High MN1 expression increases the in vitro clonogenic activity of primary mouse B-cells


Numata M., YENER M. D., SIRMA EKMEKCİ S., Aydin M., Grosveld G., Cardone M., ...Daha Fazla

LEUKEMIA RESEARCH, cilt.39, sa.8, ss.906-912, 2015 (SCI-Expanded) identifier identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 39 Sayı: 8
  • Basım Tarihi: 2015
  • Doi Numarası: 10.1016/j.leukres.2015.05.013
  • Dergi Adı: LEUKEMIA RESEARCH
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.906-912
  • Acıbadem Mehmet Ali Aydınlar Üniversitesi Adresli: Hayır

Özet

The MN1 (Meningioma 1) gene is overexpressed in certain subtypes of acute myeloid leukemia (AML) and high levels of MN1 expression in mouse bone marrow cells results in myeloid leukemia. We showed that compared with control bone marrow (BM) MN1 expression was increased (2-fold or more) in 29 out of 73 (40%) pediatric B-cell acute lymphoblastic leukemia (B-ALL) patient BM. Additional analysis of MN1 expression in sub-groups within our cohort carrying different chromosome translocations showed that carriers of the good prognostic marker t(12;21)(TEL-AML1) (n = 27) expressed significantly more MN1 than both healthy controls (n = 9) (P = 0.02) and the group carrying the t(9; 22)(BCR-ABL) (n = 9) (P = 0.001). In addition, AML1 expression was also upregulated in 31 out of 45 (68%) B-ALL patient BM compared with control and there was a significant correlation between MN1 and AML1 expression (r = 0.3552, P = 0.0167). Retroviral MN1 overexpression increased the colony forming activity of mouse Pro-B/Pre-B cells in vitro. Our results suggest that deregulated MN1 expression contributes to the pathogenesis of pediatric BALL. Further investigation into the clinical and biological significance of elevated MN1 expression in TEL-AML1(positive) leukemia might provide insight into additional molecular mechanisms contributing to B-ALL and may lead to improved treatment options for patients. (C) 2015 Elsevier Ltd. All rights reserved.