Functional Role of RUNX1 Mutations in the Etiology of Acute Myeloid Leukemia (AML)

The recruitment status of this study is unknown because the information has not been verified recently.
Verified April 2011 by Hillel Yaffe Medical Center.
Recruitment status was  Not yet recruiting
Sponsor:
Collaborator:
Weizmann Institute of Science
Information provided by:
Hillel Yaffe Medical Center
ClinicalTrials.gov Identifier:
NCT01329471
First received: March 10, 2011
Last updated: April 5, 2011
Last verified: April 2011

March 10, 2011
April 5, 2011
April 2011
April 2012   (final data collection date for primary outcome measure)
Performance of expression arrays on transfected CD34+ cells [ Time Frame: One year ] [ Designated as safety issue: No ]
Performance of expression arrays on transfected CD34+ cells (derived from human cord blood), expecting differential gene expression between the wild type RUNX1-transfected cells and mutated RUNX1-transfected cells.
Same as current
Complete list of historical versions of study NCT01329471 on ClinicalTrials.gov Archive Site
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Functional Role of RUNX1 Mutations in the Etiology of Acute Myeloid Leukemia (AML)
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The purpose of this study is to elucidate the role of RUNX1 in Acute Myeloid Leukemia (AML), in particular, the transcriptional regulation of genes by mutated forms of this protein. This research will study the effect of mutations found in AML patients

The RUNX1 gene, located at chromosomal band 21q22, is a transcription factor, crucial for hematopoiesis and the generation of hematopoietic stem cells in the embryo. RUNX1 is the most frequent target for chromosomal translocation in leukemia. In addition, point mutations in the RUNX1 gene have been found to constitute an important mode of genetic alteration in development of leukemia. Recent publications stressing the clinical need for implementing RUNX1 point mutations as both a diagnostic and unfavorable prognostic marker of AML, have aroused particular interest in the functional role of RUNX1 in this disease.

In order to pinpoint specific RUNX1 target genes involved in pre-leukemic transformation or exacerbation of existing leukemia, the investigators plan to compare expression profiles from human hematopoietic progenitors overexpressing a mutated form of RUNX1with controls (RUNX1 wild-type and knocked-down). In this study the investigators intend to collect blood, after receiving informed consent, from umbilical cords of neonates born vaginally, in order to isolate CD34+ hematopoietic progenitors. Human umbilical cord blood contains relatively high numbers of CD34+ cells, which may be frozen directly after collection and used as a source of progenitor cells for further culture or direct analysis.

Observational
Time Perspective: Prospective
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Probability Sample

Female hospital patients

Acute Myeloid Leukemia
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Umbilical cord blood
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*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Not yet recruiting
75
April 2013
April 2012   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • Consenting women who have had full-term birth

Exclusion Criteria:

  • Systemic disease
Female
18 Years to 45 Years
Yes
Not Provided
Israel
 
NCT01329471
HYMC-16-2011
Yes
Dr. Ofer Fainaru, Hillel Yaffe Medical Center
Hillel Yaffe Medical Center
Weizmann Institute of Science
Not Provided
Hillel Yaffe Medical Center
April 2011

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP