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A Rare Episode of Extensive Bone Marrow Necrosis in a Chemotherapy-naïve Patient with Multiple Myeloma Exhibiting TP53 and TET2 Mutations.
Jeon, Kibum; Kim, Hyo Jung; Kim, Miyoung; Lee, Young Kyung.
Afiliação
  • Jeon K; Department of Laboratory Medicine, Hallym University Sacred Heart Hospital, Anyang, Korea.
  • Kim HJ; Department of Internal Medicine, Hallym University Sacred Heart Hospital, Anyang, Korea.
  • Kim M; Department of Laboratory Medicine, Hallym University Sacred Heart Hospital, Anyang, Korea rabbit790622@gmail.com.
  • Lee YK; Department of Laboratory Medicine, Hallym University Sacred Heart Hospital, Anyang, Korea.
Ann Clin Lab Sci ; 50(1): 136-139, 2020 Jan.
Article em En | MEDLINE | ID: mdl-32161023
ABSTRACT
Bone marrow necrosis (BMN) is a rare life-threatening condition in which the marrow is replaced by necrotic material. Half of BMN occurrences are attributed to chemotherapy or granulocyte-colony stimulating factor treatment in patients with hematolymphoid malignancies. However, we present a patient diagnosed with both multiple myeloma and extensive BMN despite being treatment-naïve. Our patient exhibited a TP53 deletion, TET2 frameshift mutation, and a single TET2 nucleotide change. He is the third such patient reported, but the first to have his cytogenetic and molecular genetic profiles investigated using conventional cytogenetics, fluorescence in situ hybridization, and next-generation sequencing.
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Base de dados: MEDLINE Assunto principal: Doenças da Medula Óssea / Protocolos de Quimioterapia Combinada Antineoplásica / Proteína Supressora de Tumor p53 / Proteínas Proto-Oncogênicas / Proteínas de Ligação a DNA / Mieloma Múltiplo / Mutação Idioma: En Ano de publicação: 2020 Tipo de documento: Article
Buscar no Google
Base de dados: MEDLINE Assunto principal: Doenças da Medula Óssea / Protocolos de Quimioterapia Combinada Antineoplásica / Proteína Supressora de Tumor p53 / Proteínas Proto-Oncogênicas / Proteínas de Ligação a DNA / Mieloma Múltiplo / Mutação Idioma: En Ano de publicação: 2020 Tipo de documento: Article