2022-01-122022-01-122009Gülten, T. vd. (2009). "AML1 amplification and 17q25 deletion in a case of childhood acute lymphoblastic leukemia". Journal of Clinical Laboratory Analysis, 23(6), 368-371.0887-8013https://doi.org/10.1002/jcla.20343https://onlinelibrary.wiley.com/doi/10.1002/jcla.20343http://hdl.handle.net/11452/24045We report a case of childhood acute lymphoblastic leukemia (ALL) with both acute myeloid leukemia 1 (AML1) amplification and 17q25 deletion. AML1 gene is located on 21q22 and encodes a transcription factor. AML1 amplification is a common finding in childhood ALL, and itis observed as an increase in gene copy number by the FISH analysis. The mechanism of AML1 amplification is not associated with AML1 gene mutations. The 17q25 is a gene-rich chromosomal location and distinct abnormalities of this region have been observed in previous cases of different kinds of leukemia. Deletion of the 17q25 region has been reported in two leukemia patients. Septin 9 (SEPT9) and survivin genes are located on 17q25. High expression of these genes and AML1 amplification are regarded as markers in tumorigenesis and disease progression; however, more data are needed for accurate prognostic evaluation.eninfo:eu-repo/semantics/openAccess17q25AberrationAcute lymphoblastic leukemiaAML1 amplificationSEPT9AbnormalitiesGenesMedical laboratory technologyAdolescentChromosome deletionChromosomes, human, pair 17Core binding factor alpha 2 subunitFemaleGene amplificationHumansIn situ hybridization, fluorescenceKaryotypingMetaphasePrecursor cell lymphoblastic leukemia-lymphomaArticle0002726726000042-s2.0-7324914484936837123619927343Medical laboratory technologyAcute Lymphoblastic Leukemia; Chromosome 21; Pre B LymphocyteTranscription factorAcute lymphoblastic leukemiaAdolescentArticleCancer patientCarcinogenesisCase reportChromosome 17qChromosome deletionDisease courseFemaleGene amplificationGene expressionHuman