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Aberrant AML1 gene expression in the diagnosis of childhood leukemias not characterized by AML1-involved cytogenetic abnormalities.

Abstract The AML1 ( acute myeloid leukemia 1) gene, a necessary prerequisite of embryonic hematopoiesis and a critical regulator of normal hematopoietic development, is one of the most frequently mutated genes in human leukemia, involving over 50 chromosome translocations and over 20 partner genes. In the few existing studies investigating AML1 gene expression in childhood leukemias, aberrant upregulation seems to specifically associate with AML1 translocations and amplifications. The aim of this study was to determine whether overexpression also extends to other leukemic subtypes than the ones karyotypically involving AML1. We use quantitative real-time polymerase chain reaction methodology to investigate gene expression in 100 children with acute leukemias and compare them to those of healthy controls. We show that in childhood acute lymphoblastic leukemia, AML1 gene overexpression is associated with a variety of leukemic subtypes, both immunophenotypically and cytogenetically. Statistically significantly higher transcripts of the gene were detected in the acute lymphoblastic leukemia group as compared to the acute myeloid leukemia group, where AML1 overexpression appeared to associate with cytogenetic abnormalities additional to those that engage the AML1 gene, or that are reported as showing a "normal" karyotype. Collectively, our study shows that AML1 gene overexpression characterizes a broader range of leukemic subtypes than previously thought, including various maturation stages of B-cell acute lymphoblastic leukemia and cytogenetic types additional to those involving the AML1 gene.
PMID
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Authors

Mayor MeshTerms
Keywords

AML1

childhood leukemia

gene amplification

gene overexpression

overall survival

Journal Title tumour biology : the journal of the international society for oncodevelopmental biology and medicine
Publication Year Start




PMID- 28349830
OWN - NLM
STAT- MEDLINE
DA  - 20170328
DCOM- 20170407
LR  - 20170407
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 3
DP  - 2017 Mar
TI  - Aberrant AML1 gene expression in the diagnosis of childhood leukemias not
      characterized by AML1-involved cytogenetic abnormalities.
PG  - 1010428317694308
LID - 10.1177/1010428317694308 [doi]
AB  - The AML1 ( acute myeloid leukemia 1) gene, a necessary prerequisite of embryonic 
      hematopoiesis and a critical regulator of normal hematopoietic development, is
      one of the most frequently mutated genes in human leukemia, involving over 50
      chromosome translocations and over 20 partner genes. In the few existing studies 
      investigating AML1 gene expression in childhood leukemias, aberrant upregulation 
      seems to specifically associate with AML1 translocations and amplifications. The 
      aim of this study was to determine whether overexpression also extends to other
      leukemic subtypes than the ones karyotypically involving AML1. We use
      quantitative real-time polymerase chain reaction methodology to investigate gene 
      expression in 100 children with acute leukemias and compare them to those of
      healthy controls. We show that in childhood acute lymphoblastic leukemia, AML1
      gene overexpression is associated with a variety of leukemic subtypes, both
      immunophenotypically and cytogenetically. Statistically significantly higher
      transcripts of the gene were detected in the acute lymphoblastic leukemia group
      as compared to the acute myeloid leukemia group, where AML1 overexpression
      appeared to associate with cytogenetic abnormalities additional to those that
      engage the AML1 gene, or that are reported as showing a "normal" karyotype.
      Collectively, our study shows that AML1 gene overexpression characterizes a
      broader range of leukemic subtypes than previously thought, including various
      maturation stages of B-cell acute lymphoblastic leukemia and cytogenetic types
      additional to those involving the AML1 gene.
FAU - Adamaki, Maria
AU  - Adamaki M
AD  - 1 Pediatric Hematology/Oncology Unit, First Department of Pediatrics, Medical
      School, National and Kapodistrian University of Athens and "Aghia Sofia"
      Children's Hospital, Athens, Greece.
FAU - Vlahopoulos, Spiros
AU  - Vlahopoulos S
AD  - 1 Pediatric Hematology/Oncology Unit, First Department of Pediatrics, Medical
      School, National and Kapodistrian University of Athens and "Aghia Sofia"
      Children's Hospital, Athens, Greece.
FAU - Lambrou, George I
AU  - Lambrou GI
AD  - 1 Pediatric Hematology/Oncology Unit, First Department of Pediatrics, Medical
      School, National and Kapodistrian University of Athens and "Aghia Sofia"
      Children's Hospital, Athens, Greece.
FAU - Papavassiliou, Athanasios G
AU  - Papavassiliou AG
AD  - 2 Department of Biological Chemistry, Medical School, National and Kapodistrian
      University of Athens, Athens, Greece.
FAU - Moschovi, Maria
AU  - Moschovi M
AD  - 1 Pediatric Hematology/Oncology Unit, First Department of Pediatrics, Medical
      School, National and Kapodistrian University of Athens and "Aghia Sofia"
      Children's Hospital, Athens, Greece.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Tumour Biol
JT  - Tumour biology : the journal of the International Society for Oncodevelopmental
      Biology and Medicine
JID - 8409922
RN  - 0 (Core Binding Factor Alpha 2 Subunit)
RN  - 0 (RUNX1 protein, human)
SB  - IM
MH  - Case-Control Studies
MH  - Cell Line, Tumor
MH  - Child
MH  - Core Binding Factor Alpha 2 Subunit/biosynthesis/*genetics
MH  - Female
MH  - Gene Expression
MH  - Humans
MH  - Leukemia, Myeloid, Acute/*genetics/metabolism
MH  - Male
MH  - Precursor Cell Lymphoblastic Leukemia-Lymphoma/*genetics/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Survival Rate
OTO - NOTNLM
OT  - AML1
OT  - childhood leukemia
OT  - gene amplification
OT  - gene overexpression
OT  - overall survival
EDAT- 2017/03/30 06:00
MHDA- 2017/04/08 06:00
CRDT- 2017/03/29 06:00
AID - 10.1177/1010428317694308 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Mar;39(3):1010428317694308. doi: 10.1177/1010428317694308.

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