ArticleExperimental hematology & oncology2012
JAK2V617F and p53 mutations coexist in erythroleukemia and megakaryoblastic leukemic cell lines.
Article in Experimental hematology & oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
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- Molecular Landscapes and Models of Acute Erythroleukemia.HemaSphere · 2021Review
- Lineage tracing of acute myeloid leukemia reveals the impact of hypomethylating agents on chemoresistance selection.Nature communications · 2019Article
- LSD1 Inhibition Prolongs Survival in Mouse Models of MPN by Selectively Targeting the Disease Clone.HemaSphere · 2018Article
- Loss of p53 induces leukemic transformation in a murine model of Jak2 V617F-driven polycythemia vera.Oncogene · 2017Article
- A myeloid tumor suppressor role forThe Journal of experimental medicine · 2017Article
- Identification of an orally available compound with potent and broad FLT3 inhibition activity.Oncogene · 2016Article
- Dissecting Genomic Aberrations in Myeloproliferative Neoplasms by Multiplex-PCR and Next Generation Sequencing.PloS one · 2015Article
- Preclinical evaluation of bortezomib/dipyridamole novel combination as a potential therapeutic modality for hematologic malignancies.Molecular oncology · 2015Article
- Article
- B-Raf and the inhibitors: from bench to bedside.Journal of hematology & oncology · 2013Review
- Different mutations of the human c-mpl gene indicate distinct haematopoietic diseases.Journal of hematology & oncology · 2013Review
- Dysregulation of JAK-STAT pathway in hematological malignancies and JAK inhibitors for clinical application.Biomarker research · 2013Article
- SU11652 Inhibits tyrosine kinase activity of FLT3 and growth of MV-4-11 cells.Journal of hematology & oncology · 2012Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelled
backgroundJAK2V617F, a gain-of-function mutant form of tyrosine kinase JAK2, is found in the majority of patients with Ph- myeloproliferative neoplasms (MPNs), a group of chronic hematological diseases that often lead to acute leukemia. The current study is intended to find other gene mutations that collaborate with JAK2V617F to cause leukemic transformation.
methodsTotal RNA and genomic DNA were isolated from two JAK2V617F-positive cell lines, namely, erythroleukemic HEL and megakaryoblastic leukemic SET-2 cells. Candidate genes were amplified by PCR and further sequenced.
resultsHomozygous mutations of the TP53 gene which encodes tumor suppressor p53 were found in HEL and SET-2 cells. While HEL cells, which have homozygous JAK2V617F, contain a rare M133K p53 mutation, SET-2 cells, which have a heterozygous JAK2V617F mutation, contain a common R248W p53 alteration. Western blot analyses revealed high levels of p53 expression in both cells. M133K and R248W are located in the DNA binding domain of p53. Structural analyses revealed that they potentially disrupt the interaction of p53 with DNA, thereby causing loss of p53 function.
conclusionsJAK2V617F and p53 mutations coexist in leukemia cells. We believe that JAK2V617F is able to drive leukemic transformation when the function of tumor suppressor p53 is lost. The interplay of JAK2V617F with p53 may affect the progression of MPNs.
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