Diagnosed AMLs were morphologically classified according to the French-American-British (FAB) Classification (FAB Subtypes).
Although the median age for AML in adult is documented as 65 years, our study found that it to be 69.5 years, with an age range of 1- to 93 years. No association with aberrant expression was detected based on age or gender.
Among the 26 acute myeloid leukaemia patients, only 15 cases (57.2%) had the conventional CD antigen expressions of myeloid lineage – specific markers. Other 11 cases (42.3%) were AML with aberrant expression of CD markers.
cyCD3 showed aberrancy in (54.5%) of aberrant AML cases, CD7 in (45.4%), smCD3 in (9.0%), Co expression of B lymphoid markers with myeloid markers occurred in 0% in our study.
Co expression of T lymphoid markers (CD7, smCD3) with myeloid markers occurred in 23.0% cases in our study. CD13 was not expressed in 1 case out of 5 AML- M4 cases and 1 case out of 7 AML- M1. CD33 was not expressed in 1 case out of 2 AML -M0 cases.
Author(s) Details:
- C. Kariyawasan
Department of Hematology, Sri Jayewardenepura General Hospital, Sri Lanka. - L. T. Balasuriya
Department of Hematology, Sri Jayewardenepura General Hospital, Sri Lanka. - A. C. D. Ranatunga
Department of Hematology, Sri Jayewardenepura General Hospital, Sri Lanka.
Recent Global Research Developments in Aberrant Phenotype in Acute Myeloid Leukemia
Single-Cell RNA Sequencing and CAR-T Therapy: Recent advancements have highlighted the use of single-cell RNA sequencing (scRNA-seq) and CAR-T cell therapy to dissect cancer heterogeneity and tailor treatments for AML. This approach allows for a more personalized diagnosis and treatment by identifying underrepresented cellular subclones or clones resistant to therapeutic approaches [1].
Targeted Therapies: There have been significant strides in targeted therapies for AML, particularly in the last decade. Advances in molecular profiling have led to a deeper understanding of AML’s pathobiology and therapeutic vulnerabilities. This includes the development of low-intensity induction therapies and targeted oral therapies against driver mutations [2].
Integrative Genomic Analysis: Research has also focused on the integrative genomic analysis of pediatric myeloid-related acute leukemias, revealing varying immunophenotypes and the impact of mutational composition on survival outcomes [3] .
Epigenetic Dysregulation: Studies have demonstrated the critical role of epigenetic dysregulation in AML pathogenesis. Aberrant DNA methylation patterns have been identified as key factors in the disease’s development and progression [4,5] .
References
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- Bhansali, R.S., Pratz, K.W. & Lai, C. Recent advances in targeted therapies in acute myeloid leukemia. J Hematol Oncol 16, 29 (2023). https://doi.org/10.1186/s13045-023-01424-6
- Fornerod, M., Ma, J., Noort, S., Liu, Y., Walsh, M. P., Shi, L., … & Gruber, T. A. (2021). Integrative genomic analysis of pediatric myeloid-related acute leukemias identifies novel subtypes and prognostic indicators. Blood cancer discovery, 2(6), 586-599.
- Yang, X., Wong, M. P. M., & Ng, R. K. (2019). Aberrant DNA methylation in acute myeloid leukemia and its clinical implications. International journal of molecular sciences, 20(18), 4576.
- He, S., Zhou, J. & Yu, L. Aberrant DNA methylation in t(8;21) acute myeloid leukemia. GENOME INSTAB. DIS. 3, 209–216 (2022). https://doi.org/10.1007/s42764-022-00074-1