 4 copies/cell in 40%). Deregulation of MYC is responsible for uncontrolled proliferation and cellular immortalization in basal-like breast cancers. Our case demonstrates that genomic instability events associated with gene amplification may be involved in the carcinogenesis of malignant adenomyoepitheliomas.

Keyword

Adenomyoepithelioma; Breast neoplasms; c-MYC gene; In situ hybridization, fluorescent; Gene amplification

MeSH Terms

Adenomyoepithelioma*
Breast Neoplasms
Breast*
Carcinogenesis
Estrogens
Fluorescence
Gene Amplification
Genes, myc
Genomic Instability
In Situ Hybridization
In Situ Hybridization, Fluorescence
Recurrence
Estrogens
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