Cytogenetic abnormalities and monosomal karyotypes in children and adolescents with acute myeloid leukemia: correlations with clinical characteristics and outcome

Manola, Kalliopi N.; Panitsas, Fotios; Polychronopoulou, Sophia; Daraki, Aggeliki; Karakosta, Maria; Stavropoulou, Chryssa; Avgerinou, Georgia; Hatzipantelis, Emmanuel; Pantelias, Gabriel E.; Sambani, Constantina; Pagoni, Maria

doi:10.1016/j.cancergen.2013.01.001

Cited by 29 publications

(24 citation statements)

References 35 publications

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“…In those pediatric patients, the outcome seems to be dependent on other cytogenetic abnormalities in the leukemic cell [52,82]. The described poor prognostic abnormalities in adult AML of chromosomes 3q and 5q and the monosomal karyotypes are rare in children [30,83,84,85]. Overexpression of EVI1 caused by 3q26 abnormalities predicts an adverse outcome in adult AML, but EVI1 overexpression is not an independent prognostic factor in pediatric AML [86,87].…”

Section: Clinical Introductionmentioning

confidence: 99%

Pediatric AML: From Biology to Clinical Management

Rooij

2015

JCM

170

169

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Pediatric acute myeloid leukemia (AML) represents 15%–20% of all pediatric acute leukemias. Survival rates have increased over the past few decades to ~70%, due to improved supportive care, optimized risk stratification and intensified chemotherapy. In most children, AML presents as a de novo entity, but in a minority, it is a secondary malignancy. The diagnostic classification of pediatric AML includes a combination of morphology, cytochemistry, immunophenotyping and molecular genetics. Outcome is mainly dependent on the initial response to treatment and molecular and cytogenetic aberrations. Treatment consists of a combination of intensive anthracycline- and cytarabine-containing chemotherapy and stem cell transplantation in selected genetic high-risk cases or slow responders. In general, ~30% of all pediatric AML patients will suffer from relapse, whereas 5%–10% of the patients will die due to disease complications or the side-effects of the treatment. Targeted therapy may enhance anti-leukemic efficacy and minimize treatment-related morbidity and mortality, but requires detailed knowledge of the genetic abnormalities and aberrant pathways involved in leukemogenesis. These efforts towards future personalized therapy in a rare disease, such as pediatric AML, require intensive international collaboration in order to enhance the survival rates of pediatric AML, while aiming to reduce long-term toxicity.

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Section: Clinical Introductionmentioning

confidence: 99%

Pediatric AML: From Biology to Clinical Management

Rooij

2015

JCM

170

169

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“…MK is often associated with other unfavourable risk cytogenetics, such as inv (3), -5/del(5q), -7/del(7q), and rarely combined with FLT3-internal tandem duplication (ITD) or NPM1 mutations (Kayser et al, 2012;Weinberg et al, 2014). The negative influence on prognosis has been identified in AML patients with MK independently of the co-occurrence of CK (Breems et al, 2008;Medeiros et al, 2010;Fang et al, 2011;Haferlach et al, 2012;Kayser et al, 2012;Weinberg et al, 2014) and may be less pronounced in younger patients (Breems et al, 2008;Kayser et al, 2012;Manola et al, 2013;Weinberg et al, 2014). A study of MK in children with AML by Manola et al (2013) indicated an adverse prognosis with OS of 52%, but included only 15 cases with MK.…”

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confidence: 99%

Complex and monosomal karyotype are distinct cytogenetic entities with an adverse prognostic impact in paediatric acute myeloid leukaemia. A NOPHO‐DBH‐AML study

Bager

Juul-Dam

Abrahamsson³

et al. 2018

Br J Haematol

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Summary Data on occurrence, genetic characteristics and prognostic impact of complex and monosomal karyotype (CK/MK) in children with acute myeloid leukaemia (AML) are scarce. We studied CK and MK in a large unselected cohort of childhood AML patients diagnosed and treated according to Nordic Society for Paediatric Haematology and Oncology (NOPHO)‐AML protocols 1993–2015. In total, 800 patients with de novo AML were included. CK was found in 122 (15%) and MK in 41 (5%) patients. CK and MK patients were young (median age 2·1 and 3·3 years, respectively) and frequently had FAB M7 morphology (24% and 22%, respectively). Refractory disease was more common in MK patients (15% vs. 4%) and stem cell transplantation in first complete remission was more frequent (32% vs. 19%) compared with non‐CK/non‐MK patients. CK showed no association with refractory disease but was an independent predictor of an inferior event‐free survival (EFS; hazard ratio [HR] 1·43, P = 0·03) and overall survival (OS; HR 1·48, P = 0·01). MK was associated with a poor EFS (HR 1·57, P = 0·03) but did not show an inferior OS compared to non‐MK patients (HR 1·14, P = 0·62). In a large paediatric cohort, we characterized AML with non‐recurrent abnormal karyotype and unravelled the adverse impact of CK and MK on prognosis.

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“…In these pediatric patients, the outcome has been found to be dependent on other cytogenetic abnormalities in the leukemia cell [19,43]. Other poor prognostic abnormalities that have been described in adult AML, such as abnormalities of chromosomes 3q and 5q and the monsoonal karyotypes are very rare in children [44][45][46][47].…”

Section: Myeloid Leukemia 26mentioning

confidence: 99%

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

Derwich¹,

Mitkowski²,

J³

2018

Myeloid Leukemia

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Acute leukemia is the most common childhood malignancy, accounting for almost 35% of all childhood cancers. Acute myeloid leukemia (AML) represents 15-20% of pediatric acute leukemia. Majority of AML cases appear de novo, however a minority of cases can present as a secondary malignancy. AML is a highly heterogeneous disease and its diagnosis involves a combination of diagnostic analyses including morphology, immunophenotyping, cytochemistry, and leukemic blasts derived from peripheral blood or bone marrow demonstrating cytogenic and molecular characteristics. Through the identification of recurrent genetic mutations, it has been made possible to refine individual prognosis and guide therapeutic management. The current survival rate of children with AML is approximately 70%. The standard therapeutic regimen is a combination of cytarabine-and anthracycline-based regimens with allogenic stem cell transplantation in appropriate patients. Relapse in pediatric patients suffering from AML occurs in approximately 30% of cases, whereas death occurs in 5-10% of patients as a result of disease complications or chemotherapeutic side effects. In understanding the genetic basis of AML, targeted therapies will have the ability to reduce treatment-related morbidity and mortality. Here, we provide a comprehensive review of AML, its biology, diagnosis and therapeutic management in pediatric patients.

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Cytogenetic abnormalities and monosomal karyotypes in children and adolescents with acute myeloid leukemia: correlations with clinical characteristics and outcome

Cited by 29 publications

References 35 publications

Pediatric AML: From Biology to Clinical Management

Pediatric AML: From Biology to Clinical Management

Complex and monosomal karyotype are distinct cytogenetic entities with an adverse prognostic impact in paediatric acute myeloid leukaemia. A NOPHO‐DBH‐AML study

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

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