thromboxane-b2 and Carcinoma--Non-Small-Cell-Lung
thromboxane-b2 has been researched along with Carcinoma--Non-Small-Cell-Lung* in 6 studies
Trials
1 trial(s) available for thromboxane-b2 and Carcinoma--Non-Small-Cell-Lung
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Aspirin reduces adverse effects of gefitinib.
We measured serum levels of soluble (s) P-selectin and thromboxane B2 (TxB2) in patients with lung cancer treated with gefitinib, and investigated the effect of low-dose aspirin on some adverse effects of gefitinib. The serum levels of sP-selectin and TxB2 increased significantly in all patients who received gefitinib for 2 weeks. Forty patients were recruited, and 28 received gefitinib without low-dose aspirin (Group 1) and 12 were co-administered low-dose aspirin (Group 2). In Group 2, the frequency of adverse events, skin rash and diarrhea was evidently reduced by the low-dose aspirin therapy, despite having shown no remarkable change in gefitinib responsiveness between both groups. In one of the 12 patients in Group 2, aspirin therapy was suspended due to the occurrence of nasal bleeding. Four days after treatment suspension, she developed a skin lesion in her finger. However, the skin lesion improved after re-administration of aspirin without any other medications. After treatment, TxB2 significantly decreased, but not sP-selectin. These results suggest that one of the mechanisms causing gefitinib-related adverse effects depends on platelet activation. Administration of gefitinib with low-dose aspirin to lung cancer patients may prevent the development of gefitinib-related complications. Topics: Adult; Aged; Aged, 80 and over; Anti-Inflammatory Agents, Non-Steroidal; Antineoplastic Agents; Aspirin; Carcinoma, Non-Small-Cell Lung; Drug Interactions; Female; Gefitinib; Humans; Lung Neoplasms; Male; Middle Aged; P-Selectin; Platelet Activation; Platelet Aggregation Inhibitors; Prospective Studies; Quinazolines; Thromboxane B2 | 2006 |
Other Studies
5 other study(ies) available for thromboxane-b2 and Carcinoma--Non-Small-Cell-Lung
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Thromboxane synthase expression and correlation with VEGF and angiogenesis in non-small cell lung cancer.
Thromboxane synthase (TXS) metabolizes prostaglandin H2 into thromboxanes, which are biologically active on cancer cells. TXS over-expression has been reported in a range of cancers, and associated with angiogenesis and poor outcome. TXS has been identified as a potential therapeutic target in NSCLC. This study examines a link between TXS expression, angiogenesis, and survival in NSCLC.. TXS and VEGF metabolite levels were measured in NSCLC serum samples (n=46) by EIA. TXB2 levels were correlated with VEGF. A 204-patient TMA was stained for TXS, VEGF, and CD-31 expression. Expression was correlated with a range of clinical parameters, including overall survival. TXS expression was correlated with VEGF and CD-31. Stable TXS clones were generated and the effect of overexpression on tumor growth and angiogenesis markers was examined in-vitro and in-vivo (xenograft mouse model).. Serum TXB2 levels were correlated with VEGF (p<0.05). TXS and VEGF were expressed to a varying degree in NSCLC tissue. TXS was associated with VEGF (p<0.0001) and microvessel density (CD-31; p<0.05). TXS and VEGF expression levels were higher in adenocarcinoma (p<0.0001) and female patients (p<0.05). Stable overexpression of TXS increased VEGF secretion in-vitro. While no significant association with patient survival was observed for either TXS or VEGF in our patient cohort, TXS overexpression significantly (p<0.05) increased tumor growth in-vivo. TXS overexpression was also associated with higher levels of VEGF, microvessel density, and reduced apoptosis in xenograft tumors.. TXS promotes tumor growth in-vivo in NSCLC, an effect which is at least partly mediated through increased tumor angiogenesis. Topics: Carcinoma, Non-Small-Cell Lung; Humans; Lung Neoplasms; Neovascularization, Pathologic; Thromboxane B2; Thromboxane-A Synthase; Tissue Array Analysis; Vascular Endothelial Growth Factor A | 2014 |
Examination of thromboxane synthase as a prognostic factor and therapeutic target in non-small cell lung cancer.
Thromboxane synthase (TXS) metabolises prostaglandin H2 into thromboxanes, which are biologically active on cancer cells. TXS over-expression has been reported in a range of cancers, and associated with a poor prognosis. TXS inhibition induces cell death in-vitro, providing a rationale for therapeutic intervention. We aimed to determine the expression profile of TXS in NSCLC and if it is prognostic and/or a survival factor in the disease.. TXS expression was examined in human NSCLC and matched controls by western analysis and IHC. TXS metabolite (TXB2) levels were measured by EIA. A 204-patient NSCLC TMA was stained for COX-2 and downstream TXS expression. TXS tissue expression was correlated with clinical parameters, including overall survival. Cell proliferation/survival and invasion was examined in NSCLC cells following both selective TXS inhibition and stable TXS over-expression.. TXS was over-expressed in human NSCLC samples, relative to matched normal controls. TXS and TXB2 levels were increased in protein (p < 0.05) and plasma (p < 0.01) NSCLC samples respectively. TXS tissue expression was higher in adenocarcinoma (p < 0.001) and female patients (p < 0.05). No significant correlation with patient survival was observed. Selective TXS inhibition significantly reduced tumour cell growth and increased apoptosis, while TXS over-expression stimulated cell proliferation and invasiveness, and was protective against apoptosis.. TXS is over-expressed in NSCLC, particularly in the adenocarcinoma subtype. Inhibition of this enzyme inhibits proliferation and induces apoptosis. Targeting thromboxane synthase alone, or in combination with conventional chemotherapy is a potential therapeutic strategy for NSCLC. Topics: Adenocarcinoma; Apoptosis; Blotting, Western; Carcinoma, Non-Small-Cell Lung; Cell Line, Tumor; Cell Proliferation; Cyclooxygenase 2; Enzyme Inhibitors; Female; Gene Expression Regulation, Enzymologic; Gene Expression Regulation, Neoplastic; Humans; Immunohistochemistry; Lung Neoplasms; Male; Prognosis; Reverse Transcriptase Polymerase Chain Reaction; Thromboxane B2; Thromboxane-A Synthase; Tissue Array Analysis | 2011 |
Increased thromboxane B(2) levels are associated with lipid peroxidation and Bcl-2 expression in human lung carcinoma.
There is little information regarding simultaneous investigations of thromboxane A(2) (TXA(2)) lipid peroxidation and Bcl-2, three cancer-related agents, and analyses of their relationships in lung cancer. The present study was to study thromboxane B(2) (TXB(2)), a stable metabolite of TXA(2), lipid peroxidation and Bcl-2 expression in 52 non-small cell lung carcinoma (NSCLC) tissue samples. The level of thiobarbituric acid reactive substances (TBARS), an index for lipid peroxidation was significantly increased in the lung tumor tissues, compared with non-tumor tissues. TXB(2) was much higher in the tumor tissues than non-tumor tissues. Interestingly, the concentration of TXB(2) in samples from those who smoked was higher than that from those who did not smoke. The expression of Bcl-2 was significantly elevated in the tumor tissues, compared to the non-tumor tissues. There was also a positive correlation between TXB(2) and TBARS in tumor tissues; advanced stage cancers had higher levels of TXB(2). This finding supports the idea that TXB(2) may have a role in promoting tumor growth. In conclusion, our study demonstrates that the production of TXB(2) is increased in lung tumor tissues and that such an increase can result in lipid peroxidation which may be met by an elevation in Bcl-2 expression. Topics: Carcinoma, Non-Small-Cell Lung; Female; Humans; Lipid Peroxidation; Lung Neoplasms; Male; Middle Aged; Neoplasm Staging; Proto-Oncogene Proteins c-bcl-2; Thiobarbituric Acid Reactive Substances; Thromboxane B2 | 2006 |
[Study on advanced non-small cell lung cancer patients with Qi deficiency and blood stasis syndrome].
108 cases of advanced non-small cell lung cancer (NSCLC) with Qi deficiency and blood stasis syndrome (QDBS) had been studied in this paper. It has been found that: (1) QDBS existed commonly in 60.2% of NSCLC patients. (2) QDBS patients had lowered immune function and blood hypercoagulating function, as compared with healthy persons. (3) The abnormal change of immunological indexes such as TC subgroup. TXB2, 6-keto-PGF1 alpha, fibrinogen and plasmin activity as well as hemorheological indices are important pathophysiological manifestation of QDBS. Thus, the principle of supplementing Qi and activating blood circulation combined with reducing phlegm and resolving masses should be emphasized in future research. Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Carcinoma, Non-Small-Cell Lung; Diagnosis, Differential; Female; Fibrinogen; Humans; Immunity, Cellular; Lung Neoplasms; Male; Medicine, Chinese Traditional; Middle Aged; T-Lymphocyte Subsets; Thromboxane B2 | 1994 |
Evidence for prostanoid biosynthesis as a biochemical feature of certain subclasses of non-small cell carcinomas of the lung as determined in established cell lines derived from human lung tumors.
Detectable levels (greater than or equal to 0.2 pmol/10(6) cells) of one or more prostanoid species resultant to calcium ionophore A23187-induced biosynthesis from endogenous arachidonic acid were distributed in 28 cell lines derived from different histological classes of lung tumors as follows: large cell undifferentiated carcinoma (3 of 3 cell lines); adenosquamous carcinoma (1 of 2 cell lines); squamous cell carcinoma (0 of 2 cell lines); adenocarcinoma (9 of 10 cell lines); bronchioloalveolar cell carcinoma (2 of 2 cell lines); and small cell carcinoma (1 of 9 cell lines). Using the mean levels of 9 alpha,11 beta-prostaglandin F2, prostaglandin F2 alpha, prostaglandin D2, prostaglandin E2, thromboxane B2 and 6-keto-prostaglandin F1 alpha as an index of prostaglandin H (PGH) synthase activity, the distribution in cell lines representative of the different histological classes of human lung tumors exhibiting PGH synthase activity exceeding mean values greater than or equal to 2 pmol/10(6) cells was as follows: large cell undifferentiated carcinoma (3 of 3 cell lines), adenosquamous carcinoma (1 of 2 cell lines), adenocarcinoma (8 of 10) cell lines), bronchioloalveolar cell carcinoma (2 of 2 cell lines) and small cell carcinoma (0 of 9 cell lines). Three different prostanoid species accumulated to mean levels greater than or equal to 2 pmol/10(6) cells. Prostaglandin E2 levels exceeded 2 pmol/10(6) cells in 14 of the 16 cell lines in which this prostanoid accumulated to detectable levels. Cumulative levels of prostaglandin F2 alpha exceeded 2 pmol/10(6) cells in 9 of the 15 cell lines in which prostaglandin F2 alpha reached detectable levels. Detectable levels of thromboxane B2 were observed in five cell lines with thromboxane B2 accumulation exceeding 2 pmol/10(6) cells in two of the five cell lines. 9 alpha,11 beta-prostaglandin F2 and 6-keto-prostaglandin F1 alpha accumulated to detectable levels in the culture medium of one cell line, while prostaglandin D2 accumulation to detectable levels was observed in two cell lines. Stimulation of cultured human lung tumor cells exhibiting PGH synthase activity greater than or equal to 2 pmol/10(6) cells in the presence of 10(-5) M exogenous arachidonic acid resulted in a 2- to 4-fold increase in the accumulation of individual prostanoids, while the inclusion of a 10(-5) M exogenous concentration of arachidonic acid failed to stimulate detectable prostanoid production in human lung tumor cells in which PGH synt Topics: Carcinoma, Non-Small-Cell Lung; Cell Line; Humans; Kinetics; Lung Neoplasms; Prostaglandins; Thromboxane B2; Tumor Cells, Cultured | 1989 |