Results of chemical pleurodesis with mitoxantrone in malignant pleural effusion from breast cancer

Barbetakis, Nikolaos; Antoniadis, Theodoros; Tsilikas, Christodoulos

doi:10.1186/1477-7819-2-16

Cited by 23 publications

(4 citation statements)

References 38 publications

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“…Advanced breast cancer metastasized to the pleural cavity is associated with poor prognosis [2,4,40,41]. In the present study, all but one patient developed recurrent malignant pleural effusions despite multimodal therapy and died within a mean time of 3 months (range, 3 weeks to 9 months).…”

Section: Discussionmentioning

confidence: 47%

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Lysis of cancer cells by autologous T cells in breast cancer pleural effusates treated with anti-EpCAM BiTE antibody MT110

Witthauer

Schlereth

Brischwein

et al. 2008

Breast Cancer Res Treat

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In the present study, the efficacy of a new drug, i.e. the bispecific single-chain antibody MT110 targeting the epithelial antigen EpCAM and the T-cell antigen CD3 was tested ex vivo in malignant pleural effusions (MPEs). EpCAM ? epithelial cells were found in 78% of the MPEs (n = 18). Ex vivo treatment of seven MPEs resulted in a dose-dependent specific lysis of 37 ± 27% (±SD) EpCAM ? cells with 10 ng/ml (P = 0.03) and 57 ± 29.5% EpCAM ? cells with 1,000 ng/ml MT110 (P = 0.016) after 72 h. As a prerequisite for redirected lysis, stimulation of he autologous CD4 ? and CD8 ? cells in MPE by 1,000 ng/ml MT110 resulted in 21 ± 17% CD4 ? /CD25 ? and 29.4 ± 22% CD8 ? /CD25 ? cells (P = 0.016, respectively) after 72 h. This was confirmed by a 22-fold release of TNF-a and 230-fold release of IFN-c (1,000 ng/ml, 48 h, P = 0.03, respectively). Thus, relapsed breast cancer patients resistant to standard treatment might benefit from targeted therapy using MT110.Keywords Malignant pleural effusion Á Breast cancer Á Bispecific antibody Á EpCAM Á CD3 Á MT110 Á Ex vivo therapy

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Section: Discussionmentioning

confidence: 47%

“…One of the standard therapeutic strategies to prevent recurrent MPE is chemical pleurodesis using talcum. However, despite therapeutic intervention, recurrence rate is high and prognosis remains poor [3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Lysis of cancer cells by autologous T cells in breast cancer pleural effusates treated with anti-EpCAM BiTE antibody MT110

Witthauer

Schlereth

Brischwein

et al. 2008

Breast Cancer Res Treat

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“…In addition radioactive isotopes, corynebacterium parvum, interferon and recombinant interleukin-2 have been instilled in the pleural space for treatment of malignant pleural effusions. Response rate has been variable and less than optimal [ 5 ].…”

Section: Discussionmentioning

confidence: 99%

Early and late morbidity and mortality and life expectancy following thoracoscopic talc insufflation for control of malignant pleural effusions: a review of 400 cases

Barbetakis

Asteriou

Papadopoulou

et al. 2010

J Cardiothorac Surg

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BackgroundMalignant pleural effusion is a common sequelae in patients with certain malignancies. It represents a terminal condition with short median survival (in terms of months) and the goal is palliation. Aim of our study is to analyze morbidity, mortality and life expectancy following videothoracoscopic talc poudrage.Materials and methodsFrom September 2004 to October 2009, 400 patients underwent video-assisted thoracic surgery (VATS) for malignant pleural effusion. The conditions of patients were assessed and graded before and after treatment concerning morbidity, mortality, success rate of pleurodesis and median survival.ResultsThe median duration of follow up was 40 months (range 4-61 months). All patients demonstrated notable improvement in dyspnea. Intraoperative mortality was zero. The procedure was well tolerated and no significant adverse effects were observed. In hospital mortality was 2% and the pleurodesis success rate was 85%. A poor Karnofsky Performance Status and delay between diagnosis of pleural effusion and pleurodesis were statistically significant factors for in-hospital mortality. The best survival was seen in breast cancer, followed by ovarian cancer, lymphoma and pleural mesothelioma.ConclusionsVideo-assisted thoracoscopic talc poudrage is an effective and safe procedure that yields a high rate of successful pleurodesis and achieves long-term control with marked dyspnea decrease.

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“…These include both mechanical abrasion (first performed by an American surgeon, Edward Delos Churchill in 1941 [29]) and different chemical sclerosants, i.e. antibiotics (tetracycline [30], erythromycin [31], minocycline [32], doxycycline [33]), antiseptics (silver nitrate [34], iodopovidone [35]), cytostatic agents (mitomycin C [36], bleomycin [37], cytarabine [38], doxorubicin [39], etoposide [40], mitoxantrone [41], nitrogen mustard [42]), radioactive colloidal gold [43], quinacrine [44], transforming growth factor β (TGF-β) [45], autologic blood [46], lipoteichoic acid-T [47] or even bacteria ( Corynebacterium parvum [48] , Streptococcus pyogenes A3 (OK-432) [39]. The search for the ideal sclerosing agent is still ongoing.…”

Section: History Agents and Basic Mechanisms Involved In Chemical Plmentioning

confidence: 99%

Chemical pleurodesis – a review of mechanisms involved in pleural space obliteration

et al. 2019

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Chemical pleurodesis is a therapeutic procedure applied to create the symphysis between the parietal and visceral pleura by intrapleural administration of various chemical agents (e.g. talk, tetracycline, iodopovidone, etc.). The two major clinical conditions treated with chemical pleurodesis are recurrent pleural effusion (PE) and recurrent spontaneous pneumothorax. Although the history of chemical pleurodesis began over a century ago, detailed data on the mechanisms of action of sclerosing agents are highly incomplete. The following article aims to present the state of knowledge on this subject.It is believed that mesothelial cells are the main structural axis of pleurodesis. In response to sclerosing agents they secrete a variety of mediators including chemokines such as interleukin 8 (IL-8) and monocyte chemoattractant protein (MCP-1), as well as growth factors - vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), basic fibroblast growth factor (bFGF) and transforming growth factor- β (TGF-β). Numerous data suggest that intact mesothelial cells and the above cytokines play a crucial role in the initiation and maintenance of different pathways of pleural inflammation and pleural space obliteration.It seems that the process of pleurodesis is largely nonspecific to the sclerosant and involves the same ultimate pathways including activation of pleural cells, coagulation cascade, fibrin chain formation, fibroblast proliferation and production of collagen and extracellular matrix components. Of these processes, the coagulation cascade with decreased fibrinolytic activity and increased fibrinogenesis probably plays a pivotal role, at least during the early response to sclerosant administration.A better understanding of various pathways involved in pleurodesis may be a prerequisite for more effective and safe use of various sclerosants and for the development of new, perhaps more personalized therapeutic approaches.

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Results of chemical pleurodesis with mitoxantrone in malignant pleural effusion from breast cancer

Abstract: Background: Carcinoma of the breast is the second leading cause of malignant pleural effusions. This study reports on the efficacy of mitoxantrone as a sclerosing agent in patients with breast cancer who had a pleural effusion as a direct consequence of metastatic disease.

Cited by 23 publications

References 38 publications

Lysis of cancer cells by autologous T cells in breast cancer pleural effusates treated with anti-EpCAM BiTE antibody MT110

Lysis of cancer cells by autologous T cells in breast cancer pleural effusates treated with anti-EpCAM BiTE antibody MT110

Early and late morbidity and mortality and life expectancy following thoracoscopic talc insufflation for control of malignant pleural effusions: a review of 400 cases

Chemical pleurodesis – a review of mechanisms involved in pleural space obliteration

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