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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prognosis of the lung cancer patients with malignant pleural effusion is extremely poor. Intrapleural perfusion hyperthermo-chemotherapy for the treatment of malignant pleural effusion was performed in 120 lung cancer patients and showed better prognosis than conventional treatment. After successful local control by hyperthermo-chemotherapy, extrapleural pneumonectomy was performed in 8 patients with clinical N 0 or N 1 and M 0 lung cancer. All patients survived for more than 1 year. The only 1 patient survived for more than 3 years and 3 months without recurrence. Almost all patients who died within 2 years had pathological n 2, carcinomatous pericarditis, cancer invasion beyond extrapleural space and so on. Extrapleural pneumonectomy after hyperthermo-chemotherapy can be a choice of surgical treatment if the n 2 disease, pericarditis, and extrapleural invasion of disseminated cancer cells should be excluded precisely.
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PMID:[Extrapleural pneumonectomy after hyperthermo-chemotherapy for the lung cancer patients with malignant pleural effusion]. 1551 Aug 15

Unilateral breast edema usually signifies an underlying pathology of the breast and prompts extensive investigations for the purpose of an early treatment. Although breast edema has been reported with other systemic etiologies, it has not been described in patients with lung cancer. We report two cases of unilateral breast edema occurring in patients with non-small cell lung cancer and ipsilateral pleural effusion. Mammography and ultrasound of the breast both revealed increased interstitial density suggestive of fluid retention without any underlying masses. We performed a therapeutic pleurocentesis on one patient for symptomatic relief, and there was simultaneous improvement of the breast edema. We postulate a possible pathophysiology for the association between breast edema and malignant pleural effusion. The principle of management when one encounters similar cases would be to treat the underlying pleural effusion.
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PMID:Unilateral breast edema in two patients with malignant pleural effusion. 1565 37

We investigated the effectiveness and complications of intrathoracic infusion with a combination of cisplatin, OK-432, and minocycline for malignant pleural effusion. All patients were hospitalized with chest tube drainage of pleural effusion until the daily drainage volume was less than 100 ml. Twenty-five mg of minocycline, 1 to 3 KE of OK-432, and 5 to 10 mg of cisplatin were instilled into the pleural space. The administration was repeated until drainage effusion disappeared. Therapeutic effect was evaluated according to the following criteria: (1) excellent, no fluid reaccumulation for at least 4 weeks as determined by chest radiogram and clinical evaluation; (2) effective, fluid reaccumulation less than 50% of original effusion with no need of thoracentesis for symptomatic relief within 4 weeks after treatment; and (3) failure, reaccumulation of more than 50% of the original effusion requiring thoracentesis to relieve symptoms within 4 weeks of treatment. Twelve patients with malignant effusion received the combination treatment; 11 patients had primary lung cancer and one had metastatic lung tumor from cancer of the rectum. In all cases, the histology or cytology revealed adenocarcinoma. Eleven of the 12 patients had an excellent response with relief of clinical symptoms. The remaining case failed to show any improvement. Complications such as local pain, fever, nausea, and vomiting were mild and transient. We conclude that combination administration of low-dose minocycline, OK-432, and cisplatin into the thoracic cavity for malignant effusion is an effective alternative treatment with the potential for improvement of the general condition and reduced morbidity.
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PMID:[Intrathoracic infusion with a combination of low-dose minocycline, OK-432 and cisplatin for malignant pleural effusion]. 1579 17

The aim of this study was to explore the presence of interleukin (IL)-16 in pleural effusions, the correlation between IL-16 levels and cytological parameters, as well as the chemoattractant activity of IL-16 on CD4+ T-lymphocytes. Total nucleated cell and differential counts, and IL-16 concentrations in the pleural effusion from 32 patients with tuberculous pleurisy and 30 patients with lung cancer were determined. Three-colour flow cytometry was performed to determine T-lymphocyte subsets in cell pellets of pleural effusion. The chemoattractant activity of IL-16 for CD4+ T-lymphocytes was also analysed. The levels of IL-16 were significantly higher in tuberculous than in malignant effusions. However, IL-16 levels could not be used for diagnostic purposes due to significant overlap between the two groups. Positive correlations were found between the IL-16 levels and CD4+ T-cells, and pleural fluid was chemotactic for CD4+ T-cells in vitro. Intrapleural administration of IL-16 to patients produced a marked progressive influx of CD4+ T-cells into the pleural space. Compared with malignant pleural effusion, interleukin-16 appeared to be increased in tuberculous pleural effusion. Interleukin-16 levels were positively related to the numbers of CD4+ T-cells, and interleukin-16 could directly induce CD4+ T-cell infiltration into the pleural space.
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PMID:Interleukin-16 in tuberculous and malignant pleural effusions. 1580 32

EGFR mutations have been shown to correlate with the clinical responsiveness to epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI). The detection of EGFR mutations in non-small cell lung cancer (NSCLC) is important from the perspective of targeted anticancer therapy. We report the first case showing that the status of EGFR mutations can be successfully determined in malignant pleural effusion of NSCLC using polymerase chain reaction (PCR) technique, and correlated to the clinical responsiveness to gefitinib, an EGFR-TKI. This case demonstrated the importance of molecular cytology in the era of targeted therapy.
Lung Cancer 2005 Sep
PMID:EGFR mutations in malignant pleural effusion of non-small cell lung cancer: a case report. 1591 41

Malignant pleural effusion is typical of complications in advanced lung cancer patients, most of whom complain of dyspnea. The standard treatment for symptomatic pleural effusion is intrapleural administration of a chemical agent. In Japan, OK-432, a streptococcal preparation, and cisplatin (CDDP) have been among the most frequently used chemical agents. There have been very few reports on the efficacy of chemical agents for malignant pleural effusion. We compared therapeutic efficacy and toxicity of intrapleural OK-432 with CDDP in a case-control study. The subjects consisted of 32 lung cancer patients with malignant pleural effusion who were admitted to our hospital between January 2000 and June 2004. The therapeutic efficacy was assessed from duration of chest drainage after intrapleural administration, response rate, time to progression of malignant pleural effusion, and survival time. No statistically significant difference was observed for therapeutic efficacy. Although the OK-432-treated group had only grade 1 fever, chest pain, nausea, the CDDP-treated group had a grade 2 increase in creatinine and grade 3 nausea. Intrapleural OK-432 seemed to be better tolerated in the treatment of malignant pleural effusion than intrapleural CDDP.
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PMID:[Comparison of intrapleural OK-432 and cisplatin for malignant pleural effusion in lung cancer patients]. 1612 16

We developed a novel mouse model of malignant pleural effusion (MPE) by injecting Lewis lung cancer (LLC) cells directly into the pleural space of syngeneic C57B/6 mice. The pleural effusions in this model share common cellular and biochemical features with human MPEs. Implantation and growth of pleural tumors triggers a host inflammatory response characterized by a mixed inflammatory cell influx into the pleural fluid. LLC cells exhibited high basal nuclear factor (NF)-kappaB activity in vitro and in vivo, which we used to drive expression of a NF-kappaB-dependent green fluorescent protein-firefly luciferase fusion reporter construct. NF-kappaB-dependent reporter expression allowed intravital tracing of pleural tumors. Inhibition of NF-kappaB in LLC cells did not affect cell viability in culture; however, injection of LLC cells expressing a dominant NF-kappaB inhibitor resulted in decreased tumor burden, decreased pleural effusion volume, and decreased pleural effusion TNF-alpha levels. These studies indicate that tumor NF-kappaB activity regulates pleural tumor progression. This reproducible model of MPE can be used to further study the influence of specific host and tumor factors on the pathogenesis of MPE and evaluate new therapeutic strategies.
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PMID:Nuclear factor-kappaB affects tumor progression in a mouse model of malignant pleural effusion. 1621 Jun 94

Malignant pleural effusion of lung cancer is an important prognostic factor, even in minor effusions. Previous studies reported that cytological examination could not detect malignant cells in pleural dissemination cases. Therefore, we used real-time PCR as a more sensitive test to detect malignant cells. The subjects were selected from 132 primary lung cancer patients and 8 benign tumor patients as negative control. These subjects had no apparent pleural effusion or distant metastasis. All subjects were negative on cytological examination and without exfoliation evidence. The follow-up duration was 18.1 +/- 7.1 months (mean +/- SD). In the real-time PCR, the CEA-mRNA and GAPDH-mRNA parameters were measured simultaneously, and the CEA-mRNA ratio was obtained as normalized values of CEA-mRNA divided by GAPDH-mRNA. The CEA-mRNA ratio in our study was correlated with lymph node metastasis (N-factor: p = 0.0948) and lymphatic invasion (Ly-factor: p = 0.0520). Using a proportional hazard model, with recurrence or death as terminal point, the CEA-mRNA ratio affected the recurrence risk by 1.920 (95% CI: 1.104-3.340) in Stage 1a. Using log rank testing, we found significant differences in the recurrence rate between the CEA-mRNA-positive and -negative cases (p = 0.0039) at cut-off point 0.1.
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PMID:Clinical usefulness of CEA-mRNA determination in minor effusion. 1627 May 29

Malignant pleural effusion (MPE) is a poor prognostic sign for patients with non-small-cell lung cancer (NSCLC). The generation of MPE is largely regulated by vascular endothelial growth factor (VEGF), and upregulation of VEGF by Stat3 has been observed in several types of tumor cells. In this study, we demonstrate constitutively activated Stat3 in several human lung cancer cell lines and in tumor cells infiltrated in the pleurae of patients with adenocarcinoma cell lung cancer (ADCLC) and MPE. The observations suggest that activated Stat3 plays a role in the pathogenesis of ADCLC. In PC14PE6/AS2 cells, a Stat3-positive human ADCLC cell line, autocrine IL-6 activated Stat3 via JAKs, not via Src kinase. PC14PE6/AS2 cells express higher VEGF mRNA and protein than do Stat3-negative PC14PE6/AS2/dnStat3 cells. In an animal model, PC14P6/AS2/dnStat3 cells produced no MPE and less lung metastasis than did PC14P6/AS2 cells. PC14PE6/AS2 cells also expressed higher VEGF protein, microvessel density, and vascular permeability in tumors than did PC14P6/AS2/dnStat3 cells. Therefore, we hypothesize that autocrine IL-6 activation of Stat3 in ADCLC may be involved in the formation of malignant pleural effusion by upregulating VEGF. Higher levels of IL-6 and VEGF were also found in the pleural fluids of patients with ADCLC than in patients with congestive heart failure. The autocrine IL-6/Stat3/VEGF signaling pathway may also be activated in patients with ADCLC and MPE. These findings provide novel targets for the management of MPE.
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PMID:Autocrine IL-6-induced Stat3 activation contributes to the pathogenesis of lung adenocarcinoma and malignant pleural effusion. 1651 8

Malignant pleural effusion is a common and debilitating complication of advanced malignant diseases. This problem seems to affect particularly those with lung and breast cancer, contributing to the poor quality of life. Approximately half of all patients with metastatic cancer develop a malignant pleural effusion at some point, which is likely to cause significant symptoms such as dyspnea and cough. Evacuation of the pleural fluid and prevention of its re-accumulation are the main goals of management. Optimal treatment is controversial and there is no universally standard approach. Intervention options range from observation in the case of asymptomatic effusions through simple thoracentesis to more invasive methods such as chemical and mechanical pleurodesis, pleur-X catheter drainage, pleuroperitoneal shunting, and pleurectomy. The best results are reported with thoracoscopy and talc insufflation, with an acceptable morbidity. Development of novel methods to control malignant pleural effusion should be a high priority in palliative care of cancer patients. This article reviews the current, as well as, novel approaches that show some promise for the future. The aim is to identify the proper approach for each individual patient.
Lung Cancer 2006 Oct
PMID:Malignant pleural effusion, current and evolving approaches for its diagnosis and management. 1711 89


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