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. 2018 Mar 9;18(1):274.
doi: 10.1186/s12885-018-4171-6.

MYC amplification in subtypes of breast cancers in African American women

Affiliations

MYC amplification in subtypes of breast cancers in African American women

Tammey J Naab et al. BMC Cancer. .

Abstract

Background: MYC overexpression is associated with poor prognosis in breast tumors (BCa). The objective of this study was to determine the prevalence of MYC amplification and associated markers in BCa tumors from African American (AA) women and determine the associations between MYC amplification and clinico-pathological characteristics.

Methods: We analyzed 70 cases of well characterized archival breast ductal carcinoma specimens from AA women for MYC oncogene amplification. Utilizing immune histochemical analysis estrogen receptor (ER), progesterone receptor (PR), and (HER2/neu), were assessed. Cases were Luminal A (ER or PR+, Ki-67 < 14%), Luminal B (ER or PR+, Ki-67 = > 14% or ER or PR+ HER2+), HER2 (ER-, PR-, HER2+), and Triple Negative (ER-, PR-, HER2-) with basal-like phenotype. The relationship between MYC amplification and prognostic clinico-pathological characteristics was determined using chi square and logistic regression modeling.

Results: Sixty-five (97%) of the tumors showed MYC gene amplification (MYC: CEP8 > 1). Statistically significant associations were found between MYC amplification and HER2-amplified BCa, and Luminal B subtypes of BCa (p < 0.0001), stage (p < 0.001), metastasis (p < 0.001), and positive lymph node status (p = 0.039). MYC amplification was associated with HER2 status (p = 0.01) and tumor size (p = 0.01). High MYC amplification was seen in grade III carcinomas (MYC: CEP8 = 2.42), pre-menopausal women (MYC: CEP8 = 2.49), PR-negative status (MYC: CEP8 = 2.42), and ER-positive status (MYC: CEP8 = 2.4).

Conclusions: HER2 positive BCas in AA women are likely to exhibit MYC amplification. High amplification ratios suggest that MYC drives HER2 amplification, especially in HER2 positive, Luminal B, and subtypes of BCa.

Keywords: Breast cancer subtypes; FISH; Gene amplification; MYC.

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Conflict of interest statement

Ethics approval and consent to participate

This study was based on existing de-identified data and pathologic specimens. It was not deemed to be human subjects’ research, but determined to be of exempt status. Approval for this research protocol was given by the Howard University School of Medicine IRB, designated as reference number 15CMED-53.

Consent for publication

Subject consent was not required for this study. It is bound by the ruling of the US Health and Human Services Secretary’s Advisory Committee on Human Research Protections (SACHRP) under the Common Rule for exempt research and the Helsinki guidelines for establishment of IRB committees. IRB approval #15C MED 53 was obtained from the Howard University IRB for the study of de-identified materials.

Competing interests

The authors declare that they have no competing interests.

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Figures

Fig. 1
Fig. 1
FISH hybridization of MYC in breast tumor tissues. The FISH probe for MYC is labeled with a red fluorochrome, and the normal control signal for the chromosome 8 centromere is labeled in green. The nuclei of the cells are visualized via DAPI counterstaining. a 1:3 ratio of MYC to centromere signals indicating low amplification is shown. b 1:5 ration of MYC to centromere signals indicating moderate amplification is shown. c 1:1 copy ratio of MYC to centromere signals indicating no amplification of the MYC gene is shown. d 1: 8 copy ratio of MYC to centromere signals indicating high amplification is shown in the panel

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