Acute Myeloid Leukemia in Pediatric Patients: A Review About Current Diagnostic and Treatment Approaches

Derwich, Katarzyna; Mitkowski, Dorothy; J, Sadowska

doi:10.5772/intechopen.70937

“…Acute leukemias also occur when a hematopoietic stem cell acquires a sequence of mutations that confer an advantage of clonal proliferation (43, 48–52). The incidence of AML increases with age and represents 80% of adult leukemia (53) and 15–20% of childhood acute leukemiac (54). Congenital leukemia is a rare disease that is acquired in the neonatal period (45).…”

Section: Cytogenetics In the Clinic For Myeloid Malignanciesmentioning

confidence: 99%

Long Non-coding RNAs in Myeloid Malignancies

Zimța

¹

,

Tomuleasa

²

,

Sahnoune

³

et al. 2019

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Acute myeloid leukemia (AML) represents 80% of adult leukemias and 15–20% of childhood leukemias. AML are characterized by the presence of 20% blasts or more in the bone marrow, or defining cytogenetic abnormalities. Laboratory diagnoses of myelodysplastic syndromes (MDS) depend on morphological changes based on dysplasia in peripheral blood and bone marrow, including peripheral blood smears, bone marrow aspirate smears, and bone marrow biopsies. As leukemic cells are not functional, the patient develops anemia, neutropenia, and thrombocytopenia, leading to fatigue, recurrent infections, and hemorrhage. The genetic background and associated mutations in AML blasts determine the clinical course of the disease. Over the last decade, non-coding RNAs transcripts that do not codify for proteins but play a role in regulation of functions have been shown to have multiple applications in the diagnosis, prognosis and therapeutic approach of various types of cancers, including myeloid malignancies. After a comprehensive review of current literature, we found reports of multiple long non-coding RNAs (lncRNAs) that can differentiate between AML types and how their exogenous modulation can dramatically change the behavior of AML cells. These lncRNAs include: H19, LINC00877, RP11-84C10, CRINDE, RP11848P1.3, ZNF667-AS1, AC111000.4-202, SFMBT2, LINC02082-201, MEG3, AC009495.2, PVT1, HOTTIP, SNHG5, and CCAT1. In addition, by performing an analysis on available AML data in The Cancer Genome Atlas (TCGA), we found 10 lncRNAs with significantly differential expression between patients in favorable, intermediate/normal, or poor cytogenetic risk categories. These are: DANCR, PRDM16-DT, SNHG6, OIP5-AS1, SNHG16, JPX, FTX, KCNQ1OT1, TP73-AS1, and GAS5. The identification of a molecular signature based on lncRNAs has the potential for have deep clinical significance, as it could potentially help better define the evolution from low-grade MDS to high-grade MDS to AML, changing the course of therapy. This would allow clinicians to provide a more personalized, patient-tailored therapeutic approach, moving from transfusion-based therapy, as is the case for low-grade MDS, to the introduction of azacytidine-based chemotherapy or allogeneic stem cell transplantation, which is the current treatment for high-grade MDS.

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“…The most common genetic factor for its development is trisomy 21. 12 By the age of 70, about 10% of presumably normal individuals have clonal mutations in hematopoietic cells.…”

Section: Etiologymentioning

confidence: 99%

Consenso de leucemia mieloide aguda en México

Arana-Luna¹,

Alvarado-Ibarra²,

Silva-Michel³

et al. 2023

GMM

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Acute myeloid leukemia (AML) comprises a heterogeneous group of hematopoietic cell neoplasms of myeloid lineage that arise from the clonal expansion of their precursors in the bone marrow, interfering with cell differentiation, leading to a syndrome of bone marrow failure. AML is a consequence of genetic and epigenetic changes (point mutations, gene rearrangements, deletions, amplifications, and arrangements in epigenetic changes that influence gene expression) in hematopoietic precursor cells, which create a clone of abnormal cells that are capable of proliferating but cannot differentiate into mature hematopoietic cells or undergo programmed cell death. The diagnosis requires more than 20% myeloid blasts in the bone marrow and certain cytogenic abnormalities. Treatment will depend on age, comorbidities, and cytogenetic risk among the most frequent.

show abstract

“…The most common genetic factor for its development is trisomy 21. 12 By the age of 70, about 10% of presumably normal individuals have clonal mutations in hematopoietic cells.…”

Section: Etiologymentioning

confidence: 99%

Consensus in acute myeloid leukemia in Mexico

Arana-Luna¹,

Alvarado-Ibarra²,

Silva-Michel³

et al. 2022

GMM

1

0

View full text Add to dashboard Cite

Acute myeloid leukemia (AML) comprises a heterogeneous group of hematopoietic cell neoplasms of myeloid lineage that arise from the clonal expansion of their precursors in the bone marrow, interfering with cell differentiation, leading to a syndrome of bone marrow failure. AML is a consequence of genetic and epigenetic changes (point mutations, gene rearrangements, deletions, amplifications, and arrangements in epigenetic changes that influence gene expression) in hematopoietic precursor cells, which create a clone of abnormal cells that are capable of proliferating but cannot differentiate into mature hematopoietic cells or undergo programmed cell death. The diagnosis requires more than 20% myeloid blasts in the bone marrow and certain cytogenic abnormalities. Treatment will depend on age, comorbidities, and cytogenetic risk among the most frequent.

show abstract

Acute Myeloid Leukemia in Pediatric Patients: A Review About Current Diagnostic and Treatment Approaches

Cited by 4 publications

References 115 publications

Long Non-coding RNAs in Myeloid Malignancies

Long Non-coding RNAs in Myeloid Malignancies

Consenso de leucemia mieloide aguda en México

Consensus in acute myeloid leukemia in Mexico

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