Contributions
Abstract: PB1663
Type: Publication Only
Background
Acute myeloid leukemia (AML) is the most common type of hematological malignancy. It seems likely that gap junctions are involved in the communication between AML and stromal cells during disease development. Gap junctions consist of arrays of intercellular channels composed of two hemichannels or connexons, one of which is formed by six protein subunits, termed connexins (Cxs). Cxs are a conserved family of transmembrane proteins which regulate the passage of biological molecules and allow the exchange of signaling molecules between the cytoplasm of two neighboring cells. Cx43 is the major component of hematopoietic tissue and Cx32 is found on bone marrow stromal cells.
Aims
The aim of this study was to evaluate the expression of Cx 43 and Cx 32 expression profiles and to correlate their expression with disease severity and other prognostic markers in patients with AML.
Methods
This study was carried out on samples from the peripheral blood of 60 patients with AML. Detection of Cx 43 and Cx 32 expression was performed using real time polymerase chain reaction (RT-PCR)
Results
The cases were divided into 39 males (57.4%) and 21 females (42.6%). Their age ranged between 14 and 82 years with a mean value of 49.68±16.1. Cx 32 expression showed a high median fold change along with a statistically significant difference between de novo AML patients and the control group (median Cx 32=18, p=0.009). On the other hand, Cx 43 expression showed a lower median fold in comparison to the control group (median Cx 43=0.6, p=0.013).
A lower median fold change was observed in Cx 32 expression (median Cx 32=0.48), and Cx 43 expression (median Cx 43=0.1) in FAB subtype (M3) when compared with other FAB subtypes as (M1, M2, M4, M5).There was a statistically significant difference between the groups (Cx 32, p=0.009; Cx 43, p=0.002, respectively).
In addition, CD34 positive AML patients showed a significantly higher level of Cx 32 (median Cx 32=20), and Cx 43 expression (median Cx 43=0.7) against CD34 negative AML patients (median Cx 32= 0.16; median Cx 43=0.7) (Cx 32 p=0.045; Cx 43 p=0.007). No statistically significant difference was found between favorable risk patients and those with intermediate/unfavourable risk in Cx 32 and Cx 43 fold change expression.
Conclusion
Our results indicate that Cx 43 and Cx 32 may have a role in AML pathogenesis.Further studies needed to evlauate their clinical significance as prognostic factors in AML.
Session topic: 3. Acute myeloid leukemia - Biology & Translational Research
Keyword(s): Acute Myeloid Leukemia, Prognostic factor
Abstract: PB1663
Type: Publication Only
Background
Acute myeloid leukemia (AML) is the most common type of hematological malignancy. It seems likely that gap junctions are involved in the communication between AML and stromal cells during disease development. Gap junctions consist of arrays of intercellular channels composed of two hemichannels or connexons, one of which is formed by six protein subunits, termed connexins (Cxs). Cxs are a conserved family of transmembrane proteins which regulate the passage of biological molecules and allow the exchange of signaling molecules between the cytoplasm of two neighboring cells. Cx43 is the major component of hematopoietic tissue and Cx32 is found on bone marrow stromal cells.
Aims
The aim of this study was to evaluate the expression of Cx 43 and Cx 32 expression profiles and to correlate their expression with disease severity and other prognostic markers in patients with AML.
Methods
This study was carried out on samples from the peripheral blood of 60 patients with AML. Detection of Cx 43 and Cx 32 expression was performed using real time polymerase chain reaction (RT-PCR)
Results
The cases were divided into 39 males (57.4%) and 21 females (42.6%). Their age ranged between 14 and 82 years with a mean value of 49.68±16.1. Cx 32 expression showed a high median fold change along with a statistically significant difference between de novo AML patients and the control group (median Cx 32=18, p=0.009). On the other hand, Cx 43 expression showed a lower median fold in comparison to the control group (median Cx 43=0.6, p=0.013).
A lower median fold change was observed in Cx 32 expression (median Cx 32=0.48), and Cx 43 expression (median Cx 43=0.1) in FAB subtype (M3) when compared with other FAB subtypes as (M1, M2, M4, M5).There was a statistically significant difference between the groups (Cx 32, p=0.009; Cx 43, p=0.002, respectively).
In addition, CD34 positive AML patients showed a significantly higher level of Cx 32 (median Cx 32=20), and Cx 43 expression (median Cx 43=0.7) against CD34 negative AML patients (median Cx 32= 0.16; median Cx 43=0.7) (Cx 32 p=0.045; Cx 43 p=0.007). No statistically significant difference was found between favorable risk patients and those with intermediate/unfavourable risk in Cx 32 and Cx 43 fold change expression.
Conclusion
Our results indicate that Cx 43 and Cx 32 may have a role in AML pathogenesis.Further studies needed to evlauate their clinical significance as prognostic factors in AML.
Session topic: 3. Acute myeloid leukemia - Biology & Translational Research
Keyword(s): Acute Myeloid Leukemia, Prognostic factor