Acute monocytic leukemia with KMT2A::LASP1 developed 9 months after diagnosis of acute megakaryoblastic leukemia in a 2-year-old boy.
Child, Preschool
Humans
Male
Adaptor Proteins, Signal Transducing
Cytoskeletal Proteins
Leukemia, Megakaryoblastic, Acute
/ diagnosis
Leukemia, Monocytic, Acute
/ diagnosis
LIM Domain Proteins
Recurrence
Remission Induction
Retrospective Studies
Histone-Lysine N-Methyltransferase
/ genetics
Oncogene Proteins, Fusion
/ genetics
Acute megakaryoblastic leukemia
Acute monocytic leukemia
Second primary cancer
Subsequent leukemia
Therapy-related leukemia
Journal
International journal of hematology
ISSN: 1865-3774
Titre abrégé: Int J Hematol
Pays: Japan
ID NLM: 9111627
Informations de publication
Date de publication:
Oct 2023
Oct 2023
Historique:
received:
30
01
2023
accepted:
24
05
2023
revised:
23
05
2023
medline:
23
10
2023
pubmed:
14
6
2023
entrez:
14
6
2023
Statut:
ppublish
Résumé
Acute myeloid leukemia (AML) is known as one of the subsequent malignant neoplasms that can develop after cancer treatment, but it is difficult to distinguish from relapse when the preceding cancer is leukemia. We report a 2-year-old boy who developed acute megakaryoblastic leukemia (AMKL, French-American-British classification [FAB]: M7) at 18 months of age and achieved complete remission with multi-agent chemotherapy without hematopoietic stem cell transplantation. Nine months after diagnosis and 4 months after completing treatment for AMKL, he developed acute monocytic leukemia (AMoL) with the KMT2A::LASP1 chimeric gene (FAB: M5b). The second complete remission was achieved using multi-agent chemotherapy and he underwent cord blood transplantation 4 months after AMoL was diagnosed. He is currently alive and disease free at 39 and 48 months since his AMoL and AMKL diagnoses, respectively. Retrospective analysis revealed that the KMT2A::LASP1 chimeric gene was detected 4 months after diagnosis of AMKL. Common somatic mutations were not detected in AMKL or AMoL and no germline pathogenic variants were detected. Since the patient's AMoL was different from his primary leukemia of AMKL in terms of morphological, genomic, and molecular analysis, we concluded that he developed a subsequent leukemia rather than a relapse of his primary leukemia.
Identifiants
pubmed: 37314622
doi: 10.1007/s12185-023-03622-x
pii: 10.1007/s12185-023-03622-x
doi:
Substances chimiques
Adaptor Proteins, Signal Transducing
0
Cytoskeletal Proteins
0
LASP1 protein, human
0
LIM Domain Proteins
0
KMT2A protein, human
0
Histone-Lysine N-Methyltransferase
EC 2.1.1.43
Oncogene Proteins, Fusion
0
Types de publication
Case Reports
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
514-518Informations de copyright
© 2023. Japanese Society of Hematology.
Références
Quessada J, Cuccuini W, Saultier P, Loosveld M, Harrison CJ, Lafage-Pochitaloff M. Cytogenetics of pediatric acute myeloid leukemia: a review of the current knowledge. Genes (Basel). 2021;12(6):924.
doi: 10.3390/genes12060924
pubmed: 34204358
Athale UH, Razzouk BI, Raimondi SC, Tong X, Behm FG, Head DR, et al. Biology and outcome of childhood acute megakaryoblastic leukemia: a single institution’s experience. Blood. 2001;97(12):3727–32.
doi: 10.1182/blood.V97.12.3727
pubmed: 11389009
Shiba N, Ohki K, Kobayashi T, Hara Y, Yamato G, Tanoshima R, et al. High PRDM 16 expression identifies a prognostic subgroup of pediatric acute myeloid leukaemia correlated to FLT3-ITD, KMT2A-PTD, and NUP98-NSD1: the results of the Japanese Paediatric Leukaemia/Lymphoma Study Group AML-05 trial. Br J Haematol. 2016;172(4):581–91.
doi: 10.1111/bjh.13869
pubmed: 26684393
de Rooij JD, Riccardo M, van den Heuvel-Eibrink MM, Cayuela JM, Trka J, Reinhardt D, et al. Recurrent abnormalities can be used for risk group stratification in pediatric AMKL: a retrospective intergroup study. Blood. 2016;127(26):3424–30.
doi: 10.1182/blood-2016-01-695551
pubmed: 27114462
Ishida Y, Qiu D, Maeda M, Fujimoto J, Kigasawa H, Kobayashi R, et al. Secondary cancers after a childhood cancer diagnosis: a nationwide hospital-based retrospective cohort study in Japan. Int J Clin Oncol. 2016;21(3):506–16.
doi: 10.1007/s10147-015-0927-z
pubmed: 26620038
Larson RA. Etiology and management of therapy-related myeloid leukemia. Hematol Am Soc Hematol Educ Program. 2007;2007:453–9.
doi: 10.1182/asheducation-2007.1.453
Sandler ES, Friedman DJ, Mustafa MM, Winick NJ, Bowman WP, Buchanan GR. Treatment of children with epipodophyllotoxin-induced secondary acute myeloid leukemia. Cancer. 1997;79(5):1049–54.
doi: 10.1002/(SICI)1097-0142(19970301)79:5<1049::AID-CNCR24>3.0.CO;2-0
pubmed: 9041170
Hijiya N, Ness KK, Ribeiro RC, Hudson MM. Acute leukemia as a secondary malignancy in children and adolescents: current findings and issues. Cancer. 2009;115(1):23–35.
doi: 10.1002/cncr.23988
pubmed: 19072983
Bhatia S, Krailo MD, Chen Z, Burden L, Askin FB, Dickman PS, et al. Therapy-related myelodysplasia and acute myeloid leukemia after Ewing sarcoma and primitive neuroectodermal tumor of bone: a report from the Children’s Oncology Group. Blood. 2007;109(1):46–51.
doi: 10.1182/blood-2006-01-023101
pubmed: 16985182
pmcid: 1785079
Bhatia S, Robison LL, Oberlin O, Greenberg M, Bunin G, Fossati-Bellani F, Meadows AT. Breast cancer and other second neoplasms after childhood Hodgkin’s disease. N Engl J Med. 1996;334(12):745–51.
doi: 10.1056/NEJM199603213341201
pubmed: 8592547
Tomizawa D, Tawa A, Watanabe T, Saito AM, Kudo K, Taga T, et al. Excess treatment reduction including anthracyclines results in higher incidence of relapse in core binding factor acute myeloid leukemia in children. Leukemia. 2013;27(12):2413–6.
doi: 10.1038/leu.2013.153
pubmed: 23677335
Yamazaki-Suda A, Fukushima H, Suzuki R, Yamaki Y, Takada H. Severe adenovirus type F enteritis in a young child with acute myeloid leukemia. Pediatr Int. 2021;63(5):604–6. https://doi.org/10.1111/ped.14461 .
doi: 10.1111/ped.14461
pubmed: 34002473
West AH, Godley LA, Churpek JE. Familial myelodysplastic syndrome/acute leukemia syndromes: a review and utility for translational investigations. Ann NY Acad Sci. 2014;1310(1):111–8.
doi: 10.1111/nyas.12346
pubmed: 24467820
Labuhn M, Perkins K, Matzk S, Varghese L, Garnett C, Papaemmanuil E, et al. Mechanisms of progression of myeloid preleukemia to transformed myeloid leukemia in children with down syndrome. Cancer Cell. 2019;36(2):123–38.
doi: 10.1016/j.ccell.2019.06.007
pubmed: 31303423
pmcid: 6863161
Fukuhara S, Oshikawa-Kumade Y, Kogure Y, Shingaki S, Kariyazono H, Kikukawa Y, et al. Feasibility and clinical utility of comprehensive genomic profiling of hematological malignancies. Cancer Sci. 2022;113(8):2763–77.
doi: 10.1111/cas.15427
pubmed: 35579198
pmcid: 9357666
Mascarenhas J, Mughal TI, Verstovsek S. Biology and clinical management of myeloproliferative neoplasms and development of the JAK inhibitor ruxolitinib. Curr Med Chem. 2012;19(26):4399–413.
doi: 10.2174/092986712803251511
pubmed: 22830345
pmcid: 3480698
Wong SJ, Senkovich O, Artigas JA, Gearhart MD, Ilangovan U, Graham DW, et al. Structure and role of BCOR PUFD in noncanonical PRC1 assembly and disease. Biochemistry. 2020;59(29):2718–28.
doi: 10.1021/acs.biochem.0c00285
pubmed: 32628469
Kurotaki N, Harada N, Yoshiura K, Sugano S, Niikawa N, Matsumoto N. Molecular characterization of NSD1, a human homologue of the mouse Nsd1 gene. Gene. 2001;279(2):197–204.
doi: 10.1016/S0378-1119(01)00750-8
pubmed: 11733144
Dolnik A, Engelmann JC, Scharfenberger-Schmeer M, Kelkenberg-Schade S, Haldemann B, Fries T, et al. Commonly altered genomic regions in acute myeloid leukemia are enriched for somatic mutations involved in chromatin remodeling and splicing. Blood. 2012;120(18):e83–92.
doi: 10.1182/blood-2011-12-401471
pubmed: 22976956
Blanco JG, Dervieux T, Edick MJ, Mehta MK, Rubnitz JE, Shurtleff S, et al. Molecular emergence of acute myeloid leukemia during treatment for acute lymphoblastic leukemia. Proc Natl Acad Sci USA. 2001;98(18):10338–43.
doi: 10.1073/pnas.181199898
pubmed: 11526240
pmcid: 56962
Balgobind BV, Hollink IH, Arentsen-Peters ST, Zimmermann M, Harbott J, Beverloo HB, et al. Integrative analysis of type-I and type-II aberrations underscores the genetic heterogeneity of pediatric acute myeloid leukemia. Haematologica. 2011;96(10):1478–87.
doi: 10.3324/haematol.2010.038976
pubmed: 21791472
pmcid: 3186309
Smith SM, Le Beau MM, Huo D, Karrison D, Sobecks RM, Anastasi J, et al. Clinical-cytogenetic associations in 306 patients with therapy-related myelodysplasia and myeloid leukemia: the University of Chicago series. Blood. 2003;102(1):43–52.
doi: 10.1182/blood-2002-11-3343
pubmed: 12623843
Strehl S, Konig M, Meyer C, Schneider B, Harbott J, Jager U, et al. Molecular dissection of t(11;17) in acute myeloid leukemia reveals a variety of gene fusions with heterogeneous fusion transcripts and multiple splice variants. Genes Chromos Cancer. 2006;45(11):1041–9.
doi: 10.1002/gcc.20372
pubmed: 16897742