Therapeutic effects of recombinant human endostatin adenovirus in a mouse model of malignant pleural effusion

Fang, Fang; Chen, Ping; Wu, Xin; Yang, Li; Yang, Xun; Xi, Zhen; Zhou, Bin; Zhou, Xi Kun; Qian, Zhi; Bo, Xiaochen; Wei, Yu Quan

doi:10.1007/s00432-009-0555-y

Cited by 10 publications

(13 citation statements)

References 41 publications

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“…Moreover, inhibition of multiple tumor-to-host signalling events in mouse models of MPE resulted in dramatic reductions in pleural fluid accumulation without affecting tumor growth [51][52][53][54][55] . To date…”

Section: Medical Regulation Of Pleural Fluid Formationmentioning

confidence: 99%

Translational Research in Pleural Infection and Beyond

Lee

Idell

Stathopoulos

2016

Chest

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The incidence of pleural infection has been rising in recent years. Intrapleural therapy with tissue plasminogen activator (tPA) and deoxyribonuclease (DNase) has significantly reduced the need for surgery, and its impact on clinical care is rising worldwide. Efforts are underway to optimize the delivery regimen and establish the short and longer term effects of this therapy. The complex interactions of bacterial infection within the pleura with inflammatory responses and clinical interventions (antibiotics and tPA/DNase or other fibrinolysins) require further studies to improve future treatment options. Intrapleural instillation of tPA potently induces pleural fluid formation, principally via a monocyte chemotactic protein (MCP)-1 dependent mechanism. Activation of transcriptional programs in pleural resident cells and infiltrating cells during pleural infection and malignancy results in the local secretion of a cocktail of proinflammatory signaling molecules (including MCP-1) within the pleural confines that contributes to effusion formation. Understanding the biology of these molecules and their interaction may provide novel targets for pleural fluid control.

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Section: Medical Regulation Of Pleural Fluid Formationmentioning

confidence: 99%

Translational Research in Pleural Infection and Beyond

Lee

Idell

Stathopoulos

2016

Chest

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“…Strikingly, most of them were pro-inflammatory molecules, including tumor necrosis factor (TNF), chemokine ligand (CCL)2 and osteopontin (OPN), highlighting the importance of the newly described models (16–19). Vasculature-targeted mediators other than VEGF were next implicated in promoting or halting MPE formation, with examples being angiopoietins and endostatin, respectively (20–22).…”

Section: Pleural Tumors As Mpe-driving Forcesmentioning

confidence: 99%

Malignant Pleural Effusion

Stathopoulos

Kalomenidis

2012

Am J Respir Crit Care Med

152

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Malignant pleural effusion (MPE) poses a significant clinical problem. Current non-etiologic management is suboptimal in terms of efficacy and safety. In light of recent research progress, we propose herein a new view of MPE development, which may rapidly translate into meaningful changes in therapeutics. In addition to tumor-induced impairment of pleural fluid drainage, pertinent findings point towards another pathway to MPE formation: a vicious loop of interactions between pleural-based tumor cells and the host vasculature and immune system that results in increased net fluid production via enhanced plasma extravasation into the pleural space. The ability of tumor cells to trigger this cascade likely rests on a specific and distinct transcriptional repertoire, which results in important vasoactive events in the pleural space. While the characterization of tumor-derived factors responsible for MPE development is in the making, an additional, indirect path to MPE was recently demonstrated: tumor cells recruit and co-opt host cells and mediators, which in turn, amplify tumor cell-primed fluid leakage and impact tumor cell functions. Importantly, recent evidence suggests that the biologic events that culminate in clinical MPE are likely amenable to therapeutic inhibition and even prevention. In this perspective, the scientific basis for an update of current concepts of MPE formation is highlighted. Key questions for future research are posed. Finally, a vision for novel, effective, safe and convenient treatment modalities that can be offered to outpatients with MPE is set forth.

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“…These mice underwent in vivo bioluminescence imaging weekly. One week after NUGC-4-Luc cell injection, mice were randomly divided into four groups with seven mice each and were injected intraperitoneally with the following: group 1, cisplatin (purchased from QiLu Pharmaceutical Co., Shandong, China; 1 mg/kg) at days 1–3 + endostar (purchased from Simcere Pharmaceutical Co., Jiangsu, China; 8 mg/kg) at days 4–7; group 2, endostar (8 mg/kg) at days 1–4 + cisplatin (1 mg/kg) at days 5–7; group 3, endostar (8 mg/kg) + cisplatin (1 mg/kg) at days 1, 4 and 7; group 4 (control group), 50 μ L of normal saline at days 1–7 [ 10 , 22 ]. Each group was treated for two consecutive weeks and underwent imaging weekly.…”

Section: Methodsmentioning

confidence: 99%

Effects of Combined Simultaneous and Sequential Endostar and Cisplatin Treatment in a Mice Model of Gastric Cancer Peritoneal Metastases

Jia

Ren

et al. 2017

Gastroenterology Research and Practice

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Objective. Aimed to study the effects of endostar and cisplatin using an in vivo imaging system (IVIS) in a model of peritoneal metastasis of gastric cancer. Methods. NUGC-4 gastric cancer cells transfected with luciferase gene (NUGC-4-Luc) were injected i.p. into nude mice. One week later, mice were randomly injected i.p.: group 1, cisplatin (d1–3) + endostar (d4–7); group 2, endostar (d1–4) + cisplatin (d5–7); group 3, endostar + cisplatin d1, 4, and 7; group 4, saline for two weeks. One week after the final administration, mice were sacrificed. Bioluminescent data, microvessel density (MVD), and lymphatic vessel density (LVD) were analyzed. Results. Among the four groups, there were no significant differences in the weights and in the number of cancer cell photons on days 1 and 8 (P > 0.05). On day 15, the numbers in groups 3 and 1 were less than that in group 2 (P < 0.05). On day 21, group 3 was significantly less than group 2 (P < 0.05). MVD of group 4 was less than that of groups 1 and 2 (P < 0.01). There was no significant difference between groups 2 and 3 (P > 0.05) or in LVD number among the four groups (P > 0.05). Conclusions. IVIS® was more useful than weight, volume of ascites, and number of peritoneal nodules. The simultaneous group was superior to sequential groups in killing cancer cells and inhibiting vascular endothelium. Cisplatin-endostar was superior to endostar-cisplatin in killing cancer cells, while the latter in inhibiting peritoneal vascular endothelium.

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Therapeutic effects of recombinant human endostatin adenovirus in a mouse model of malignant pleural effusion

Abstract: Our work provides a rationale for future studies toward evaluating the effectiveness of the adenovirus-based endostatin therapy for MPE.

Cited by 10 publications

References 41 publications

Translational Research in Pleural Infection and Beyond

Translational Research in Pleural Infection and Beyond

Malignant Pleural Effusion

Effects of Combined Simultaneous and Sequential Endostar and Cisplatin Treatment in a Mice Model of Gastric Cancer Peritoneal Metastases

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