ArticleMolecular cytogenetics2014
Genomic amplification of MYC as double minutes in a patient with APL-like leukemia.
Article in Molecular cytogenetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 18 citations in OpenAlex.
- Acute Promyelocytic Leukemia with double minute chromosomes: a rare case with high relapse risk.Oxford medical case reports · 2025Article
- Myeloid neoplasms with MYC-positive double minutes: towards recognition as a distinct entity.Blood cancer journal · 2025Article
- The role of extrachromosomal DNA in tumorigenesis and progression.Frontiers in oncology · 2025Review
- Current understanding of extrachromosomal circular DNA in cancer pathogenesis and therapeutic resistance.Journal of hematology & oncology · 2020Review
- The biogenesis and roles of extrachromosomal oncogene involved in carcinogenesis and evolution.American journal of cancer research · 2020Review
- Association between the methylation status of theOncology letters · 2016Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute promyelocytic leukemia (APL) is a subtype of acute myeloid leukemia (AML) characterized by a PML-RARA fusion due to a translocation t(15;17). Its sensitivity to treatment with all-trans retinoic acid (ATRA), which causes differentiation of the abnormal promyelocytes, combined with anthracycline based chemotherapy makes it the best curable subtype of acute myeloid leukemia. A rapid and accurate diagnosis is needed in the first place to prevent (more) bleeding problems. Here we present a patient with a leukemia with an APL-like morphology but no detectable PML-RARA fusion, as demonstrated by RT-PCR and cytogenetic analysis.
resultsUnexpectedly, karyotyping revealed numerous double minutes (dmins). Fluorescence in situ hybridization (FISH) with DNA probes specific for the MYC-region showed the presence of multiple MYC amplicons. SNP-array analysis uncovered amplification of the 8q24.13-q24.21 region, including the MYC-gene, flanked by deletions in 8q24.13 and 8q24.21-q24.22, and a homozygous deletion in 9p21.3, flanked by heterozygous deletions in the same chromosome region.
conclusionsThe diagnosis was revised to AML, not otherwise specified (AML, NOS) and therefore therapy with ATRA was discontinued.
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