Double minute chromosomes in acute myeloid leukemia and myelodysplastic syndromes are associated with complex karyotype, monosomal karyotype, TP53 deletion, and TP53 mutations

References

• Levan A, Levan G. Have double minutes functioning centromeres? Hereditas. 1978;88(1):81–92.
   PubMed Web of Science ®Google Scholar
• Barker PE, Hsu TC. Are double minutes chromosomes? Exp Cell Res. 1978;113(2):456–458.
   PubMed Web of Science ®Google Scholar
• Haaf T, Schmid M. Analysis of double minutes and double minute-like chromatin in human and murine tumor cells using antikinetochore antibodies. Cancer Genet Cytogenet. 1988;30(1):73–82.
   PubMedGoogle Scholar
• Lin CC, Meyne J, Sasi R, et al. Apparent lack of telomere sequences on double minute chromosomes. Cancer Genet Cytogenet. 1990;48(2):271–274.
   PubMedGoogle Scholar
• Furuya T, Morgan R, Berger CS, et al. Presence of telomeric sequences on deleted chromosomes and their absence on double minutes in cell line HL-60. Cancer Genet Cytogenet. 1993;70(2):132–135.
   PubMedGoogle Scholar
• Krawczun MS, Camargo M, Cervenka J. Patterns of BrDU incorporation in homogenously staining regions and double minutes. Cancer Genet Cytogenet. 1986;21(3):257–265.
   PubMedGoogle Scholar
• Takayama S, Uwaike Y. Analysis of the replication mode of double minutes using the PCC technique combined with BrDU labelling. Chromosoma. 1988;97(3):198–203.
   PubMed Web of Science ®Google Scholar
• Oobatake Y, Shimizu N. Double-strand breakage in the extrachromosomal double minutes triggers their aggregation in the nucleus, micronucleation, and morphological transformation. Genes Chromosomes Cancer. 2020;59(3):133–143.
   PubMed Web of Science ®Google Scholar
• Storlazzi CT, Fioretos T, Surace C, et al. MYC-containing double minutes in hematologic malignancies: evidence in favor of the episome model and exclusion of MYC as the target gene. Hum Mol Genet. 2006;15(6):933–942.
   PubMed Web of Science ®Google Scholar
• Zhu J, Yu Y, Meng X, et al. De novo-generated small palindromes are characteristic of amplicon boundary junction of double minutes. Int J Cancer. 2013;133(4):797–806.
   PubMed Web of Science ®Google Scholar
• Mitelman F, Johansson B, Mertens FE. Mitelman database of chromosome aberrations and gene fusions in cancer; 2020. [cited 2020 Nov 8]. Available from: https://mitelmandatabase.isb-cgc.org.
   Google Scholar
• Meng X, Qi X, Guo H, et al. Novel role for non-homologous end joining in the formation of double minutes in methotrexate-resistant colon cancer cells. J Med Genet. 2015;52(2):135–144.
   PubMed Web of Science ®Google Scholar
• Yu L, Zhao Y, Quan C, et al. Gemcitabine eliminates double minute chromosomes from human ovarian cancer cells. PLOS One. 2013;8(8):e71988.
   PubMed Web of Science ®Google Scholar
• Thomas L, Stamberg J, Gojo I, et al. Double minute chromosomes in monoblastic (M5) and myeloblastic (M2) acute myeloid leukemia: two case reports and a review of literature. Am J Hematol. 2004;77(1):55–61.
   PubMed Web of Science ®Google Scholar
• Huh YO, Tang G, Talwalkar SS, et al. Double minute chromosomes in acute myeloid leukemia, myelodysplastic syndromes, and chronic myelomonocytic leukemia are associated with micronuclei, MYC or MLL amplification, and complex karyotype. Cancer Genet. 2016;209(7–8):313–320.
   PubMed Web of Science ®Google Scholar
• T Ang G, DiNardo C, Zhang L, et al. MLL gene amplification in acute myeloid leukemia and myelodysplastic syndromes is associated with characteristic clinicopathological findings and TP53 gene mutation. Hum Pathol. 2015;46(1):65–73.
   PubMed Web of Science ®Google Scholar
• Bruckert P, Kappler R, Scherthan H, et al. Double minutes and c-MYC amplification in acute myelogenous leukemia: are they prognostic factors? Cancer Genet Cytogenet. 2000;120(1):73–79.
   PubMedGoogle Scholar
• Fan Y, Mao R, Lv H, et al. Frequency of double minute chromosomes and combined cytogenetic abnormalities and their characteristics. J Appl Genetics. 2011;52(1):53–59.
   PubMed Web of Science ®Google Scholar
• Benner SE, Wahl GM, Von Hoff DD. Double minute chromosomes and homogeneously staining regions in tumors taken directly from patients versus in human tumor cell lines. Anticancer Drugs. 1991;2(1):11–25.
   PubMed Web of Science ®Google Scholar
• Arber DA, Orazi A, Hasserjian R, et al. The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia. Blood. 2016;127(20):2391–2405.
   PubMed Web of Science ®Google Scholar
• Dohner H, Estey E, Grimwade D, et al. Diagnosis and management of AML in adults: 2017 ELN recommendations from an international expert panel. Blood. 2017;129(4):424–447.
   PubMed Web of Science ®Google Scholar
• Breems DA, Van Putten WL, De Greef GE, et al. Monosomal karyotype in acute myeloid leukemia: better indicator of poor prognosis than a complex karyotype. J Clin Oncol. 2008;26(29):4791–4797.
   PubMed Web of Science ®Google Scholar
• Vaidya R, Caramazza D, Begna KH, et al. Mosomal karyotype in primary myelofibrosis is detrimental to both overall and leukemia free survival. Blood. 2011;117(21):5612–5615.
   PubMed Web of Science ®Google Scholar
• National Cancer Institute. SEER cancer statistics review, 1975-2015: overview, median age at diagnosis; 2018. Available from: https://seer.cancer.gov/csr/1975_2018/
   Google Scholar
• Schanz J, Tuchler H, Sole F, et al. Monosomal karyotype in MDS: explaining the poor prognosis? Leukemia. 2013;27(10):1988–1995.
   PubMed Web of Science ®Google Scholar
• Korbel JO, Campbell PJ. Criteria for inference of chromothripsis in cancer genomes. Cell. 2013;152(6):1226–1236.
   PubMed Web of Science ®Google Scholar
• L Abbate A, Tolomeo D, Cifola I, et al. MYC-containing amplicons in acute myeloid leukemia: genomic structures, evolution, and transcriptional consequences. Leukemia. 2018;32(10):2152–2166.
   PubMed Web of Science ®Google Scholar
• Stephens PJ, Greenman CD, Fu B, et al. Massive genomic rearrangement acquired in a single catastrophic event during cancer development. Cell. 2011;144(1):27–40.
   PubMed Web of Science ®Google Scholar
• Rausch T, Jones DT, Zapatka M, et al. Genome sequencing of pediatric medulloblastoma links catastrophic DNA rearrangements with TP53 mutations. Cell. 2012;148(1–2):59–71.
   PubMed Web of Science ®Google Scholar
• Gao JH, Chen YH, Mina A, et al. Unique morphologic and genetic characteristics of acute myeloid leukemia with chromothripsis: a clinicopathologic study from a single institution. Hum Pathol. 2020;98:22–31.
   PubMed Web of Science ®Google Scholar
• Tefferi A, Idossa D, Lasho TL, et al. Mutations and karyotype in myelody plastic syndromes: TP53 clusters with monosomal karyotype, RUNX1 with trisomy21, and SF3B1 with inv(3)(q21q26.2)and del(11q). Blood Cancer J. 2017;7(12):658.
   PubMedGoogle Scholar
• Bochtler T, Granzow M, Stölzel F, et al. Marker chromosomes can arise from chromothripsis and predict adverse prognosis in acute myeloid leukemia. Blood. 2017;129(10):1333–1342.
   PubMed Web of Science ®Google Scholar
• Yin Y, Tainsky MA, Bischoff FZ, et al. Wild-type p53 restores cell cycle control and inhibits gene amplification in cells with mutant p53 alleles. Cell. 1992;70(6):937–948.
   PubMed Web of Science ®Google Scholar
• Livingstone LR, White A, Sprouse J, et al. Altered cell cycle arrest and gene amplification potential accompany loss of wild-type p53. Cell. 1992;70(6):923–935.
   PubMed Web of Science ®Google Scholar
• Stengel A, Kern W, Haferlach T, et al. The impact of TP53 mutations and TP53 deletions on survival varies between AML, ALL, MDS and CLL Fan analysis of 3307 cases. Leukemia. 2017;31(3):705–711.
   PubMed Web of Science ®Google Scholar
• Rucker FG, Schlenk RF, Bullinger L, et al. TP53 alterations in acute myeloid leukemia with complex karyotype correlate with specific copy number alterations, monosomal karyotype, and dismal outcome. Blood. 2012;119(9):2114–2121.
   PubMed Web of Science ®Google Scholar