Case Report: Identification of a novel LYN::LINC01900 transcript with promyelocytic phenotype and TP53 mutation in acute myeloid leukemia
Acute myeloid leukemia (AML) is a malignant disease of myeloid hematopoietic stem/progenitor cells characterized by the abnormal proliferation of primitive and naive random cells in the bone marrow and peripheral blood. Acute promyelocytic leukemia (APL) is a type (AML-M3) of AML. Most patients with...
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Frontiers Media S.A.
2023-12-01
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Online Access: | https://www.frontiersin.org/articles/10.3389/fonc.2023.1322403/full |
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author | Chengjun Hu Qiuxin Dai Ruiyi Zhang Huanping Yang Man Wang Kaili Gu Jiangang Yang Wenjun Meng Ping Chen Maozhong Xu |
author_facet | Chengjun Hu Qiuxin Dai Ruiyi Zhang Huanping Yang Man Wang Kaili Gu Jiangang Yang Wenjun Meng Ping Chen Maozhong Xu |
author_sort | Chengjun Hu |
collection | DOAJ |
description | Acute myeloid leukemia (AML) is a malignant disease of myeloid hematopoietic stem/progenitor cells characterized by the abnormal proliferation of primitive and naive random cells in the bone marrow and peripheral blood. Acute promyelocytic leukemia (APL) is a type (AML-M3) of AML. Most patients with APL have the characteristic chromosomal translocation t(15; 17)(q22; q12), forming PML::RARA fusion. The occurrence and progression of AML are often accompanied by the emergence of gene fusions such as PML::RARA, CBFβ::MYH11, and RUNX1::RUNX1T1, among others. Gene fusions are the main molecular biological abnormalities in acute leukemia, and all fusion genes act as crucial oncogenic factors in leukemia. Herein, we report the first case of LYN::LINC01900 fusion transcript in AML with a promyelocytic phenotype and TP53 mutation. Further studies should address whether new protein products may result from this fusion, as well as the biological function of these new products in disease occurrence and progression. |
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institution | Directory Open Access Journal |
issn | 2234-943X |
language | English |
last_indexed | 2024-03-09T10:42:15Z |
publishDate | 2023-12-01 |
publisher | Frontiers Media S.A. |
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series | Frontiers in Oncology |
spelling | doaj.art-18da46bc10894d3eae5c15cf9b7a2a8d2023-12-01T13:23:38ZengFrontiers Media S.A.Frontiers in Oncology2234-943X2023-12-011310.3389/fonc.2023.13224031322403Case Report: Identification of a novel LYN::LINC01900 transcript with promyelocytic phenotype and TP53 mutation in acute myeloid leukemiaChengjun Hu0Qiuxin Dai1Ruiyi Zhang2Huanping Yang3Man Wang4Kaili Gu5Jiangang Yang6Wenjun Meng7Ping Chen8Maozhong Xu9Department of Hematology, The Affiliated Jiangyin Hospital of Southeast University Medical College, Jiangyin, Jiangsu, ChinaDepartment of Hematology, The Affiliated Jiangyin Hospital of Southeast University Medical College, Jiangyin, Jiangsu, ChinaSuzhou Jsuniwell Medical Laboratory, Suzhou, ChinaSuzhou Jsuniwell Medical Laboratory, Suzhou, ChinaJiangsu Institute of Hematology, National Clinical Research Center for Hematologic Diseases, NHC Key Laboratory of Thrombosis and Hemostasis, The First Affiliated Hospital of Soochow University, Suzhou, ChinaSuzhou Jsuniwell Medical Laboratory, Suzhou, ChinaDepartment of Hematology, The Affiliated Jiangyin Hospital of Southeast University Medical College, Jiangyin, Jiangsu, ChinaDepartment of Hematology, The Affiliated Jiangyin Hospital of Southeast University Medical College, Jiangyin, Jiangsu, ChinaSuzhou Jsuniwell Medical Laboratory, Suzhou, ChinaDepartment of Hematology, The Affiliated Jiangyin Hospital of Southeast University Medical College, Jiangyin, Jiangsu, ChinaAcute myeloid leukemia (AML) is a malignant disease of myeloid hematopoietic stem/progenitor cells characterized by the abnormal proliferation of primitive and naive random cells in the bone marrow and peripheral blood. Acute promyelocytic leukemia (APL) is a type (AML-M3) of AML. Most patients with APL have the characteristic chromosomal translocation t(15; 17)(q22; q12), forming PML::RARA fusion. The occurrence and progression of AML are often accompanied by the emergence of gene fusions such as PML::RARA, CBFβ::MYH11, and RUNX1::RUNX1T1, among others. Gene fusions are the main molecular biological abnormalities in acute leukemia, and all fusion genes act as crucial oncogenic factors in leukemia. Herein, we report the first case of LYN::LINC01900 fusion transcript in AML with a promyelocytic phenotype and TP53 mutation. Further studies should address whether new protein products may result from this fusion, as well as the biological function of these new products in disease occurrence and progression.https://www.frontiersin.org/articles/10.3389/fonc.2023.1322403/fullacute myeloid leukemiaLYN::LINC01900promyelocytic phenotypelncRNA fusionmutation |
spellingShingle | Chengjun Hu Qiuxin Dai Ruiyi Zhang Huanping Yang Man Wang Kaili Gu Jiangang Yang Wenjun Meng Ping Chen Maozhong Xu Case Report: Identification of a novel LYN::LINC01900 transcript with promyelocytic phenotype and TP53 mutation in acute myeloid leukemia Frontiers in Oncology acute myeloid leukemia LYN::LINC01900 promyelocytic phenotype lncRNA fusion mutation |
title | Case Report: Identification of a novel LYN::LINC01900 transcript with promyelocytic phenotype and TP53 mutation in acute myeloid leukemia |
title_full | Case Report: Identification of a novel LYN::LINC01900 transcript with promyelocytic phenotype and TP53 mutation in acute myeloid leukemia |
title_fullStr | Case Report: Identification of a novel LYN::LINC01900 transcript with promyelocytic phenotype and TP53 mutation in acute myeloid leukemia |
title_full_unstemmed | Case Report: Identification of a novel LYN::LINC01900 transcript with promyelocytic phenotype and TP53 mutation in acute myeloid leukemia |
title_short | Case Report: Identification of a novel LYN::LINC01900 transcript with promyelocytic phenotype and TP53 mutation in acute myeloid leukemia |
title_sort | case report identification of a novel lyn linc01900 transcript with promyelocytic phenotype and tp53 mutation in acute myeloid leukemia |
topic | acute myeloid leukemia LYN::LINC01900 promyelocytic phenotype lncRNA fusion mutation |
url | https://www.frontiersin.org/articles/10.3389/fonc.2023.1322403/full |
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