Literature DB >> 12358913

Frequent co-expression of HoxA9 and Meis1 genes in infant acute lymphoblastic leukaemia with MLL rearrangement.

Toshihiko Imamura1, Akira Morimoto, Mami Takanashi, Shigeyoshi Hibi, Tohru Sugimoto, Eiichi Ishii, Shinsaku Imashuku.   

Abstract

We studied the expression of HoxA9 and Meis1 by reverse transcriptase-polymerase chain reaction analysis in leukaemic cells from cases of infant acute lymphoblastic leukaemia (ALL, n = 27) and childhood ALL (n = 29). These two genes were co-expressed significantly more frequently in infant ALL than in childhood ALL (19/27 vs0/29 cases, P < 0.001) and were highly associated with MLL gene rearrangement in infant ALL cases (P < 0.001). These findings indicate that the HoxA9 and Meis1 genes are closely associated with MLL gene rearrangement in the development of infant ALL, which represents a distinct entity of childhood ALL.

Entities:  

Mesh:

Substances:

Year:  2002        PMID: 12358913     DOI: 10.1046/j.1365-2141.2002.03803.x

Source DB:  PubMed          Journal:  Br J Haematol        ISSN: 0007-1048            Impact factor:   6.998


  30 in total

1.  Hoxa9 and Meis1 are key targets for MLL-ENL-mediated cellular immortalization.

Authors:  Bernd B Zeisig; Tom Milne; María-Paz García-Cuéllar; Silke Schreiner; Mary-Ellen Martin; Uta Fuchs; Arndt Borkhardt; Sumit K Chanda; John Walker; Richard Soden; Jay L Hess; Robert K Slany
Journal:  Mol Cell Biol       Date:  2004-01       Impact factor: 4.272

2.  The role of meis1 in primitive and definitive hematopoiesis during zebrafish development.

Authors:  Ana Cvejic; Jovana Serbanovic-Canic; Derek L Stemple; Willem H Ouwehand
Journal:  Haematologica       Date:  2010-11-03       Impact factor: 9.941

3.  Persistent transactivation by meis1 replaces hox function in myeloid leukemogenesis models: evidence for co-occupancy of meis1-pbx and hox-pbx complexes on promoters of leukemia-associated genes.

Authors:  Gang G Wang; Martina P Pasillas; Mark P Kamps
Journal:  Mol Cell Biol       Date:  2006-05       Impact factor: 4.272

Review 4.  Hypoxia and metabolic properties of hematopoietic stem cells.

Authors:  Cheng Cheng Zhang; Hesham A Sadek
Journal:  Antioxid Redox Signal       Date:  2013-06-21       Impact factor: 8.401

5.  Meis1 programs transcription of FLT3 and cancer stem cell character, using a mechanism that requires interaction with Pbx and a novel function of the Meis1 C-terminus.

Authors:  Gang G Wang; Martina P Pasillas; Mark P Kamps
Journal:  Blood       Date:  2005-03-08       Impact factor: 22.113

6.  Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis.

Authors:  Leila Dardaei; Elena Longobardi; Francesco Blasi
Journal:  Proc Natl Acad Sci U S A       Date:  2014-02-27       Impact factor: 11.205

7.  RNA-binding protein IGF2BP3 targeting of oncogenic transcripts promotes hematopoietic progenitor proliferation.

Authors:  Jayanth Kumar Palanichamy; Tiffany M Tran; Jonathan M Howard; Jorge R Contreras; Thilini R Fernando; Timothy Sterne-Weiler; Sol Katzman; Masoud Toloue; Weihong Yan; Giuseppe Basso; Martina Pigazzi; Jeremy R Sanford; Dinesh S Rao
Journal:  J Clin Invest       Date:  2016-03-14       Impact factor: 14.808

8.  HOXA9 modulates its oncogenic partner Meis1 to influence normal hematopoiesis.

Authors:  Yu-Long Hu; Steve Fong; Christina Ferrell; Corey Largman; Wei-Fang Shen
Journal:  Mol Cell Biol       Date:  2009-07-20       Impact factor: 4.272

9.  Meis1 regulates postnatal cardiomyocyte cell cycle arrest.

Authors:  Ahmed I Mahmoud; Fatih Kocabas; Shalini A Muralidhar; Wataru Kimura; Ahmed S Koura; Suwannee Thet; Enzo R Porrello; Hesham A Sadek
Journal:  Nature       Date:  2013-04-17       Impact factor: 49.962

10.  Upregulation of Flt3 is a passive event in Hoxa9/Meis1-induced acute myeloid leukemia in mice.

Authors:  A Staffas; L S Arabanian; S Y Wei; A Jansson; S Ståhlman; P Johansson; L Fogelstrand; J Cammenga; F Kuchenbauer; L Palmqvist
Journal:  Oncogene       Date:  2016-09-12       Impact factor: 9.867

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.