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Sayedian F, Senft JR, Spruill MD, et al. c-MYC Amplification in Acute Myelogenous Leukemia Evolving from Double Minutes (dmins) to Homogeneously Staining Region (hsr). J Assoc Genet Technol. 2014;40(2):64-7
Sayedian, F., Senft, J. R., Spruill, M. D., Wenger, S. L., & Vos, J. A. (2014). c-MYC Amplification in Acute Myelogenous Leukemia Evolving from Double Minutes (dmins) to Homogeneously Staining Region (hsr). Journal of the Association of Genetic Technologists, 40(2), 64-7.
Sayedian, Farzaneh, et al. "c-MYC Amplification in Acute Myelogenous Leukemia Evolving from Double Minutes (dmins) to Homogeneously Staining Region (hsr)." Journal of the Association of Genetic Technologists vol. 40,2 (2014): 64-7.
Sayedian F, Senft JR, Spruill MD, Wenger SL, Vos JA. c-MYC Amplification in Acute Myelogenous Leukemia Evolving from Double Minutes (dmins) to Homogeneously Staining Region (hsr). J Assoc Genet Technol. 2014;40(2):64-7. PMID: 26029796.
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J Assoc Genet Technol. 2014;40(2):64-7.

c-MYC Amplification in Acute Myelogenous Leukemia Evolving from Double Minutes (dmins) to Homogeneously Staining Region (hsr).

Journal of the Association of Genetic Technologists

Farzaneh Sayedian, Jamie R Senft, Michelle D Spruill, Sharon L Wenger, Jeffrey A Vos

Affiliations

  1. Department of Pathology, 1 Medical Center Drive, Morgantown, West Virginia University, Morgantown, WV.

PMID: 26029796

Abstract

A bone marrow biopsy of a 68-year-old woman revealed 59% blasts and immature monocytes, consistent with acute myeloid leukemia (AML) with monocytic features. Occasional hypolobated megakaryocytes and decreased iron stores were also present. A peripheral blood sample showed 7% blasts in addition to monocytosis, macrocytic anemia and thrombocytopenia. Molecular testing was negative for FLT3-ITD, NPM1 and CEBPA. Fluorescence in situ hybridization (FISH) probes were negative for t(8;21), t(15;17), inversion 16 and 11q23 rearrangements. The karyotype was 46,XX,del(20)(q11.2q13.1),~50dmin[3]/47,idem,+4[13]/47,idem,+22[2]/46,XX[2]. FISH confirmed that the double minutes were c-MYC positive with cryptic deletion of the c-MYC FISH signal on one of the chromosome 8s. Two months post-diagnosis, 57% of our patient's cells were still positive for c-MYC amplification; however, by four months only 8% of cells were positive for c-MYC amplification. After seven months, the patient's karyotype had the 20q deletion, X chromosome loss and a ring chromosome that consisted of a homogeneously staining region (hsr) containing c-MYC amplification. This case demonstrates that gene amplification in the form of double minutes can transform into a more stable hsr.

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