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Research Paper|Volume 8, Issue 11|pp 2936—2947

Molecular pathway activation features of pediatric acute myeloid leukemia (AML) and acute lymphoblast leukemia (ALL) cells

Ivan Petrov1,2,3, Maria Suntsova1,4, Olga Mutorova1,5, Maxim Sorokin6,7, Andrew Garazha1,3, Elena Ilnitskaya2, Pavel Spirin8, Sergey Larin1, Olga Kovalchuk9, Vladimir Prassolov8, Alex Zhavoronkov1,2, Alexander Roumiantsev1, Anton Buzdin1,4,6
  • 1D. Rogachev Federal Research Center of Pediatric Hematology, Oncology and Immunology, Moscow, 117198, Russia
  • 2First Oncology Research and Advisory Center, Moscow, 117997, Russia
  • 3Moscow Institute of Physics and Technology, Dolgoprudny, Moscow region, 141700, Russia
  • 4Group for Genomic Regulation of Cell Signaling Systems, Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Moscow, 117997, Russia
  • 5Morozov Pediatric Clinical Hospital, Moscow, 101000, Russia
  • 6National Research Centre “Kurchatov Institute”, Centre for Convergence of Nano-, Bio-, Information and Cognitive Sciences and Technologies, Moscow, 123182, Russia
  • 7Pathway Pharmaceuticals, Wan Chai, Hong Kong, Hong Kong SAR
  • 8Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Mosow, Russia,119991
  • 9Department of Biological Sciences, University of Lethbridge, Lethbridge, AB, T1K3M4, Canada
Received: August 6, 2016Accepted: November 4, 2016Published: November 19, 2016

Abstract

Acute lymphoblast leukemia (ALL) is characterized by overproduction of immature white blood cells in the bone marrow. ALL is most common in the childhood and has high (>80%) cure rate. In contrast, acute myeloid leukemia (AML) has far greater mortality rate than the ALL and is most commonly affecting older adults. However, AML is a leading cause of childhood cancer mortality. In this study, we compare gene expression and molecular pathway activation patterns in three normal blood, seven pediatric ALL and seven pediatric AML bone marrow samples. We identified 172/94 and 148/31 characteristic gene expression/pathway activation signatures, clearly distinguishing pediatric ALL and AML cells, respectively, from the normal blood. The pediatric AML and ALL cells differed by 139/34 gene expression/pathway activation biomarkers. For the adult 30 AML and 17 normal blood samples, we found 132/33 gene expression/pathway AML-specific features, of which only 7/2 were common for the adult and pediatric AML and, therefore, age-independent. At the pathway level, we found more differences than similarities between the adult and pediatric forms. These findings suggest that the adult and pediatric AMLs may require different treatment strategies.