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

Christopher A. Febres-Aldana; Odille Mejia-Mejia; Kritika Krishnamurthy; Thomas Mesko; Robert Poppiti

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저자정보: Christopher A. Febres-Aldana (Arkadi M. Rywlin Department of Pathology and Laboratory Medicine Mount Sinai Medical Center Miami) Odille Mejia-Mejia (Arkadi M. Rywlin Department of Pathology and Laboratory Medicine Mount Sinai Medical Center Miami) Kritika Krishnamurthy (Arkadi M. Rywlin Department of Pathology and Laboratory Medicine Mount Sinai Medical Center Miami) Thomas Mesko (Section of Surgical Oncology Mount Sinai Medical Center Miami Beach FL USA) Robert Poppiti (Arkadi M. Rywlin Department of Pathology and Laboratory Medicine Mount Sinai Medical Center Miami)

저널정보: 한국유방암학회 Journal of Breast Cancer Journal of Breast Cancer Vol.23 No.1

발행연도: 2020.1

수록면: 93 - 99 (7page)

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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.

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

참고문헌 (12)

참고문헌 신청

Rasbridge SA / 1998 / Adenomyoepithelioma of the breast with malignant features / Virchows Arch 432:123~130

McLaren BK / 2005 / Adenomyoepithelioma: clinical, histologic, and immunohistologic evaluation of a series of related lesions / Am J Surg Pathol 29:1294~1299

Lubin D / 2019 / Adenomyoepitheliomas of the breast frequently harbor recurrent hotspot mutations in PIK3-AKT pathway-related genes and a subset show genetic similarity to salivary gland epithelial-myoepithelial carcinoma / Am J Surg Pathol 43:1005~1013

Geyer FC / 2018 / Recurrent hotspot mutations in HRAS Q61 and PI3K-AKT pathway genes as drivers of breast adenomyoepitheliomas / Nat Commun 9:1816

Baum JE / 2019 / Mammary epithelial-myoepithelial carcinoma : report of a case with HRAS and PIK3CA mutations by next-generation sequencing / Int J Surg Pathol 27:441~445

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이 논문의 저자 정보

Christopher A. Febres-Aldana

소속기관 Arkadi M. Rywlin Department of Pathology and Laboratory Medicine Mount Sinai Medical Center Miami