Placental ABCA1 Expression Is Increased in Spontaneous Preterm Deliveries Compared with Iatrogenic Preterm Deliveries and Term Deliveries.

OBJECTIVE: Abnormal expression of ABCA1 and ABCG1 in the placenta can elicit lipid metabolism disorder and adverse pregnancy outcomes. However, whether it is associated with preterm delivery remains unclear. Our present study aimed to evaluate the relationship between abnormal expression of ABCA1 or ABCG1 and preterm delivery. METHODS: Maternal blood and placental tissues from women with spontaneous deliveries (SPD), iatrogenic deliveries (IPD), and term deliveries (TD) were collected. The lipid content and expression of ABCA1 and ABCG1 were subsequently measured. RESULTS: Compared with IPD and TD groups, the HDL, TD, LDL, and TC levels were lower in the maternal blood but higher (except TC) in the cord blood of the SPD group. The extracellular lipid content in the placentas of the SPD group was also notably lower relative to the IPD and TD groups. Moreover, the protein and mRNA expressions of ABCA1 in the placentas of the SPD group were significantly higher compared with the IPD and TD groups; however, there was no obvious difference among the three groups in the protein and mRNA expressions of ABCG1. CONCLUSIONS: Abnormal expression of ABCA1 may be associated with the dysregulation of placental lipid metabolism and the occurrence or development of SPD.

E-26 Transformation-specific Related Gene Expression and Outcomes in Cytogenetically Normal Acute Myeloid Leukemia: A Meta-analysis / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>The E-26 transformation-specific related gene (ERG) is frequently expressed in cytogenetically normal acute myeloid leukemia (CN-AML). Herein, we performed a meta-analysis to investigate the relationship between the prognostic significance of ERG expression and CN-AML.</p><p><b>METHODS</b>A systematic review of PubMed database and other search engines were used to identify the studies between January 2005 and November 2016. A total of 667 CN-AML patients were collected from seven published studies. Of the 667 patients underwent intensive chemotherapy, 429 had low expression of ERG and 238 had high expression of ERG. Summary odds ratio (OR) and the 95% confidence interval (CI) for the ERG expression and CN-AML were calculated using fixed- or random-effects models. Heterogeneity was assessed using Chi-squared-based Q- statistic test and I2 statistics. All statistical analyses were performed using R.3.3.1 software packages (R Foundation for Statistical Computing, Vienna, Austria) and RevMan5.3 (Cochrane Collaboration, Copenhagen, Denmark).</p><p><b>RESULTS</b>Overall, patients with high ERG expression had a worse relapse (OR = 2.5127, 95% CI: 1.5177-4.1601, P = 0.0003) and lower complete remission (OR = 0. 3495, 95% CI: 0.2418-0.5051, P< 0.0001). With regard to the known molecular markers, both internal tandem duplications of the fms-related tyrosine kinase 3 gene (OR = 3.8634, 95% CI: 1.8285-8.1626, P = 0.004) and brain and acute leukemia, cytoplasmic (OR = 3.1538, 95% CI: 2.0537-4.8432, P< 0.0001) were associated with the ERG expression. In addition, the results showed a statistical significance between French-American-British (FAB) classification subtype (minimally differentiated AML and AML without maturation, OR = 4.7902, 95% CI: 2.7772-8.2624, P< 0.0001; acute monocytic leukemia, OR = 0.2324, 95% CI: 0.0899-0.6006, P = 0.0026) and ERG expression.</p><p><b>CONCLUSION</b>High ERG expression might be used as a strong adverse prognostic factor in CN-AML.</p>

Establishment and pathologic analysis of imatinib-resistant gastrointestinal stromal tumor xenografts / 中华病理学杂志

<p><b>OBJECTIVE</b>To establish and characterize imatinib-resistant gastrointestinal stromal tumor (GIST) xenografts. Further provided an ideal experimental platform through the imatinib-resistant GIST xenografts to investigate the mechanism of resistance to imatinib.</p><p><b>METHODS</b>Imatinib-resistant GIST cells were injected under the skin of athymic nude mice to establish animal models of human imatinib-resistant GIST. The molecular and histopathologic features of GIST xenografts were also analysed and compared with their counterpart of cell lines.</p><p><b>RESULTS</b>The xenograft tumor models had been established by subcutaneously injection of GIST cells into nude mice. Immunohistochemistry results showed CD117 expression was positive in GIST-PR2 xenograft tumor, but negative in GIST-R. In GIST-PR1, tumor areas showing rhabdomyoblastic differentiation were presented next to areas with classic GIST morphology. The rhabdomyoblastic component demonstrated consistently positivity for desmin and myogenin, whereas CD117 was completely negative. The mutation profiles of these xenograft tumors were the same as their counterpart of cell lines.</p><p><b>CONCLUSIONS</b>Human GIST xenografts with mutation in c-kit have been established from imatinib-resistant GIST lines. Those models will enable further studies on mechanisms of resistance, combination therapies and allow testing of novel targeted therapies.</p>