ArticleCancer genomics & proteomics
Therapy-induced Deletion in 11q23 Leading to Fusion of
Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Outcomes of acute myeloid leukemia with KMT2A (MLL) rearrangement: a multicenter study of TROPHY group.Blood cancer journal · 2025Article
- The causal effects of 2,821 protein level ratios on non-small cell lung cancer: a two-sample Mendelian randomization study.Translational cancer research · 2025Article
- Targeting ARHGEF12 promotes neuroblastoma differentiation, MYCN degradation, and reduces tumorigenicity.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- An interactive analysis of the mouse oviductal miRNA profiles.Frontiers in cell and developmental biology · 2022Article
- KMT2A-ARHGEF12, a therapy related fusion with poor prognosis.Molecular biology reports · 2021Review
- Autophagy-related circRNA evaluation reveals hsa_circ_0001747 as a potential favorable prognostic factor for biochemical recurrence in patients with prostate cancer.Cell death & disease · 2021Article
- Acute Undifferentiated Leukemia With a Balanced t(5;10)(q35;p12) Resulting in Fusion ofCancer genomics & proteomicsArticle
- NovelCancer genomics & proteomicsArticle
- Interstitial Deletions Generating Fusion Genes.Cancer genomics & proteomicsReview
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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
BACKGROUND/
aimFusion of histone-lysine N-methyltransferase 2A gene (KMT2A) with the Rho guanine nucleotide exchange factor 12 gene (ARHGEF12), both located in 11q23, was reported in some leukemic patients. We report a KMT2A-ARHGEF12 fusion occurring during treatment of a pediatric acute myeloid leukemia (AML) with topoisomerase II inhibitors leading to a secondary acute lymphoblastic leukemia (ALL). MATERIALS AND
methodsMultiple genetic analyses were performed on bone marrow cells of a girl initially diagnosed with AML.
resultsAt the time of diagnosis with AML, the t(9;11)(p21;q23)/KMT2A-MLLT3 genetic abnormality was found. After chemotherapy resulting in AML clinical remission, a 2 Mb deletion in 11q23 was found generating a KMT2A-ARHGEF12 fusion gene. When the patient later developed B lineage ALL, a t(14;19)(q32;q13), loss of one chromosome 9, and KMT2A-ARHGEF12 were detected.
conclusionThe patient sequentially developed AML and ALL with three leukemia-specific genomic abnormalities in her bone marrow cells, two of which were KMT2A-rearrangements.
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