ArticleLeukemia2009
The molecular anatomy of the FIP1L1-PDGFRA fusion gene.
Article in Leukemia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00015587 (Chemical Exposures and Leukemia Risks and Childhood Leukemia and Environmental Exposure), which is not on this map. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Chemical Exposures and Leukemia Risks and Childhood Leukemia and Environmental Exposure
Who cites it
12 citing papers in PubMed, 29 citations in OpenAlex.
- Article
- Long read nanopore DNA sequencing with adaptive sampling to identify tyrosine kinase fusion genes.Leukemia · 2026Article
- Novel BMP2K::PDGFRA fusion in an unusual myeloid/lymphoid neoplasm with eosinophilia.Journal of hematopathology · 2025Article
- A Critical Case of Chronic Eosinophilic Leukemia: Diagnostic Criteria and Response to Cytarabine.Case reports in oncological medicine · 2025Article
- Integration of Genomic Sequencing Drives Therapeutic Targeting of PDGFRA in T-Cell Acute Lymphoblastic Leukemia/Lymphoblastic Lymphoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Which Second-Line Tyrosine Kinase Inhibitor(s) for Chronic Myeloid Leukemia?Current treatment options in oncology · 2023Review
- A neoplasm with FIP1L1-PDGFRA fusion presenting as pediatric T-cell lymphoblastic leukemia/lymphoma without eosinophilia.Cancer genetics · 2017Article
- Hypothesis: Artifacts, Including Spurious Chimeric RNAs with a Short Homologous Sequence, Caused by Consecutive Reverse Transcriptions and Endogenous Random Primers.Journal of Cancer · 2015Review
- Article
- Identification of JAK2 as a mediator of FIP1L1-PDGFRA-induced eosinophil growth and function in CEL.PloS one · 2012Article
- FIP1L1/RARA with breakpoint at FIP1L1 intron 13: a variant translocation in acute promyelocytic leukemia.Haematologica · 2011Article
- Screening for diverse PDGFRA or PDGFRB fusion genes is facilitated by generic quantitative reverse transcriptase polymerase chain reaction analysis.Haematologica · 2010Article
Corrections and comments
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Authors and funding
19 authors at 10 institutions in 4 countries.
Funding
Abstract
The FIP1L1-PDGFRA fusion gene is a recurrent molecular abnormality in patients with eosinophilia-associated myeloproliferative neoplasms. We characterized FIP1L1-PDGFRA junction sequences from 113 patients at the mRNA (n=113) and genomic DNA (n=85) levels. Transcript types could be assigned in 109 patients as type A (n=50, 46%) or B (n=47, 43%), which were created by cryptic acceptor splice sites in different introns of FIP1L1 (type A) or within PDGFRA exon 12 (type B). We also characterized a new transcript type C (n=12, 11%) in which both genomic breakpoints fell within coding sequences creating a hybrid exon without use of a cryptic acceptor splice site. The location of genomic breakpoints within PDGFRA and the availability of AG splice sites determine the transcript type and restrict the FIP1L1 exons used for the creation of the fusion. Stretches of overlapping sequences were identified at the genomic junction site, suggesting that the FIP1L1-PDGFRA fusion is created by illegitimate non-homologous end-joining. Statistical analyses provided evidence for clustering of breakpoints within FIP1L1 that may be related to DNA- or chromatin-related structural features. The variability in the anatomy of the FIP1L1-PDGFRA fusion has important implications for strategies to detect the fusion at diagnosis or for monitoring response to treatment.
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