Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026986 (myelodysplastic syndrome)
 14,926 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We established a nested case-control study cohort of myelodysplastic syndrome patients (n = 435). And 41 patients had conditions progressing to leukemia (case group = 41), 342 patients had no leukemic transformation (control group = 342), and 52 patients died. Bone marrow mononuclear cell of the patients in the case group and after the evolution were analyzed for the gene expression microarray test (self-control study), whereas the bone marrow mononuclear cell of the paired patients extracted at diagnosis were analyzed for the gene expression microarray test (case-control study). By incorporating the results of above two studies, we identified the genes related to the transformation of myelodysplastic syndrome to acute leukemia. A total of 958 deregulated genes were identified via bioinformatics analysis. Further analyses identified a subset of six genes that help distinguish between the case and control groups. These genes are TUBB, PSMD1, SLC7A5, ATG3, TUBB2C, and TIMM10. The combined gene expression microarray test and nested case-control study method identified a subset of six genes that help distinguish between the case and control groups. The six genes may play critical roles in the evolution of myelodysplastic syndrome to acute leukemia.
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PMID:Prospective nested case-control study of feature genes related to leukemic evolution of myelodysplastic syndrome. 2306 73

Based on the nested case-control study cohort and gene expression profile, we have picked up a subset of six genes to distinguish the leukemia group and control group stably. ATG3 is the only down regulated gene. This research is to investigate the effect of ATG3 gene over expression by lentivirus on SKM-1 cell line and myelodysplastic syndrome to leukemic transformation. Human SKM-1 cells were transfected with ATG3-GFP recombinant lentiviral vectors and compared with cells transfected with GFP lentiviral vectors. Western blot was performed to detect the ATG3 protein. Cell proliferation was assessed by cell counting kit-8. Cell vitality was tested by Trypan Blue. Cell apoptosis was determined by Annexin V Apoptosis Detection Kit APC. Observe and compare the changes on growth curve, cell vitality and cell apoptosis. After 72 h of transfection, satisfactory transfection efficiency (> 90 %) was observed. SKM-1 cell line showed a statistically significant (P < 0.05) overexpression of ATG3, parallel to significantly (P < 0.05) inhibited cell proliferation. The cell vitality of ATG3 overexpression was significantly (P < 0.05) lower than negative control. Cell apoptosis analysis by flow cytometer demonstrated decreased proportion of early apoptosis and increased that of late apoptosis and death (P < 0.05). Over expressed ATG3 gene and protein, the SKM-1 cell line was inhibited in proliferation and cell vitality. It was promoted from early apoptosis to late apoptosis and death. The malignancy of SKM-1 cell line was decreased after transfection. ATG3 gene and its gene family may play an important role in transformation of myelodysplastic syndrome.
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PMID:Lentiviral vector-mediate ATG3 overexpression inhibits growth and promotes apoptosis of human SKM-1 cells. 2442 Aug 57