Small Cell Lung Cancer

Small-cell lung cancer

Small cell lung cancer (SCLC) accounts for about 13 % of all lung cancer cases, with about 29,000 new cases diagnosed annually in the USA [1]. The incidence of SCLC is declining, due in part to decreased smoking rates, increased use of filtered cigarettes, and changes in pathologic criteria for classifying SCLC [2].

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Small cell lung cancer.

Management of Small Cell Lung Cancer: ACCP Evidence-Based Clinical Practice Guidelines (2nd Edition)

PURPOSETo determine the response rate, survival, and toxicity of irinotecan (CPT-11), a topoisomerase I inhibitor, combined with etoposide, a topoisomerase II inhibitor, in refractory or relapsed small-cell lung cancer (SCLC).PATIENTS AND METHODSTwenty-five patients with refractory or relapsed SCLC were entered onto the trial. All 25 patients had been pretreated with some form of cisplatin-based combination chemotherapy and had also received previous etoposide- or anthracyclinecontaining chemotherapy. The median time off chemotherapy was 6.7 months (range, 0.9 to 23.5). Patients were treated at 4-week intervals using CPT-11 (a starting dose of 70 mg/m2 intravenously on days 1, 8, and 15) plus etoposide (80 mg/m2 intravenously on days 1 to 3), with a subsequent dose based on toxicity. In addition, recombinant human granulocyte colony-stimulating factor (rhG-CSF; 2 microg/kg/d) was given from day 4 to day 21, except on the days of CPT-11 administration.RESULTSAll patients were assessable for toxicity and su...

Combination of irinotecan and etoposide for treatment of refractory or relapsed small-cell lung cancer.

Successful treatment of primary pulmonary angiosarcoma.

To assess the effect and toxicity of hypotonic cisplatin treatment (HPT) consisting of the intrapleural administration of cisplatin in distilled water for malignant pleural effusion in patients with non-small-cell lung cancer (NSCLC). Non-small-cell lung cancer patients with cytologically proven and previously untreated malignant pleural effusion were enrolled into this study. Firstly, the lung was fully re-expanded by a tube thoracostomy, and then 25 mg cisplatin in 500 ml of distilled water was instilled through a chest tube and then the tube was clamped. After 1 h, the tube was declamped and allowed to drain. The chest tube was removed when the pleural effusion volume decreased to 200 ml or less per day. A complete response (CR) was considered to occur when the pleural effusion disappeared. A partial response (PR) was determined to occur when the volume of pleural effusion remained under ¼ of hemithorax. The response at 4 weeks was evaluated by an extramural review. Out of 84 patients enrolled from February 1998 to August 2002, 80 patients were eligible and analysed in the present study. The toxicity of HPT was acceptable. Neither a haematological toxicity of any grade nor grade 4 nonhaematological toxicity was observed. Grade 3 nonhaematological toxicities were observed, including nausea (4%), vomiting (3%), pyothorax (1%) and dyspnoea (1%). The median time of drainage from HTP was 4 days. Twenty-seven (34%) and 39 (49%) patients achieved CR and PR, respectively, for an overall response rate of 83% (95% confidence interval, 74–91%). The median duration of the response was 206 days. The median survival time of all patients was 239 days. Hypotonic cisplatin treatment for malignant pleural effusion of NSCLC is therefore considered to be feasible and effective. A phase III study of HPT is thus warranted.

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Intrapleural hypotonic cisplatin treatment for malignant pleural effusion in 80 patients with non-small-cell lung cancer: a multi-institutional phase II trial.

Aims: We analyzed the association of ABCB1 polymorphisms with erlotinib-induced toxicity and the pharmacokinetics in patients with non-small-cell lung cancer. Materials & methods: After erlotinib 150 mg was administered to 50 patients, ABCB1 polymorphisms were analyzed via either TaqMan® assays or direct nucleotide sequencing. Plasma concentrations were measured by HPLC. Results: The trough concentration at steady state in patients with the ABCB1 1236TT–2677TT–3435TT genotype was higher compared with others groups (p = 0.021) and patients carrying this genotype had a higher risk of developing higher grade 2 toxicity (p = 0.012). Conclusion: The present study suggested that the ABCB1 1236TT–2677TT–3435TT genotype was associated with higher plasma concentration and the risk of developing higher toxicity in patients treated with erlotinib. Original submitted 5 August 2011; Revision submitted 30 November 2011

Association of ABCB1 polymorphisms with erlotinib pharmacokinetics and toxicity in Japanese patients with non-small-cell lung cancer

. Side effects, such as skin rash and diarrhea, are commonly seen at a single dose of 150 mg/day; in extreme cases, these toxicities can lead to discontinuation of therapy. As the severity of skin rash is strongly associated with improved clinical outcome, skin rash may be a surrogate marker for a favorable clinical outcome. The BR 21 study demonstrated a correlation between the development of a higher grade 2 skin rash and efficacy in patients treated with erlotinib

Sunao Ushijima

Papers

Combination of irinotecan and etoposide for treatment of refractory or relapsed small-cell lung cancer.

Successful treatment of primary pulmonary angiosarcoma.

Intrapleural hypotonic cisplatin treatment for malignant pleural effusion in 80 patients with non-small-cell lung cancer: a multi-institutional phase II trial.

Association of ABCB1 polymorphisms with erlotinib pharmacokinetics and toxicity in Japanese patients with non-small-cell lung cancer

Association of ABCB1 polymorphisms with erlotinib pharmacokinetics and toxicity in Japanese