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1.
Chinese Journal of Cancer Biotherapy ; (6): 1026-1033, 2018.
Artigo em Chinês | WPRIM | ID: wpr-801677

RESUMO

@# Objective: The present study was aimed to explore the role and distinctive mechanism of SPIDR, the key regulatory protein of homologous recombination pathway, in progression of small cell lung cancer (SCLC). Methods: 60 SCLC specimens and 44 normal lung tissues were collected from the patients undergoing tumor resection and bronchoscopic puncture in Shanghai Pulmonary Hospital Affiliated to Tongji University from January 2013 to January 2015. The expression of SPIDR in clinical samples and NCIH446 (SCLC cell line) and MRC-5 (normal cell line) were assayed by Real-time PCR. The role of SPIDR in SCLC was investigated in vivo and in vitro by the expression of SPIDR were artificially modified in NCI-H446. Results: Smoking was significantly associated with the occurrence of SCLC (P<0.01). The expression of SPIDR mRNAin SCLC tissues was lower than that of normal lung tissues (P <0.01), and the SPIDR transcriptional and translational levels of NCI-H446 cells were also lower than that of MRC-5.Although there is no significant changes of cell growth rate and susceptibility to cisplatin and etoposide in the NCI-H446 cells overexpressing SPIDR. However, the volume of xenograft tumors of overexpressed SPIDR group decreased by 58.99% (P<0.01) and 61.84% (P<0.01) than that of the original NCI-H446 cells and the NCI-H446 cells transfected with vector (pMSCV) and the average tumor mass decreased by 61.70% (P<0.01) and 70.25% (P<0.01) respectively. When the fetal bovine serum content in the medium was reduced to 3%, the growth rate of NCI-H446 cells overexpressing SPIDR was 22.33% (P<0.01) and 20.24% (P<0.05) lower than that of the original NCIH446 cells and control group, the similar results were obtained from the 1% serum concentration experiment as well. Conclusion: The expression of SPIDR, the key regulatory protein in the DNAdouble strand break homologous recombination repair pathway, was significantly suppressed in SCLC tissues, which markedly accelerated the growth of NCI-H446 cells in vivo and reduced the reliance of NCIH446 cells to the serum. The detailed mechanism is worthy of further investigation.

2.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 717-720, 2011.
Artigo em Chinês | WPRIM | ID: wpr-248596

RESUMO

The purpose of this paper was to evaluate the relationship between the thrombosis and secretory duct dilation,lesion size,clinical types,nature (primary or recurrent) and duration of illness in the development of ranula.A total of 229 cases of sublingual gland cysts were treated with surgical resection from Jan.1990 to Feb.2010.The patients' data were investigated on histopathological findings,size of ranula,the clinical types,nature of ranula (primary or recurrent) and duration of illness.Sections from the paraffin-embeded blocks were HE-stained.CK expression was immunohistochemically detected.Among 229 cases the incidence of venous thrombosis was 58.52%.The incidence of venous thrombosis with or without duct dilation was 73.25% and 26.39% respectively,with a significant difference between the two groups (P<0.005).The incidence of venous thrombosis of ranulas with diameter larger or less than 3 cm was 72.22% and 46.28% (P<0.005).The incidence of venous thrombosis of oral ranula,plunging ranula and mixed ranula was 49.37%,77.19% and 85.71% respectively,with a significant difference found between oral and plunging or mixed ranula (P<0.01).The incidence of venous thrombosis in ranula patients with duration of illness longer or less than 3 months was 69.77% and 51.75% (P<0.01).The incidence of venous thrombosis with recurrent and primary ranulas was 51.85% and 64.85%,without a significant difference noted between them (P>0.05).It is concluded that the formation of venous thrombosis was related to the dilation of secretory duct,lesion size,clinical types,duration of lesion but formation of venous thrombosis was not related to the nature (primary or recurrent) of ranulas.

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