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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

Expression levels (LN) of genes with statistically significant difference between AML and CML. The above box plots show significant difference in expression for cyclin D3 in the CD34 positive fraction. There was no significant difference in expression level of Mhouse between AML and CML. LN, natural logarithm; Mhouse, mean of three housekeeping genes expression levels; N, number of samples in each group.
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Figure 1: Expression levels (LN) of genes with statistically significant difference between AML and CML. The above box plots show significant difference in expression for cyclin D3 in the CD34 positive fraction. There was no significant difference in expression level of Mhouse between AML and CML. LN, natural logarithm; Mhouse, mean of three housekeeping genes expression levels; N, number of samples in each group.

Mentions: Cyclin D3 was expressed at significantly higher levels in CML (p≤ 0.04); however, the remainder of the genes indicated that there was no significant difference between the two groups (Figs 1 and 2). The mean ranks for each of the genes between AML and CML indicated upregulation of cyclin D3 in CML in comparison with AML in the CD34+ve fraction, whereas it was upregulated in the total BM fraction, and there was no significant difference (p≤0.39). The mean rank analysis revealed downregulation of adipsin in CML in the total BM fraction, although there was no significant difference (p≤0.08). The mean rank plots showed general trends in the relative expression levels for each Indicator genes between AML and CML. In the total BM and CD34-ve fractions, most of the genes were highly expressed in AML, compared to CML; however, in the CD34+ fraction similar numbers of genes demonstrated a higher expression in AML and CML.


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)

Expression levels (LN) of genes with statistically significant difference between AML and CML. The above box plots show significant difference in expression for cyclin D3 in the CD34 positive fraction. There was no significant difference in expression level of Mhouse between AML and CML. LN, natural logarithm; Mhouse, mean of three housekeeping genes expression levels; N, number of samples in each group.
© Copyright Policy
Related In: Results  -  Collection

License
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getmorefigures.php?uid=PMC4402154&req=5

Figure 1: Expression levels (LN) of genes with statistically significant difference between AML and CML. The above box plots show significant difference in expression for cyclin D3 in the CD34 positive fraction. There was no significant difference in expression level of Mhouse between AML and CML. LN, natural logarithm; Mhouse, mean of three housekeeping genes expression levels; N, number of samples in each group.
Mentions: Cyclin D3 was expressed at significantly higher levels in CML (p≤ 0.04); however, the remainder of the genes indicated that there was no significant difference between the two groups (Figs 1 and 2). The mean ranks for each of the genes between AML and CML indicated upregulation of cyclin D3 in CML in comparison with AML in the CD34+ve fraction, whereas it was upregulated in the total BM fraction, and there was no significant difference (p≤0.39). The mean rank analysis revealed downregulation of adipsin in CML in the total BM fraction, although there was no significant difference (p≤0.08). The mean rank plots showed general trends in the relative expression levels for each Indicator genes between AML and CML. In the total BM and CD34-ve fractions, most of the genes were highly expressed in AML, compared to CML; however, in the CD34+ fraction similar numbers of genes demonstrated a higher expression in AML and CML.

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