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肿瘤形成评论综述™
SJR: 0.631 SNIP: 0.503 CiteScore™: 2

ISSN 打印: 0893-9675
ISSN 在线: 2162-6448

肿瘤形成评论综述™

DOI: 10.1615/CritRevOncog.2017024465
pages 157-185

Homeobox Gene Involvement in Normal Hematopoiesis and in the Pathogenesis of Childhood Leukemias

Maria Adamaki
Biomedical Applications Unit, Institute of Biology, Medicinal Chemistry and Biotechnology, National Hellenic Research Foundation, 11635 Athens, Greece
Maria Goulielmaki
Biomedical Applications Unit, Institute of Biology, Medicinal Chemistry and Biotechnology, National Hellenic Research Foundation, 11635 Athens, Greece
Ioannis Christodoulou
Biomedical Applications Unit, Institute of Biology, Medicinal Chemistry and Biotechnology, National Hellenic Research Foundation, 11635 Athens, Greece
Spiros Vlahopoulos
Biomedical Applications Unit, Institute of Biology, Medicinal Chemistry and Biotechnology, National Hellenic Research Foundation, 11635 Athens, Greece; Horemio Research Institute, First Department of Pediatrics, Aghia Sophia Children's Hospital, National and Kapodistrian University of Athens, Athens, Greece
Vassilis Zoumpourlis
Biomedical Applications Unit, Institute of Biology, Medicinal Chemistry and Biotechnology, National Hellenic Research Foundation, 11635 Athens, Greece

ABSTRACT

Homeobox (HOX) genes are a superfamily of highly conserved genes with essential functions in many aspects of mammalian development. Their expression is tightly regulated throughout the duration of definitive hematopoiesis, so the pathogenetic mechanism that leads to leukemia suggests that malignant transformation is directly intertwined with the deregulation of HOX gene expression. Even though HOX gene involvement has been reviewed extensively in adult leukemias, childhood leukemias have received much less attention and mainly in the context of leukemias harboring MLL (mixed-lineage leukemia) gene translocations. In recent years, scientific evidence has highlighted HOX gene involvement in the development of other subtypes of childhood leukemias and added HOX gene family members that were previously unrelated to the pathogenesis of childhood leukemia. This has significant implications when considering both the risk stratification of pediatric patients and potential targets for successful therapy. Through the identification of HOX target genes, their resulting interactions, and the cognate signaling pathways, we hope to gain a better understanding of the molecular mechanism(s) underlying the ectopic activation of these genes in childhood leukemias and subsequently to reveal new molecular targets for successful therapy in cases of poor prognosis or resistant disease.


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