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10.3390/jcm4010127

http://scihub22266oqcxt.onion/10.3390/jcm4010127
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C4470244!4470244!26237023
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suck abstract from ncbi

pmid26237023      J+Clin+Med 2015 ; 4 (1): 127-49
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  • Pediatric AML: From Biology to Clinical Management #MMPMID26237023
  • de Rooij JDE; Zwaan CM; van den Heuvel-Eibrink M
  • J Clin Med 2015[Jan]; 4 (1): 127-49 PMID26237023show ga
  • 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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