View clinical trials related to Lung Adenocarcinoma.
Filter by:Folic acid (FA; folate) in the dose of 350-1,000 μg daily should be supplemented, daily, starting 7 days before the first dose of pemetrexed based chemotherapy and should be continued while the patient is on therapy and for 21 days after cessation of therapy. Vitamin B12 injections (1,000 μg i.m.) should also be started 1 week before the first dose of chemotherapy. However, the evidence for delaying chemotherapy by seven days for the purpose of giving vitamin B12 and FA supplementation is not robust. Observational and prospective single arm studies have not shown any increased toxicity if pemetrexed was started earlier than the recommended duration of supplementation. In a resource constrained setting, this will lead to one additional visit and 1-week chemotherapy delay which may be inconvenient for patients. Hence an open label, randomized control trial is being undertaken to evaluate if there are any differences in pemetrexed related hematological toxicity amongst patients who receive delayed initiation of chemotherapy (following 5 - 7 days of vitamin B12 and FA supplementation; Delayed Arm) as compared to those in whom vitamin B12 and FA supplementation is starting simultaneously (within 24 hours) of initiation of chemotherapy (Immediate Arm).
This is a prospective, randomized, open, multicenter phase Ⅱ study to evaluate the efficacy of cytokine-induced killer cells combined chemotherapy in stage Ⅳ naive EGFR wild-type lung adenocarcinoma.
The purpose of this study is to compare effects of erlotinib and pemetrexed as maintenance therapy for lung adenocarcinoma. Primary Outcome is the progression free survival (PFS). Based on prediction of different potential benefit groups, this study may help the oncologist to optimize and improve the maintenance therapy plan for lung adenocarcinoma.
This study was proposed to validate the efficacy of gefitinib as first-line therapy in advanced lung adenocarcinoma with EGFR mutation determined by plasma cf-DNA.
This randomized phase II trial studies how well chemotherapy and radiation therapy given with or without metformin hydrochloride works in treating patients with stage III non-small cell lung cancer. Drugs used in chemotherapy, such as carboplatin and paclitaxel, work in different ways to stop the growth of tumor cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Radiation therapy uses high-energy x-rays to kill tumor cells and shrink tumors. Metformin hydrochloride may shrink tumors and keep them from coming back. It is not yet known whether chemotherapy and radiation therapy is more effective when given with or without metformin hydrochloride in treating stage III non-small cell lung cancer.
Cancers occur when the molecules that control normal cell growth (genes and proteins) are altered. Changes in the tumor genes and in the genes of normal cells are called "alterations." Many of these alterations can be detected by directly examining cancer cells in a tumor or circulating in blood. Several alterations that occur repeatedly in certain types of cancers have already been identified. These discoveries ahve led to the development of new drugs that "target" those alterations. More remain to be discovered. Some of the alterations are found in genes. Genes are composed of DNA "letters," which contain the instructions that tell the cells in our bodies how to grow and work. Genes make proteins which actually carry out the instructions in our cells. We would like to use your DNA to look for alterations in the genes in cancer cells and blood cells using a technology called "sequencing." Gene sequencing is a way of reading the DNA to identify errors in genes that may contribute to the behavior of cells. Some changes in genes occur only in cancer cells. Others occur in normal cels as well, in the genes that may have been passed from parent to child. This research study will examine both kinds of genes. The purpose of this research study is to perform gene sequencing (gene tests) on your cancer cells (obtained from biopsies or surgery) and normal tissues (usually blood). The results of the gene tests will be used to try to develop better ways to treat and prevent cancers. We will also study better ways to communicate the results of these complex gene tests to you and your doctors, and to help you and your doctors use this information to choose the best paths for treatment. As part of this work, we may also learn things about the genes in your normal cells; some of that information will also be shared wtih you and your doctors if you so choose. Importantly, this study will use tissue specimens that have already been collected and stored in the pathology department as part of your clinical care or as part of other research studies you may be participating in. In this study, gene tests will be performed on material only after the necessary clinical tests have been performed. In general, no additional invasive procedures will be required.
This registry is intended to measure the effect of myPlan Lung Cancer™ test has on treatment decisions of Surgeons when added to standard clinical-pathological parameters in patients with early stage NSCLC.The sponsor is conducting two parallel registries, with one directed at Surgeons (ONC003) and the other at Oncologists (ONC006).This registry is specific to Surgeons (ONC003). Outcomes measures on lung cancer relapse and death from any cause will be collected.
This prospective, open-label, single arm, non-interventional study will investigate the effectiveness of bevacizumab monotherapy in participants with lung adenocarcinoma who previously received 4 to 6 cycles of induction platinum doublet plus bevacizumab.
This is a Prospective, open-label, parallel, multi-center, Phase III randomized trial to evaluate the efficacy and safety of video-assisted thoracoscopic segmentectomy versus Lobectomy in treating patients with Lung adenocarcinoma in situ or with microinvasion.
The p63 gene is a recently discovered member of the p53 family located at chromosome 3q27Many studies have reported that overexpression of p63 can mimic p53 activities by binding DNA, activating transcription, and inducing apoptosis. Various studies proved p63 as a marker of basal cells in normal salivary glands, breast, prostate, respiratory and squamous epithelia, and of tumor cells from various malignancies. Still, p63 has been the subject of relatively few studies in lung adenocarcinoma, and breast carcinoma, and no study has described the correlation of p63 with pancreatic ductal adenocarcinoma. In the current study, we aim to evaluate the prognostic value of the expression of p63 in the lung adenocarcinoma, breast adenocarcinoma, and pancreatic ductal adenocarcinoma. We will achieve this aim by collecting clinical data retrospectively from the patients' medical records as well as assessing the histological sections and performing immunohistochemical staining for p63.