MYC amplification in subtypes of breast cancers in African American women.

Autor: Naab TJ; Department of Pathology, Howard University College of Medicine, Howard University Hospital, 2041 Georgia Avenue Rm. 1M-06, Washington DC, NW, 20060, USA., Gautam A; Department of Oncology, University of Massachusetts Medical School, 373 Plantation street Suite# 318, Worcester, MA, 01581, England., Ricks-Santi L; Cancer Research Center, Department of Biological Sciences, Hampton University, 100 E. Queen Street, Hampton, VA, 23668, USA., Esnakula AK; Department of Pathology, Immunology and Laboratory Medicine, University of Florida College of Medicine, P.O. Box 100275, 1600 SW Archer Road, Gainesville, FL, 32610-0275, USA., Kanaan YM; Department of Microbiology, Howard University College of Medicine, 2041 Georgia Avenue Rm. 1M-06, Washington DC, NW, 20060, USA., DeWitty RL; Department of Surgery, Howard University Hospital, 2041 Georgia Avenue, Washington DC, NW, 20060, USA., Asgedom G; Department of Medicine, Howard University Hospital, 2041 Georgia Avenue, Washington DC, NW, 20060, USA., Makambi KH; Department of Biostatistics, Bioinformatics, and Biomathematics, Lombardi Comprehensive Cancer Center, Georgetown University, 4000 Reservoir Road, Washington, DC, NW, 20057, USA., Abawi M; Inherited Cancer Program, GeneDx, 207 Perry Pkwy, Gaithersburg, MD, 20877, USA., Blancato JK; Department of Oncology, Lombardi Comprehensive Cancer Centre, Georgetown University Medical Centre, 3800 Reservoir Road, Washington DC, NW, 20007, USA. blancatj@georgetown.edu.
Jazyk: angličtina
Zdroj: BMC cancer [BMC Cancer] 2018 Mar 09; Vol. 18 (1), pp. 274. Date of Electronic Publication: 2018 Mar 09.
DOI: 10.1186/s12885-018-4171-6
Abstrakt: 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.
Databáze: MEDLINE
Externí odkaz:
Nepřihlášeným uživatelům se plný text nezobrazuje