View clinical trials related to Lung Cancer.
Filter by:Background: - Mithramycin is a drug that was first tested as a cancer therapy in the 1960s. It acted against some forms of cancer, but was never accepted as a treatment. Research suggests that it may be useful against some cancers of the chest, such as lung and esophageal cancer or mesothelioma. Researchers want to see if mithramycin can be used to treat these types of cancer. Objectives: - To see if mithramycin is safe and effective against different chest cancers. Eligibility: - Individuals at least 18 years of age who have lung, esophagus, pleura, or mediastinum cancers. Design: - Participants will be screened with a physical exam and medical history. Blood and urine samples will be collected. Imaging studies and tumor tissue samples will be used to monitor the cancer before treatment. - Participants will receive mithramycin every day for 7 days, followed by 7 days without treatment. Each 14-day round of treatment is called a cycle. - Treatment will be monitored with frequent blood tests and imaging studies. - Participants will continue to take the drug for as long as the side effects are not severe and the tumor responds to treatment.
Cancer patients are highly variable in their body composition, specifically in the proportion of fat and muscle. Some patients tend to gain fat and lose muscle (or lean body mass) at the same time. These patients can develop severe muscle wasting, termed sarcopenia. Patients with sarcopenia have more severe treatment related toxicity requiring delays, dose reductions and stopping of treatment, and have reduced survival. One potential explanation for this is that patients with sarcopenia have a reduced volume of lean body mass into which chemotherapy drugs are distributed, resulting in a higher concentration and greater toxicity. This study will randomize lung cancer patients to either the standard dosing strategy based on body surface area or experimental, personalized dosing based on lean body mass. Based on retrospective findings in this patient population, the investigators expect to find that severe toxicity will be reduced for sarcopenic patients on the personalized dosing arm based on lean body mass.
To collect data of all patients who have undergone Endobronchial ultrasound for diagnosis or staging of suspected lung cancer
Advanced non-small-cell lung cancer (NSCLC) patients without epidermal growth factor receptor (EGFR) mutations show a poor prognosis. Gemcitabine combined with cisplatin chemotherapy is an effective treatment measures for EGFR mutation-negative NSCLC patients, but the prognosis remains poor. Chemotherapy combined with targeted monoclonal antibody treatment may be better treatment options in these patients. Monoclonal antibodies, such as bevacizumab, can block tumor growth in different ways. Bevacizumab blocks the ability of tumors to grow new blood vessels and spread. It is not yet known whether cisplatin and gemcitabine is more effective when given alone or with bevacizumab. This randomized trial studies how well giving cisplatin and gemcitabine alone or in combination with Bevacizumab (Avastin) works in treating patients with stage IIIB/IV non-squamous NSCLC without EGFR mutations.
The overall goal of this research is to enhance the investigators understanding of the pathways involved in lung cancer, and to identify new biomarkers and/or therapeutic targets. By comparing gene expression between normal lung tissue and tumors growing in lung-specific C/EBPa KO mice, the investigators have identified the Bmi-1 proto-oncogene as being abnormally upregulated in C/EBPa-deleted tumors. Subsequently, the investigators have validated this observation in human lung cancer, implicating the investigators KO mice are an effective discovery tool for lung cancer research. Through similar approaches, the investigators have already identified (Sonic Hedgehog, SHH), and plan to identify other pathways which are abnormally regulated in C/EBPa-/- tumors. In parallel, the investigators will proceed to define the clinical relevance of the SHH pathway and the other newly-discovered molecular aberrations, by analyzing their expression and correlate it to C/EBPa expression on the samples of patients with NSCLC at NUHS. If the investigators preliminary data on Bmi-1 will be confirmed, this proto-oncogene may generate useful correlates that could be used in diagnosis and treatment of lung cancer, as well as identify new prognostic/predictive markers in lung cancer. Similarly, SHH pathway-components may behave as potential biomarkers and therapeutic tools for C/EBPa-related lung cancers. This proposal seeks to test the hypothesis that pathways which are dysregulated in lung tumors growing in a lung-specific C/EBPa KO model can be utilized as discovery tools to identify genes involved in human lung cancer pathogenesis.
In 2011, there was an estimated 233,000 cases of invasive breast cancer, and 39,970 deaths from breast cancer in the United States. The vast majority of patients are diagnosed with Stage I-III resectable and potentially curable disease, and for these patients, the most pressing questions are whether adjuvant endocrine or chemotherapy are indicated, and if so, how to determine whether these treatments are working. Adjuvant systemic therapy reduces relative recurrence rates by 30-50%, depending on the age of the patient and tumor characteristics. However, patients with early stage disease often do not bear measurable markers of disease such as an elevated cancer antigen 27-29 (CA27.29) or circulating tumor cells. Patients with early stage breast cancer are typically treated with adjuvant therapy based on historical evidence showing that such therapy prolongs survival in this population. Lung cancer is the most common malignancy and the leading cause of cancer-related death in the U.S. Approximately 220,000 new cases of lung cancer are diagnosed in the U.S. every year. Unfortunately, lung cancers are often diagnosed at later stages than breast cancer, due in part to little/no effective screening for lung cancer. As with breast cancer, patients are commonly treated with chemotherapeutic agents, but treatment regimens can take several weeks to months to elicit clinically detectable anti-tumor effects. A biomarker to assess early tumor response to therapy would benefit this patient population. The contents of dying tumor cells can be detected in the bloodstream, and this may be enhanced by the leaky vasculature of solid tumors. Protein biomarkers of tumor cell death are difficult to detect due to the complex nature of plasma and the lack of technical sensitivity. In contrast, DNA is easier to detect through polymerase chain reaction (PCR) amplification. Indeed, circulating tumor DNA has been detected in plasma from patients with osteosarcoma, breast cancer, and colorectal cancer. Until recently, it was impractical to develop an assay to routinely quantify circulating tumor DNA due to heterogeneity between patients and tumors. Advances in genomic technology now permit sequencing a tumor genome to identify patient-specific genomic aberrations. Major genomic alterations (i.e., insertions, amplifications, deletions, inversions, translocations) can be readily detected using PCR primers which will recognize tumor DNA but not normal DNA. While this strategy may be generally applicable to diverse types of solid tumors, two issues are apparent in breast cancer. Firstly, the incidence of chromosomal rearrangements varies widely. Whole-genome sequencing of 15 breast tumors revealed a range of 1-231 major genomic alterations (mean= 68), where 2 tumors had 1 alteration, and 9 tumors had > 20 alterations. Single-base point mutations are more common but difficult to reliably detect using PCR. Therefore, the investigators must consider that a small subset of patients may have a limited number of genomic alterations available for this assay. Secondly, intratumoral heterogeneity may mean that some genomic alterations are not present in every tumor cell. Such heterogeneity has been inferred from FISH and immunohistochemistry (IHC) studies for many years, and is now being verified at the genomic level. The investigators must consider that only a subpopulation of tumor cells may be sensitive to cytotoxic therapy, so changes in the levels of circulating tumor DNA may only be reflected with analysis of genomic alterations specific to the sensitive cells.
The goal of the investigators study is to investigate the role of a hormone named Activin A (ActA) in the development of the skeletal muscle atrophy caused by cancer. According to the investigators hypothesis, ActA could be released by the tumor and activate a muscle atrophy gene program. To answer this question, the investigators plan first to compare circulating levels of ActA in cancer patients with and without cachexia. In a second step, the investigators would like to assess whether ActA circulating levels are predictive for the development of cachexia and short survival.
Lung cancer is the first cause of death among cancer patients. Non Small Cell lung cancer (NSCLS) represents about 80-85% of the cases. Of this, about 80% presents with locally advanced or metastatic disease. Important to mention the number of patients that progress or recur in central nervous system (CNS). It has been reported that patients with adenocarcinoma, who are under 60 years and with elevated carcinoembryonic antigen (CEA) are in the highest risk to develop brain metastasis. In small cell lung cancer, treatment with prophylactic cranial irradiation (PCI) is the standard of care in patients without progression after locoregional or systemic treatment because the proven benefit in overall survival (OS) and progression free survival (PFS). However, in NSCLC PCI has not been able to prove any survival benefit, only in CNS PFS, probably because there is no trial, to our knowledge, of PCI in NSCLC that include only the specific group of patients considered in high risk of developing brain metastasis.
The purpose of this study is to evaluate the effect of food on the pharmacokinetics (PK) of the experimental drug, entinostat, in women with breast cancer and men and women with non-small cell lung cancer. The safety and tolerability of entinostat will also be evaluated when entinostat is given by itself as well as with the approved drugs, exemestane (Aromasin®) or erlotinib (Tarceva®). A biomarker (chemical "marker" in the blood/tissue that may be related to your response to the study drug) will also be tested.
This research study is a Phase II clinical trial. Phase II clinical trials test the effectiveness of an investigational drug to learn whether the drug works in treating a specific cancer. "Investigational" means that the drug is still being studied and that research doctors are trying to find out more about it-such as the safest dose to use, the side effects it may cause, and if the drug is effective for treating different types of cancer. It also means that the FDA has not approved the drug for this type of cancer, or for any use outside of research studies. When cancer spreads from the primary tumor, one of the most commons sites it spreads to is bone. When cancer spreads to bone there can be significant symptoms such as pain. Cabozantinib works by blocking signaling that leads to cancer growth as well as blocking the growth of new blood vessels (angiogenesis) that help to feed a tumor. Cabozantinib has been studied or is being studied in research studies as a possible treatment for various types of cancer, including prostate cancer, brain cancer, thyroid cancer, lung cancer and kidney cancer. Previous clinical research studies indicate that cabozantinib may also have activity against cancer once it has spread to the bones. The purpose of this study is to find out if cabozantinib is effective in treating cancer that has spread to the bone.