Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149925 (small cell lung cancer)
 6,491 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred and six consecutive small cell lung cancer patients were treated by a combination regimen COMVp (CTX 1,000-1,400 mg IV D 1,8; VCR 1-2 mg IV D 1,8; MTX 20-40 mg IV or IM D 3,5,10,12; VP-16 100 mg IV drip D 3-7; three weeks as a cycle and 2-3 cycles as a course) in our hospital during 1983 to 1984. Among the 95 patients who were evaluated, 10 (10.5%) gave CR, 57 (60%) PR, 19 (20%) no change and 9 (9.5%) progression. The overall response rate was 70.5%. In this paper, factors influencing the response and side effects are also analysed. The data show that COMVp regimen is one of the good front line combination chemotherapy regimens currently available in the management of small cell lung cancer.
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PMID:[COMVp regimen in the treatment of small cell lung cancer--report of 106 patients]. 282 52

Induced hypertension chemotherapy (IHC) using angiotensin II was applied for patients with lung cancer who had not been treated previously, and the results compared with those of preceding conventional chemotherapy as a sequential control. Twenty-nine patients with non-small cell lung cancer (non-SCLC) were treated with MTX and MMC. Response rate among evaluable cases was 23.1% (3/13) for conventional chemotherapy and 18.2% (2/11) for IHC. Twenty-eight patients with small cell lung cancer (SCLC) were treated with VCR, CPA and ACNU. Among evaluable cases, both chemotherapy groups with and without IHC showed the same response rate, 66.7% (8/12). With respect to response rate, there were no differences between conventional chemotherapy and IHC for non-SCLC or SCLC.
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PMID:[Experience with induced hypertension chemotherapy for lung cancer]. 298 59

Phase II-III trials of oral VP 16-213 (VP 16) were conducted in non-Hodgkin lymphoma (NHL) and small cell lung cancer (SCLC). Of 29 heavily pretreated patients (pts) with NHL treated VP 16 at a dose of 200 mg/d days 1-5 q 3w, there were 3 CRs and 6 PRs (CR + PR : 31%) lasting 16 (7-185) weeks. Of 19 pts with NHL in stages III-IV treated by a non-cross alternating regimen consisting of AVCP (ADM, VCR, CPM, PDN)/EMLP (VP 16, MTX, L-ASP PDN), there were 4 CRs (21%) and 14 PRs (74%) lasting a median duration of 4.5 months. A combination consisting of VCR. VP 16 and CPM (VEC) was administered to a total of 29 pts with SCLC. Nine out of 10 pts with LD and 10 out of 19 pts with ED were attained CR after 2 cycles of VEC and subsequent irradiation to primary tumor. A median survival time of CR (LD + ED) exceeded one year while that of PR was 7+ months. These results indicated that oral VP 16 has significant activity for NHL and SCLC and lack of cross resistance to conventional drugs used for NHL.
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PMID:[VP 16-213]. 387 41

Methotrexate (MTX) in high doses (3 to 7.5 g/m2) with leucovorin rescue (HDMTX-LCV) can be delivered on a weekly basis in a setting of proper pharmacologic monitoring. Myelosuppression occurs in 28 per cent of the patients and in 8 per cent of the courses and usually results from delayed MTX excretion secondary to mild reversible nephrotoxicity. The incidence of tumor regression was 50 per cent in head and neck cancer; 59 per cent in non-Hodgkin's lymphoma; 40 per cent in small cell lung cancer; 24 to 50 per cent in breast cancer and 50 per cent in osteogenic carcinoma, for an over-all response rate of 39 per cent (70 of 178) in patients with disseminated cancer. HDMTX-LCV is not recommended for the conventional treatment of metastatic cancer because of the potential for toxicity and the fact that the response rates cited are probably not superior to those which can be achieved by conventional doses of MTX. However, the relative lack of myelosuppression and mucositis, when compared to conventional unrescued MTS, and the achievement of therapeutic concentrations of MTX in the central nervous system with the HDMTX-LCV program have led to its incorporation into clinical trials of combination chemotherapy.
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PMID:High dose methotrexate with leucovorin rescue. Rationale and spectrum of antitumor activity. 696 19

We reviewed recent reports on apoptosis and summarized the presentations at the Shirafu Cancer Symposium, 1993. The study of programmed cell death, apoptosis, has become one of the mainstream in cell biology, particularly in immunology, developmental biology and oncology. To determine whether the apoptotic cell death induced by anti-cancer agents could be inhibited by bcl-2, we established a bcl-2-transfected human small cell lung cancer cell line, SBC-3/Bcl-2. SBC-3/Bcl-2 showed higher resistance to ADM, CPT-11 and MMC compared with the parental line SBC-3. Agarose gel electrophoresis showed typical DNA fragmentation of SBC-3 following treatment with CPT-11 or MMC. In contrast, the same concentration of the drugs did not induce DNA fragmentation in SBC-3/Bcl-2. However, there was no difference in sensitivity to CDDP, VP-16, ACNU, MTX and Taxol between SBC-3 and SBC-3/Bcl-2 (Ohmori, T. et al. Biochem. Biophys. Res. Commun. 1993). These studies indicate that bcl-2 can modulate the cytotoxicity of some anti-cancer agents by inhibiting the process of apoptosis. We speculate that some apoptotic pathways are bcl-2-sensitive and others bcl-2-independent.
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PMID:[Anticancer agents and apoptosis]. 810 88

To determine whether the apoptotic cell death induced by anti-cancer agents could be inhibited by bcl-2, we established a bcl-2-transfected human small cell lung cancer cell line, SBC-3/Bcl2. SBC-3/Bcl2 showed higher resistance to ADM, CPT-11 and MMC compared with the parental line SBC-3, with relative resistance values of 3.4, 7.6 and 5.7, respectively. However, there was no difference in sensitivity to CDDP, VP-16, ACNU, MTX and taxol between SBC-3 and SBC-3/Bcl2. Agarose gel electrophoresis showed typical DNA fragmentation of SBC-3 following treatment with CPT-11 or MMC, in a concentration-dependent manner. In contrast, the same concentration of the drugs did not induce DNA fragmentation in SBC-3/Bcl2. Treatment with CDDP resulted in the same degree of DNA fragmentation in SBC-3 and SBC-3/Bcl2. These studies indicate that bcl-2 can modulate the cytotoxicity of some anti-cancer agents by inhibiting the process of apoptosis.
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PMID:Apoptosis of lung cancer cells caused by some anti-cancer agents (MMC, CPT-11, ADM) is inhibited by bcl-2. 847 31

We reviewed recent investigations on apoptosis related to anticancer chemotherapy. The study of programmed cell death, apoptosis, has become one of the main stream in cellular biology, particularly in immunology, developmental biology and oncology. To determine whether the apoptotic cell death induced by anticancer agents could be inhibited by bcl-2 oncogene, we established a bcl-2 transfected human small cell lung cancer cell line, SBC-3/Bcl-2. SBC-3/Bcl-2 showed higher resistance to ADM, CPT-11 and MMC compared to the parental line SBC-3. Agarose gel electrophoresis showed typical DNA fragmentation of SBC-3 following treatment with CPT-11 or MMC. In contrast, the same concentration of the drugs did not induce DNA fragmentation in SBC-3/Bcl-2. However, there was no difference in sensitivity to CDDP, VP-16, ACNU, MTX and Taxol between SBC-3 and SBC-3/Bcl-2 (Ohmori T, et al: Biochem Biophys Res Commun 1993). These results suggest that bcl-2 can modulate the cytotoxicity of some anticancer agents by inhibiting the process of apoptosis. We speculate that some apoptotic pathways are bcl-2-dependent and others bcl-2-independent.
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PMID:[Anticancer agents and apoptosis]. 858 98

The aim of our study was to assess frequency of death from myocardial infarction in patients (pts) treated for small cell lung cancer (SCLC). 33 out of 845 patients treated for SCLC died from myocardial infarction. All patients were smokers. In 6 patients coexisted hypertension, in 2--diabetes and in 5--obesity. Eight patients have had cardiac disease in anamnesis. All patients were treated with one or more number of cardiotoxic drugs as DDP, VCR or VBL, E, MTX and ADR which are able to cause ischemic heart disease or myocardial infarction. Sixteen out of 33 patients have had radiotherapy of lung tumour. Death from myocardial infarction occurred from 0.5 up till 98.5 months from the beginning of start treatment. Eighteen men died from myocardial infarction in the first year of treatment. Risk of death from myocardial infarction was 15 times greater in men with SCLC than in men of the polish population at the same age and at the same time.
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PMID:[Myocardial infarction as a cause of death in patients treated for small cell lung cancer]. 1080 90