View clinical trials related to Lung Neoplasms.
Filter by:The purpose of this clinical trial is to find out how successfully non-small-cell lung cancer patients are able to give an immune response to injections of the immunotherapeutic product GSK1572932A, and to find out more about the safety of this treatment. A course of eight injections will be administered over 21 weeks; including screening for suitability and all tests, the duration of the study for a patient will be 30-35 weeks. During this period various tests will be performed, including physical examinations and blood tests. The Protocol Posting has been updated in order to comply with the FDA Amendment Act, Sep 2007.
This amended expansion phase of the protocol is to further the experience at a dose level of 150 mg CPT eq/m2 in patients with Stage IV non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) and to test for preliminary anti-tumor activity in these tumor types. The MTD was initially defined as 113 mg CPT equivalents(eq)/m2 in the dose escalation part of the study. However, in the initial expansion phase (Protocol Amendment 11), 11 patients (10 NSCLC patients and 1 gastric cancer patients) were dosed at 113 mg CPT eq/m2 and less bone marrow toxicity was observed as compared to more heavily pre-treated patients in the dose escalation part of the study. Therefore, this amended expansion phase will investigate the safety and anti-tumor effects of a dose of 150 mg CPT eq/m2. The study will also determine: - The safety and tolerability of XMT-1001 at 150 mg CPT eq/m2 - The pharmacokinetics (PK) of XMT-1001 (how XMT-1001 behaves in the body) in patients Stage IV non-small cell lung carcinoma (NSCLC) and small cell lung cancer - Evidence of XMT-1001 anti-tumor activity at 150 mg CPT eq/m2
This is a phase II trial of abraxane and carboplatin in extensive stage small cell lung cancer to examine overall response rate, time to progressive disease, survival time, and assessment of toxicity profile for Carboplatin and Abraxane.
RATIONALE: Pemetrexed disodium and sorafenib may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Sorafenib may also stop the growth of tumor cells by blocking blood flow to the tumor. Giving pemetrexed disodium together with sorafenib may kill more tumor cells. PURPOSE: This randomized phase II trial is studying pemetrexed disodium and sorafenib to see how well they work compared with pemetrexed disodium alone as second-line therapy in treating patients with stage IIIB or stage IV non-small cell lung cancer.
This is a single-arm, open-label, multicenter, international pilot study to evaluate changes that occur in 2-deoxy-2-[18F]fluoro-D-glucose (FDG)- and 3'-deoxy-3'-[18F]fluorothymidine(FLT)-PET (Positron Emission Tomography) imaging as a result of treatment with erlotinib in patients with recurrent or refractory non−small cell lung cancer (NSCLC). The study will enroll approximately 30 patients at approximately 4 sites in Australia and 2 sites in the United States.
As a single agent, paclitaxel has a response rate of 33% and 25-29% in SCLC patients with sensitive relapse and with resistant relapse, respectively. As a single agent, gemcitabine also has a response rate 16% and 6-13% in SCLC patients with sensitive relapse and with resistant relapse, respectively. Because of single-agent activity, different mechanism of action, non-overlapping toxicities, and beneficial pharmacologic interaction, paclitaxel and gemcitabine combinations are attractive for testing in clinical trials.
Oxaliplatin is a diaminocyclohexane platinum compound, with a mechanism of action similar to that of cisplatin. Oxaliplatin has a more manageable toxicity profile than cisplatin, with no renal toxicity and a lower incidence of hematological and gastrointestinal toxicities. Gemcitabine and oxaliplatin are both active in NSCLC with no overlapping toxicity. Preclinical studies show a synergistic effect of the gemcitabine-oxaliplatin combination. The combination of gemcitabine-oxaliplatin is attractive in NSCLC patients as it may improve the therapeutic index.
Oxaliplatin has a more manageable toxicity profile than cisplatin, with no renal toxicity and a lower incidence of hematological and gastrointestinal toxicities. The combination of gemcitabine-oxaliplatin is attractive in NSCLC patients as it may improve the therapeutic index. Given the potential advantages of oxaliplatin and th finding that the addition of chemotherapy improves survival in the postoperative adjuvant setting, we conduct a phase II trial to compare adjuvant gemcitabine-oxaliplatin with gemcitabine-cisplatin in patients with completely resected stage IB, II or IIIA NSCLC
It is suggested that a bimodal or trimodal approach combining neoadjuvant chemotherapy with or without radiotherapy followed by surgery provides a potentially superior method of enhancing resectability and improving locoregional control and survival compared to radiotherapy alone followed by surgery. Unsolved questions are the identification of the best induction strategy, the impact of surgery on long-term survival, and the contribution of radiation therapy in this setting. Thus, the investigators conduct a phase II trial to compare neoadjuvant chemotherapy with concurrent chemoradiotherapy in patients with biopsy proven N2 stage IIIA NSCLC to address optimal induction strategy.
3-Hydroxy-3-methylglutaryl CoA reductase inhibitors, commonly referred to as the statins, have proven therapeutic and preventative effects in cardiovascular diseases. Recently, there are emerging interests in their use as anticancer agents based on preclinical evidence of their antiproliferative, proapoptotic, anti-invasive, and radiosensitizing properties. Inhibition of 3-hydroxy-3-methylglutaryl CoA reductase by the statins interferes with the rate-limiting step of the mevalonate pathway, leading to reduced levels of mevalonate and its downstream products, many of which play important roles in critical cellular functions such as membrane integrity, cell signaling, protein synthesis, and cell cycle progression. Perturbations of these processes in neoplastic cells by the statins may therefore result in control of tumor initiation, growth, and metastasis. The statins have demonstrated growth inhibitory activity in cancer cell lines and preclinical tumor models in animals. Simvastatin, a member of the statin family, profoundly impaired basal and growth factor-stimulated SCLC cell growth in vitro and induced apoptosis. SCLC cells treated with simvastatin were sensitized to the effects of the chemotherapeutic agent etoposide. Moreover, SCLC tumour growth in vivo was inhibited by simvastatin. Therefore, the investigators will conduct this phase II trial to evaluate the efficacy & toxicity of irinotecan/cisplatin plus simvastatin in patients with chemo-naïve ED-SCLC.