{"title":"MYC-r with a non-IG partner concurrently with a cryptic t(12;21) in B-lymphoblastic leukemia: A case and prognostic significance","authors":"Prasad Koduru , Weina Chen , Franklin Fuda , Martha Pacheco , Rolando Garcia","doi":"10.1016/j.cancergen.2025.01.008","DOIUrl":null,"url":null,"abstract":"<div><div>B-lymphoblastic leukemia (B-ALL) in children is characterized by recurrent chromosomal rearrangements that mostly have prognostic value. <em>MYC</em> rearrangements (<em>MYC</em>-r), typically associated with Burkitt lymphoma or mature B-cell neoplasms are infrequent in B-ALL. We report here a unique case of childhood B-ALL with concurrent <em>MYC</em>-r with a non-<em>IG</em> partner and a cryptic t(12;21). Leukemic cells had lymphoblastic morphology. Immunophenotypically, leukemic blasts were CD10 (+, slightly bright), CD15 (few +), CD19 (+), CD20 (+, partial), CD22 (+), CD34 (-), CD38 (+, slightly variably), CD45 (+, partial), cytoplasmic CD79a (+), HLA-DR (+), surface Ig (-), MPO (-), and TdT (+, partially). This immunophenotype was consistent with B-ALL. Cytogenetically, the karyotype was complex including a t(4;8)(q31;q24), and FISH analysis showed <em>MYC</em>-r, <em>ETV6</em>::<em>RUNX1</em> and loss of <em>ETV6</em> allele. The patient has been in complete remission for 11 years following the diagnosis. We reviewed cases of B-ALL with double leukemogenic alterations and <em>MYC</em>-r with non-<em>IG</em> partners to understand the clinical outcome in these rare patients.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"292 ","pages":"Pages 85-91"},"PeriodicalIF":1.4000,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer Genetics","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S221077622500016X","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
引用次数: 0
Abstract
B-lymphoblastic leukemia (B-ALL) in children is characterized by recurrent chromosomal rearrangements that mostly have prognostic value. MYC rearrangements (MYC-r), typically associated with Burkitt lymphoma or mature B-cell neoplasms are infrequent in B-ALL. We report here a unique case of childhood B-ALL with concurrent MYC-r with a non-IG partner and a cryptic t(12;21). Leukemic cells had lymphoblastic morphology. Immunophenotypically, leukemic blasts were CD10 (+, slightly bright), CD15 (few +), CD19 (+), CD20 (+, partial), CD22 (+), CD34 (-), CD38 (+, slightly variably), CD45 (+, partial), cytoplasmic CD79a (+), HLA-DR (+), surface Ig (-), MPO (-), and TdT (+, partially). This immunophenotype was consistent with B-ALL. Cytogenetically, the karyotype was complex including a t(4;8)(q31;q24), and FISH analysis showed MYC-r, ETV6::RUNX1 and loss of ETV6 allele. The patient has been in complete remission for 11 years following the diagnosis. We reviewed cases of B-ALL with double leukemogenic alterations and MYC-r with non-IG partners to understand the clinical outcome in these rare patients.
期刊介绍:
The aim of Cancer Genetics is to publish high quality scientific papers on the cellular, genetic and molecular aspects of cancer, including cancer predisposition and clinical diagnostic applications. Specific areas of interest include descriptions of new chromosomal, molecular or epigenetic alterations in benign and malignant diseases; novel laboratory approaches for identification and characterization of chromosomal rearrangements or genomic alterations in cancer cells; correlation of genetic changes with pathology and clinical presentation; and the molecular genetics of cancer predisposition. To reach a basic science and clinical multidisciplinary audience, we welcome original full-length articles, reviews, meeting summaries, brief reports, and letters to the editor.