
Contributions
Abstract: PB1615
Type: Publication Only
Background
The partition-defective 3 (PARD-3) gene is essential for the disassembly of the tight/ adhesive junctions and epithelial-mesenchymal transition (EMT) which is critical for tumor spreading. Previous research has shown that PARD-3 protein expression is frequently lost in primary esophageal squamous cell carcinoma(ESCC). In the progression of non-small-cell lung cancer (NSCLC), PARD-3 has also been verified to contribute to EMT, invasion, and chemoresistance in NSCLC. The effect of PARD-3 expression on adult B-cell acute lymphoblastic leukemia (ALL) has not been identified.
Aims
The purpose of this study was to investigate the transcriptional level of PARD-3 in adult B cell acute lymphoblastic leukemia.
Methods
A real-time quantitative reverse transcription-polymerase chain reaction assay based on Taq-Man fluorescence methodology was used to quantify the PARD-3 mRNA copy number in the bone marrow cells from patients with adult leukemia. Normal marrow samples from the allogeneic stem cell transplantation donors were served as control. Informed consent was obtained for every marrow sample.
Results
Expression levels of the PARD-3 in leukemia patients and normal donor marrow are shown in Figure 1. These results showed that the relative levels of PARD-3 gene expression in marrow from 32 newly diagnosed B-cell ALL (median 92.84%; range 0.002%~316.201%) was significantly higher than those of marrow from the 20 healthy donors (median 13.74%; range 2.93%~41.15%; P=0.004). Significant PARD-3 mRNA over expression was found in the de novo B-cell ALL patients compared with 32 treated B-cell ALL patients (median 10.46%; range 0.415%~64.489%) who achieved complete remission or 32 de novo AML (median 11.638%; range 0.021%~114.169%; P<0.0001). The expression levels of PARD-3 was higher in 6 refractory/relapsed B-cell ALL patients (median 110.315%; range 1.276%~499.772%) than that of newly diagnosed B-cell ALL, but no statistical significant difference was observed (P=0.72). Besides, no statistical significant difference was observed in 32 newly diagnosed AML (median 11.638%, range 0.021%~114.169%) and 20 healthy donors (P=0.72), but it was higher in BALL-1 and NALM6 cells from B cell ALL cell lines than in other cells from AML cell lines (Figure 1).
Conclusion
These observations suggest that PARD-3 is overexpressed in B-cell acute lymphoblastic leukemia and may play a role in the pathogenesis of B-cell acute lymphoblastic leukemia.
Session topic: 1. Acute lymphoblastic leukemia – Biology & Translational Research
Keyword(s): Acute lymphoblastic leukemia, PCR
Abstract: PB1615
Type: Publication Only
Background
The partition-defective 3 (PARD-3) gene is essential for the disassembly of the tight/ adhesive junctions and epithelial-mesenchymal transition (EMT) which is critical for tumor spreading. Previous research has shown that PARD-3 protein expression is frequently lost in primary esophageal squamous cell carcinoma(ESCC). In the progression of non-small-cell lung cancer (NSCLC), PARD-3 has also been verified to contribute to EMT, invasion, and chemoresistance in NSCLC. The effect of PARD-3 expression on adult B-cell acute lymphoblastic leukemia (ALL) has not been identified.
Aims
The purpose of this study was to investigate the transcriptional level of PARD-3 in adult B cell acute lymphoblastic leukemia.
Methods
A real-time quantitative reverse transcription-polymerase chain reaction assay based on Taq-Man fluorescence methodology was used to quantify the PARD-3 mRNA copy number in the bone marrow cells from patients with adult leukemia. Normal marrow samples from the allogeneic stem cell transplantation donors were served as control. Informed consent was obtained for every marrow sample.
Results
Expression levels of the PARD-3 in leukemia patients and normal donor marrow are shown in Figure 1. These results showed that the relative levels of PARD-3 gene expression in marrow from 32 newly diagnosed B-cell ALL (median 92.84%; range 0.002%~316.201%) was significantly higher than those of marrow from the 20 healthy donors (median 13.74%; range 2.93%~41.15%; P=0.004). Significant PARD-3 mRNA over expression was found in the de novo B-cell ALL patients compared with 32 treated B-cell ALL patients (median 10.46%; range 0.415%~64.489%) who achieved complete remission or 32 de novo AML (median 11.638%; range 0.021%~114.169%; P<0.0001). The expression levels of PARD-3 was higher in 6 refractory/relapsed B-cell ALL patients (median 110.315%; range 1.276%~499.772%) than that of newly diagnosed B-cell ALL, but no statistical significant difference was observed (P=0.72). Besides, no statistical significant difference was observed in 32 newly diagnosed AML (median 11.638%, range 0.021%~114.169%) and 20 healthy donors (P=0.72), but it was higher in BALL-1 and NALM6 cells from B cell ALL cell lines than in other cells from AML cell lines (Figure 1).
Conclusion
These observations suggest that PARD-3 is overexpressed in B-cell acute lymphoblastic leukemia and may play a role in the pathogenesis of B-cell acute lymphoblastic leukemia.
Session topic: 1. Acute lymphoblastic leukemia – Biology & Translational Research
Keyword(s): Acute lymphoblastic leukemia, PCR