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Expression profiling of microarray gene signatures in acute and chronic myeloid leukaemia in human bone marrow.

Sakhinia E, Estiar MA, Andalib S, Rezamand A - Iran J Ped Hematol Oncol (2015)

Bottom Line: No statistically significant difference was observed in expression for any gene among CML cases.HOXA9 experienced a non-significant upregulation in AML; however, in combination with proteoglycan 1 distinguished between AML and normal samples in the CD34- fraction in unsupervised clustering.The evidence from the present study suggests that the genes discriminatory between ALL and AML are uninformative in the context of CML and normal BM, excepting for distinction with AML.

View Article: PubMed Central - PubMed

Affiliation: Connective Tissue Disease Research Center, Department of Medical Genetics, Tabriz University of Medical Sciences, Tabriz, Iran.

ABSTRACT

Background: Classification of cancer subtypes by means of microarray signatures is becoming increasingly difficult to ignore as a potential to transform pathological diagnosis; nonetheless, measurement of Indicator genes in routine practice appears to be arduous. In a preceding published study, we utilized real-time PCR measurement of Indicator genes in acute lymphoid leukaemia (ALL) and acute myeloid leukaemia (AML) as a way of application of microarray gene signatures. More to the point, the specificity of such genes for this distinction was investigated by their measurement in cases afflicted with chronic myeloid leukaemia (CML) and with normal bone marrow (BM).

Material and method: Mononuclear cells were sorted into unselected (total), CD34+ve, and CD34-ve fractions, mRNA globally amplified by using PolyA PCR. Moreover, the level of expression of 17 Indicator genes was identified by using real-time PCR.

Results: No statistically significant difference was observed in expression for any gene among CML cases. Cyclin D3 (p≤0.04) was exclusively upregulated in CML in the CD34+ fraction, notwithstanding upregulation of HkrT-1 (p≤0.02) and fumarylacetoacetate (p≤0.03) in AML. HOXA9 experienced a non-significant upregulation in AML; however, in combination with proteoglycan 1 distinguished between AML and normal samples in the CD34- fraction in unsupervised clustering. Unsupervised clustering distinguished among AML and the other diagnostic groups.

Conclusion: The evidence from the present study suggests that the genes discriminatory between ALL and AML are uninformative in the context of CML and normal BM, excepting for distinction with AML.

No MeSH data available.


Related in: MedlinePlus

Mean ranks for Indicator genes in AML and Normal BM in each of the three fractions. Mean ranks (y-axes) for each gene, calculated using the Mann– Whitney in the AML and Normal BM groups (total, CD34+ and CD34-), sorted based on gene mean rank for AML
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Figure 5: Mean ranks for Indicator genes in AML and Normal BM in each of the three fractions. Mean ranks (y-axes) for each gene, calculated using the Mann– Whitney in the AML and Normal BM groups (total, CD34+ and CD34-), sorted based on gene mean rank for AML

Mentions: Statistically significant different expression was found in several genes between AML and the normal BM. In particular, there was an upregulation in the total BM fraction, adipsin (p≤0.03), and HkrT-1 (p≤0.02) in AML. Nevertheless, an upregulation was observed in fumarylacetoacetate (p≤0.014), and LTC4 synthase (p≤0.014), HOXA9 (p≤0.01), and c-myb (p≤0.01) in the CD34 positive and negative fractions, in AML, in comparison with normal BM (Fig 4). There is a difference in expression between AML and normal BM in the mean rank plot for each gene (Fig 5), whereas a wide separation of the curves for AML and normal BM was observed.


Expression profiling of microarray gene signatures in acute and chronic myeloid leukaemia in human bone marrow.

Sakhinia E, Estiar MA, Andalib S, Rezamand A - Iran J Ped Hematol Oncol (2015)

Mean ranks for Indicator genes in AML and Normal BM in each of the three fractions. Mean ranks (y-axes) for each gene, calculated using the Mann– Whitney in the AML and Normal BM groups (total, CD34+ and CD34-), sorted based on gene mean rank for AML
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4402154&req=5

Figure 5: Mean ranks for Indicator genes in AML and Normal BM in each of the three fractions. Mean ranks (y-axes) for each gene, calculated using the Mann– Whitney in the AML and Normal BM groups (total, CD34+ and CD34-), sorted based on gene mean rank for AML
Mentions: Statistically significant different expression was found in several genes between AML and the normal BM. In particular, there was an upregulation in the total BM fraction, adipsin (p≤0.03), and HkrT-1 (p≤0.02) in AML. Nevertheless, an upregulation was observed in fumarylacetoacetate (p≤0.014), and LTC4 synthase (p≤0.014), HOXA9 (p≤0.01), and c-myb (p≤0.01) in the CD34 positive and negative fractions, in AML, in comparison with normal BM (Fig 4). There is a difference in expression between AML and normal BM in the mean rank plot for each gene (Fig 5), whereas a wide separation of the curves for AML and normal BM was observed.

Bottom Line: No statistically significant difference was observed in expression for any gene among CML cases.HOXA9 experienced a non-significant upregulation in AML; however, in combination with proteoglycan 1 distinguished between AML and normal samples in the CD34- fraction in unsupervised clustering.The evidence from the present study suggests that the genes discriminatory between ALL and AML are uninformative in the context of CML and normal BM, excepting for distinction with AML.

View Article: PubMed Central - PubMed

Affiliation: Connective Tissue Disease Research Center, Department of Medical Genetics, Tabriz University of Medical Sciences, Tabriz, Iran.

ABSTRACT

Background: Classification of cancer subtypes by means of microarray signatures is becoming increasingly difficult to ignore as a potential to transform pathological diagnosis; nonetheless, measurement of Indicator genes in routine practice appears to be arduous. In a preceding published study, we utilized real-time PCR measurement of Indicator genes in acute lymphoid leukaemia (ALL) and acute myeloid leukaemia (AML) as a way of application of microarray gene signatures. More to the point, the specificity of such genes for this distinction was investigated by their measurement in cases afflicted with chronic myeloid leukaemia (CML) and with normal bone marrow (BM).

Material and method: Mononuclear cells were sorted into unselected (total), CD34+ve, and CD34-ve fractions, mRNA globally amplified by using PolyA PCR. Moreover, the level of expression of 17 Indicator genes was identified by using real-time PCR.

Results: No statistically significant difference was observed in expression for any gene among CML cases. Cyclin D3 (p≤0.04) was exclusively upregulated in CML in the CD34+ fraction, notwithstanding upregulation of HkrT-1 (p≤0.02) and fumarylacetoacetate (p≤0.03) in AML. HOXA9 experienced a non-significant upregulation in AML; however, in combination with proteoglycan 1 distinguished between AML and normal samples in the CD34- fraction in unsupervised clustering. Unsupervised clustering distinguished among AML and the other diagnostic groups.

Conclusion: The evidence from the present study suggests that the genes discriminatory between ALL and AML are uninformative in the context of CML and normal BM, excepting for distinction with AML.

No MeSH data available.


Related in: MedlinePlus