Utations can induce the resistance and poor prognosis of myeloid neoplasms.15 The role of SETBP1 nonhotspot mutations is at the moment elusive, such as what occurred with SETBP1 N272D in our case. As well as SETBP1 mutations, a nonreceptor tyrosine kinase JAK3 mutation is identified because the secondary mutation in juvenile myelomonocytic leukemia (JMML), whereas the latter is involved not in the initiation but the progression of JMML, thus indicating a poor prognosis.16 JAK3 mutation is a driver mutation frequently reported in T lineage acute lymphoblastic leukemia. Recurrent JAK3 V722I is reported in malignant struma ovarii, that is a certain ovarian teratoma.17 Constant with JAK3 V722I, the mutation web-site of JAK3 I688F is situated inside the same protein domain (protein kinase 1), as a result potentially harboring a equivalent function. When relating to the case, we propose the following hypothesis. Initial, the mutation burden brought on by chemotherapies with platinum-based drugs and radiotherapy in the major solid tumor influences the evolution of hematopoietic cells and further progression to secondary leukemia. Second, the leukemic situations originating from a PM-GCTs progenitor cell are capable of undergoing hematopoietic differentiation into the subsequent hematological malignancy, which is constant with an earlier study.18 Lastly, a competing hypothesis is the fact that there’s a shared precursor in the germ cell lineage harboring the p53 pathway alteration for the principal malignant GCT plus the secondary MCL, and also the latter is steadily created within the setting of additional “driver mutations”, which can be supported by the most recent proof.7 Future research to explore the potential germline genetic predisposition for the development of hematologic neoplasms within the setting of PM-GCTs are potential. There had been some defects within this case.Sorcin/SRI Protein Species First, on account of clinical laboratory limitations, the concentration of serum tryptase was not examined to investigate the correlation amongst tryptase expression and leukemic improvement.IL-21 Protein Molecular Weight In addition, the patient’s relatives refused to execute gene sequencing, and specimens within the period of PM-GCTs have been also not examined for genetic alterations.PMID:23819239 Therefore, it can be tricky to figure out no matter whether these gene mutations are germline or somatic.ConclusionIn this case, acute MCL preceded by malignant mediastinal GCT had related clinical symptoms and morphological manifestations but distinctly diverse genetic profiles than principal MCL. The characteristic morphology of MCL delivers probably the most pivotal proof that led our diagnosis in the right direction. A competing hypothesis is the fact that there’s a popular embryonal cancer stem cell involving the PM-GCTs along with the secondary MCL, plus the latter is progressively created inside the setting of added “driver mutations”. Future research to explore the possible germline genetic predisposition for the improvement of hematologic neoplasms within the setting of PM-GCTs are prospective.doi.org/10.2147/CMAR.SCancer Management and Investigation 2022:DovePressPowered by TCPDF (tcpdf.org)DovepressWang et alAbbreviationsMCL, Mast cell leukemia; MCs, Mast cells; SM, Systemic mastocytosis; GCT, Germ cell tumor; AML, Acute myeloid leukemia; PBMCs, Peripheral blood mononuclear cells; PCR, Polymerase chain reaction; LDH, Lactate dehydrogenase; PET/CT, Positron emission tomography/computed tomography; NSE, Nonspecific esterase; POX, Peroxidase; NASDCE, Naphthol AS-D chloroacetate esterase staining; PM-GCTs, Key mediastinal GCTs;.