{"title":"Lineage switch in B-lineage Acute Lymphoblastic Leukemia at relapse: a report","authors":"Hershavardhini K , Likhitha Bhukya , Abhilasha S","doi":"10.1016/j.phoj.2025.100461","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>Lineage switch is an uncommon phenomenon at time of relapse and the mechanisms by which this occurs are unclear, but may represent an expanded pre-therapy sub-clone, clonal evolution of the original leukemia, or development of a new clone that may be therapy-related. Here we present two cases which explains the etiology of lineage switch being therapy-related clonal selection.</div></div><div><h3>Case report</h3><div>Case 1: A 9-year-old male child treated for pre-B ALL at our centre on chemotherapy relapsed with AML in the 8th cycle of the maintenance phase. Case 2: A 6-year-old female diagnosed with pre-B ALL relapsed with AML in the 5th cycle of maintenance therapy. Both of these cases at time of relapse also showed a <em>TP53</em> gene mutation, confirmed by next generation sequencing.</div></div><div><h3>Conclusion</h3><div>In this report, we have reported a lineage switch in two patients at time of relapse of pre-B ALL, in association with <em>T</em><em>P53</em> mutation with a poor outcome.</div></div>","PeriodicalId":101004,"journal":{"name":"Pediatric Hematology Oncology Journal","volume":"10 3","pages":"Article 100461"},"PeriodicalIF":0.0000,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pediatric Hematology Oncology Journal","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2468124525000294","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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Abstract
Background
Lineage switch is an uncommon phenomenon at time of relapse and the mechanisms by which this occurs are unclear, but may represent an expanded pre-therapy sub-clone, clonal evolution of the original leukemia, or development of a new clone that may be therapy-related. Here we present two cases which explains the etiology of lineage switch being therapy-related clonal selection.
Case report
Case 1: A 9-year-old male child treated for pre-B ALL at our centre on chemotherapy relapsed with AML in the 8th cycle of the maintenance phase. Case 2: A 6-year-old female diagnosed with pre-B ALL relapsed with AML in the 5th cycle of maintenance therapy. Both of these cases at time of relapse also showed a TP53 gene mutation, confirmed by next generation sequencing.
Conclusion
In this report, we have reported a lineage switch in two patients at time of relapse of pre-B ALL, in association with TP53 mutation with a poor outcome.
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