| Literature DB >> 24745672 |
Siham Bibi1, Florent Langenfeld1, Sylvie Jeanningros1, Fabienne Brenet2, Erinn Soucie2, Olivier Hermine3, Gandhi Damaj4, Patrice Dubreuil5, Michel Arock6.
Abstract
In all variants of mastocytosis, activating KIT mutations are frequently found. In adults, neoplastic mast cells (MCs) cells show the KIT mutation D816V, whereas in children, MCs invading the skin are frequently positive for non-KIT D816V mutations. The clinical course and prognosis of the disease vary among patients with systemic mastocytosis (SM). Additional KIT-independent molecular defects might cause progression. Additional oncogenic lesions have recently been identified in advanced SM. In advanced SM the presence of additional genetic lesions or altered signaling worsening the prognosis might lead to the use of alternative therapies such as combined antisignaling targeted treatments or stem cell transplantation.Entities:
Keywords: ASXL1; KIT; Mutation; Signaling; Spliceosome; Systemic mastocytosis; TET2; Targeted therapy
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Year: 2014 PMID: 24745672 DOI: 10.1016/j.iac.2014.01.009
Source DB: PubMed Journal: Immunol Allergy Clin North Am ISSN: 0889-8561 Impact factor: 3.479