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Critical Reviews™ in Oncogenesis
SJR: 0.631 SNIP: 0.503 CiteScore™: 2

ISSN Imprimer: 0893-9675
ISSN En ligne: 2162-6448

Critical Reviews™ in Oncogenesis

DOI: 10.1615/CritRevOncog.v15.i1-2.40
pages 91-115

Structural and Expression Changes of Septins in Myeloid Neoplasia

Nuno Cerveira
Department of Genetics, Portuguese Oncology Institute, Portugal
Joana Santos
Department of Genetics, Portuguese Oncology Institute, Porto, Portugal
Manuel R. Teixeira
Department of Genetics, Portuguese Oncology Institute, Rua Dr. António Bernardino de Almeida, 4200-072 Porto, Portugal; and Abel Salazar Biomedical Sciences Institute (ICBAS), Porto, Portugal

RÉSUMÉ

Septins are an evolutionarily conserved family of GTP-binding proteins that associate with cellular membranes and the actin and microtubule cytoskeletons. Fourteen septin genes have been characterized to date (SEPT1 to SEPT14) in humans. Septins have been reported to be misregulated in various human diseases, including neurological disorders, infection, and neoplasia. In this review, we describe what is known thus far about septin deregulation in myeloid neoplasia. Septin abnormalities in myeloid neoplasia can be divided into two major groups. First, some septins (SEPT2, SEPT5, SEPT6, SEPT9, and SEPT11) have been repeatedly identified as in-frame fusion partners of the MLL gene in de novo and therapy-related myeloid neoplasia, in both children and adults. Second, deregulation of the expression of septin family genes in hematological cancers can be observed either with or without the concomitant presence of MLL gene fusions. Although current hypotheses regarding the roles of septins in oncogenesis remain speculative for the most part, the fundamental roles of septins in cytokinesis, membrane remodeling, and compartmentalization can provide some clues on how abnormalities in the septin cytoskeleton could be involved in neo-plastic disorders.


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