Gemcitabine and small cell lung cancer

Scarpati, Michele Della Vittoria; Vicidomini, Giovanni; Santini, Mario

doi:10.1016/s0169-5002(01)00237-9

Cited by 6 publications

(2 citation statements)

References 2 publications

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“…The conventional treatment of lung cancer includes surgery, radiation and chemotherapy. Various chemotherapy drugs, including doxorubicin, 5‐fluorouracil, cisplatin, etoposide and gemcitabine, have been used to treat lung cancer [1–3]. Unfortunately, all of these anticancer drugs affect not only pathological tumour cells, but also normal cells, especially bone marrow cells or intestinal epithelia with high turnover rate, causing serious complications and toxicity.…”

Section: Introductionmentioning

confidence: 99%

7,8‐Dihydroxy‐4‐methylcoumarin induces apoptosis of human lung adenocarcinoma cells by ROS‐independent mitochondrial pathway through partial inhibition of ERK/MAPK signaling

et al. 2007

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Coumarins have attracted intense interest in recent years because they have been identified from natural sources, especially green plants and have diverse pharmacological properties. In this study, we investigated whether 7,8-dihydroxy-4-methylcoumarin (DHMC) caused apoptosis in A549 human non-small cell lung carcinoma cells (NSCLC) and, if so, by what mechanisms. Here, we show that, in A549 human NSCLC cells, DHMC induces apoptosis through mitochondria-mediated caspase-dependent pathway. Although an increase in the levels of reactive oxygen species (ROS) was observed, pre-treatment with antioxidant showed no protective effect against DHMC-induced apoptosis. In addition, our immunoblot data revealed that DHMC treatment led to down-regulation of Bcl-xl, Bax, p21, Cox-2, p53 and upregulation of c-Myc. Results in the present study for the first time suggest that DHMC induces apoptosis in human lung A549 cells through partial inhibition of ERK/ MAPK signaling.

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Section: Introductionmentioning

confidence: 99%

7,8‐Dihydroxy‐4‐methylcoumarin induces apoptosis of human lung adenocarcinoma cells by ROS‐independent mitochondrial pathway through partial inhibition of ERK/MAPK signaling

et al. 2007

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“…However, cancer chemotherapy has progressed since its introduction into clinical practice and represents the most promising treatment modality. Various chemotherapy drugs, including doxorubicin, 5‐fluorouracil, cisplatin, etoposide and gemcitabine, have been used to treat lung cancer (Scarpati et al ., 2001; Worden & Kalemkerian, 2000; Yang et al ., 2002). But all of these anticancer drugs affect not only pathological tumour cells, but also normal cells, especially bone marrow cells or intestinal epithelia with high turnover rate, causing serious complications and toxicity.…”

Section: Introductionmentioning

confidence: 99%

Effector mechanism of magnolol‐induced apoptosis in human lung squamous carcinoma CH27 cells

Yang

Hsieh

Tsai

et al. 2003

British J Pharmacology

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Magnolol, an active component isolated from the root and stem bark of Magnolia officinalis, has been reported to exhibit antitumour effects, but little is known about its molecular mechanisms of action. Magnolol inhibited proliferation of human lung squamous carcinoma CH27 cells at low concentrations (10–40 μM), and induced apoptosis at high concentrations (80–100 μM). Treatment with 80 μM magnolol significantly increased the expression of Bad and Bcl‐XS proteins, whereas it decreased the expression of Bcl‐XL. Overexpression of Bcl‐2 protected CH27 cells against magnolol‐triggered apoptosis. Magnolol treatment resulted in accumulation of cytosolic cytochrome c and activation of caspase‐9 and downstream caspases (caspase‐3 and ‐6). Pretreatment with z‐VAD‐fmk markedly inhibited magnolol‐induced cell death, but did not prevent cytosolic cytochrome c accumulation. Magnolol induced a modest and persistent JNK activation and ERK inactivation in CH27 cells without evident changes in the protein levels. The responsiveness of JNK and ERK to magnolol suggests the involvement of these kinases in the initiation of the apoptosis process. These results indicate that regulation of the Bcl‐2 family, accumulation of cytosolic cytochrome c, and activation of caspase‐9 and caspase‐3 may be the effector mechanisms of magnolol‐induced apoptosis. British Journal of Pharmacology (2003) 138, 193–201. doi:

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Is long term gemcitabine useful in small cell lung cancer?

Dediu

2002

Lung Cancer

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Gemcitabine and small cell lung cancer

Cited by 6 publications

References 2 publications

7,8‐Dihydroxy‐4‐methylcoumarin induces apoptosis of human lung adenocarcinoma cells by ROS‐independent mitochondrial pathway through partial inhibition of ERK/MAPK signaling

7,8‐Dihydroxy‐4‐methylcoumarin induces apoptosis of human lung adenocarcinoma cells by ROS‐independent mitochondrial pathway through partial inhibition of ERK/MAPK signaling

Effector mechanism of magnolol‐induced apoptosis in human lung squamous carcinoma CH27 cells

Is long term gemcitabine useful in small cell lung cancer?

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