Case Report
Copyright ©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Cases. Aug 26, 2023; 11(24): 5780-5788
Published online Aug 26, 2023. doi: 10.12998/wjcc.v11.i24.5780
Focal lymphoblastic transformation of chronic myelogenous leukemia develops into erythroid leukemia: A case report
Wei Wang, Ya-Ling Chen, Pan-Pan Gou, Pei-Lin Wu, Kun-Sheng Shan, Dong-Liang Zhang
Wei Wang, Ya-Ling Chen, Pan-Pan Gou, Kun-Sheng Shan, Dong-Liang Zhang, Department of Hematology, The 909th Hospital of PLA (Southeast Hospital Affiliated to Xiamen University), Zhangzhou 363000, Fujian Province, China
Pei-Lin Wu, Department of Hematology, The 175th Hospital of PLA (Southeast Hospital Affiliated to Xiamen University), Zhangzhou 363000, Fujian Province, China
Author contributions: Wang W contributed to the design of the report and drafted the manuscript; Chen YL and Shan KS treated the patient; Gou PP, Wu PL, and Zhang DL revised the manuscript; and all the authors have read and approved the final version of the manuscript.
Supported by Nanjing Military Region Innovation Project, No. 15MS108; and the Youth Nursery Fund, No. 18Y024.
Informed consent statement: Written informed consent was obtained from the patient for the publication of this case report and any accompanying images.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
CARE Checklist (2016) statement: The authors have read the CARE Checklist (2016), and the manuscript was prepared and revised according to the CARE Checklist (2016).
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Wei Wang, PhD, Chief Physician, Doctor, Department of Hematology, The 909th Hospital of PLA (Southeast Hospital Affiliated to Xiamen University), Zhanghua Street of Xiangcheng District, Zhangzhou 363000, Fujian Province, China. wangwei220012@163.com
Received: May 19, 2023
Peer-review started: May 19, 2023
First decision: June 13, 2023
Revised: July 3, 2023
Accepted: July 24, 2023
Article in press: July 24, 2023
Published online: August 26, 2023
Processing time: 97 Days and 21.5 Hours
Abstract
BACKGROUND

We present a case of focal lymphoblastic transformation to erythroid leukemia following acute myeloblastic transformation in a patient with chronic myelogenous leukemia (CML) and discuss its mechanism of occurrence and development.

CASE SUMMARY

The presence of the Philadelphia (Ph) chromosome was identified through karyotype analysis, while the BCR-ABL fusion gene was detected using quantitative real-time polymerase chain reaction of the peripheral blood sample. Fluorescence in situ hybridization was used to detect the expression of the BCR-ABL gene in the lymphoma. Antigen expression and gene mutations in the primitive cells were detected by flow cytometry. The analysis confirmed the presence of CML along with focal lymphoblastic transformation to erythroid leukemia. Additionally, the patient was found to have secondary erythroid leukemia, along with multiple new gene mutations and abnormalities in complex karyotypes of chromosomes.

CONCLUSION

Our findings suggest a possible molecular basis for the focal lymphoblastic transformation secondary to myeloblastic transformation in patients with CML.

Keywords: Chronic myelogenous leukemia; Blast crisis; Focal lymphoblastic transformation; Pure erythroid leukemia; Case report

Core Tip: A case of focal lymphoblastic transformation into erythroid leukemia following acute myeloblastic transformation in a chronic myelogenous leukemia patient is presented, and the mechanism of its occurrence and development is discussed. Multiple new gene mutations and abnormalities in complex karyotypes of chromosomes were found to be the major reason.