title: Stem cell factor SALL4, a potential prognostic marker for myelodysplastic syndromes.
abstract: BACKGROUND
  Myelodysplastic syndromes (MDS) are a group of heterogeneous diseases with variable clinical course. Predicting disease progression is difficult due to lack of specific molecular marker(s). SALL4 plays important roles in normal hematopoiesis and leukemogenesis. SALL4 transgenic mice develop MDS prior to acute myeloid leukemia (AML) transformation. However, the role of SALL4 in human MDS has not been extensively investigated. In this study, we evaluate the diagnostic/prognostic value of SALL4 in MDS by examining its expression levels in a cohort of MDS patients.
  
  
  METHODS
  Fifty-five newly diagnosed MDS, twenty MDS-AML, and sixteen post-treatment MDS patients were selected for our study along with ten healthy donors.
  
  
  RESULTS
  We demonstrated that SALL4 was over-expressed in MDS patients and proportionally increased in MDS patients with high grade/IPSS scores. This expression pattern was similar to that of Bmi-1, an important marker in predicting MDS/AML progression. In addition, the level of SALL4 was positively correlated with increased blast counts, high-risk keryotypes and increased significantly in MDS-AML transformation. Furthermore, higher level of SALL4 expression was associated with worse survival rates and SALL4 level decreased following effective therapy.
  
  
  CONCLUSIONS
  To the best of our knowledge, this is the largest series and the first to report the expression pattern of SALL4 in detail in various subtypes of MDS in comparison to that of Bmi-1. We conclude that SALL4 is a potential molecular marker in predicting the prognosis of MDS.
authors.forename: Fei
authors.initials: F
authors.lastname: Wang
authors.forename: Ye
authors.initials: Y
authors.lastname: Guo
authors.forename: Qian
authors.initials: Q
authors.lastname: Chen
authors.forename: Zhuo
authors.initials: Z
authors.lastname: Yang
authors.forename: Ning
authors.initials: N
authors.lastname: Ning
authors.forename: Yujuan
authors.initials: Y
authors.lastname: Zhang
authors.forename: Yonggang
authors.initials: Y
authors.lastname: Xu
authors.forename: Xiaodong
authors.initials: X
authors.lastname: Xu
authors.forename: Chunrong
authors.initials: C
authors.lastname: Tong
authors.affiliation: Department of Clinical Laboratory, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China. lchai@partners.org.
authors.forename: Li
authors.initials: L
authors.lastname: Chai
authors.forename: Wei
authors.initials: W
authors.lastname: Cui
mesh_terms: D000328:Adult; D000368:Aged; D000818:Animals; D016022:Case-Control Studies; D045744:Cell Line, Tumor; D018450:Disease Progression; D005260:Female; D006801:Humans; D008297:Male; D008822:Mice, Transgenic; D008875:Middle Aged; D048054:Mitogen-Activated Protein Kinase 7; D009190:Myelodysplastic Syndromes / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D011379:Prognosis; D014157:Transcription Factors / Q000096:biosynthesis* / Q000235:genetics; D055815:Young Adult
chemical_list: C472575:SALL4 protein, human; D014157:Transcription Factors; C481581:MAPK7 protein, human; D048054:Mitogen-Activated Protein Kinase 7