View clinical trials related to Non-Small Cell Lung Cancer.
Filter by:Molecular residual disease (MRD) has strong relationship with clinical outcome in multiple solid tumors. Here, the investigators try to verify the negative predictive value of undetectable MRD, which is considered as a superior prognostic factor for resected NSCLC patients, and not requiring excessive adjuvant therapy. Stage IB-IIIA resected NSCLC patients with landmark and longitudinal undetectable MRD are enrolled and under close surveillance in this study.
This study investigates fluorine-18-AlphaVBeta6-BP ([18F]-αvβ6-BP) as a Positron Emission (PET) imaging agent in Non-Small Cell Lung Cancer (NSCLC) patients with brain metastases. Investigators hypothesize that [18F]-αvβ6-BP PET/Computed Tomography (CT) is a sensitive tool for disease assessment in patients with metastatic NSCLC, including those with brain metastases.
TC-510 is a novel cell therapy that consists of autologous genetically engineered T cells expressing two synthetic constructs: first, a single-domain antibody that recognizes human Mesothelin, fused to the CD3-epsilon subunit which, upon expression, is incorporated into the endogenous T cell receptor (TCR) complex and second, a PD-1:CD28 switch receptor, which is expressed on the surface of the T cell, independently from the TCR. The PD-1:CD28 switch receptor comprises the PD-1 extracellular domain fused to the CD28 intracellular domain via a transmembrane domain. Thus, the switch is designed to produce a costimulatory signal upon engagement with PD-L1 on cancer cells.
This study will explore the best dose of radiation to be used when treating stage I-III non-small cell lung cancer (NSCLC) with stereotactic body radiation therapy (SBRT) or hypo-fractionated radiotherapy (HypoFrx-RT) that is delivered in combination with an immune checkpoint inhibitor. Treatments with SBRT or HypoFrx-RT for locally confined NSCLC show positive response which may be further augmented when they are combined with an immune checkpoint inhibitor. Currently, it is not understood what radiation dose is most suitable for such combined treatments and their clinical efficacy in the treatment of early stage (ES) NSCLC. Therefore, this study can help researchers gain insight into what a safe and effective SBRT or HypoFrx-RT dose will be when such radiotherapeutic approaches are combined with concurrent and adjuvant administration of an immune checkpoint inhibitor in the treatment of ES NSCLC.
Lung cancer is the most common type of cancer occurring in both males and females worldwide (WHO statistics, 2018), and the 5-year survival rate for advanced NSCLC is low (between 6% and 33%, depending on the stage. The rat sarcoma (RAS) proto-oncogene has been identified as an oncogenic driver of tumorigenesis in several cancers, including NSCLC. The RAS proteins can be mutationally activated at codons 12, 13, or 61, leading to human cancers. Different tumor types are associated with mutations in certain isoforms of RAS, with Kirsten rat sarcoma viral oncogene homolog (KRAS) being the most frequently mutated isoform in most cancers. While the role of KRAS mutations in human cancers has been known for decades, no anti-cancer therapies specifically targeting KRAS mutations have been successfully developed, largely because the protein has been intractable for inhibition by small molecules. AMG 510 is a small molecule that specifically and irreversibly inhibits the KRAS G12C mutated protein. Nonclinical studies of AMG 510 have demonstrated inhibition of growth and regression of cells and tumors harboring KRAS p.G12C, and in clinical Study 20170543, AMG 510 demonstrated antitumor activity in KRAS p.G12C mutated NSCLC. These data suggest that inhibition of KRAS G12C may have therapeutic benefit for subjects with KRAS p.G12C driven cancers. Recently development of liquid biopsy technology has enabled detection of KRAS-driven cancer with plasma ctDNA analysis. Therefore, in this study, we aim to conduct a phase 2 trial of sotorasib in KRAS G12C mutant-patients, and conduct pre-treatment and post-treatment biopsies using tissue and liquid to identify novel mechanisms of acquired resistance to sotorasib in these patients. Total sample size is 37 patients, Sotorasib will be given 960mg daily until disease progression or unacceptable toxicity.
Our study aimed to evaluate the correlation between test reagent specific gene test results and the efficacy of relevant targeted drugs in patients with non-small cell lung cancer, and to support the continued registration of test reagents.
To evaluate the efficacy and safety of recombinant human endostatin /PD-1 mab combined with first-line chemotherapy in the treatment of driver gene negative advanced non-small cell lung cancer.
Lung cancer represents the most frequent neoplastic disease worldwide, with an annual incidence of over 2 million cases, which represents 11.6% of all cancer diagnoses. Further, it constitutes the main cause of cancer-related deaths. Among the lung cancer types, non-small cell lung cancer represents 80-85% of cases, and the majority of patients are diagnosed with locally advanced or metastatic disease, and 5-year survival rates remain discouraging in most world regions, ranging from 8-18%. Advances in molecular biology have led to the discovery of several molecular targets and development of targeted therapy for patients with specific molecular subtypes of NSCLC. One of the most widely studied is the epidermic growth factor receptor (EGFR), which has been long recognized as a key modulator for specific tumor cell functions, and thus it has been used in drug development strategies. Mutations in the EGFR gene are reported in 15% of all NSCLC cases, though incidence varies widely and in Mexico up to 34% of patients present with tumors with EGFR mutations. Treatment of patients with tumors with these characteristics is based on specific tyrosine kinase inhibitors (TKIs), achieving higher objective response rates and improved progression-free survival (PFS) compared with chemotherapy-based schemes. Nonetheless, despite the initial response, most patients treated with TKIs will eventually develop resistance mechanisms and present progressive disease. Consequently, the development of novel strategies to overcome TKI resistance and improve PFS of patients with NSCLC with epidermic growth factor receptor mutations (EGFRm) is priority. Up to 30% of patients with NSCLC present with somatic mutations in the liver kinase B1 (LKB1) gene, which acts as a tumor suppressor through inhibition of mammilian target of rapamycin (mTOR). In a study which included 24 patients with LKB1 expression who received treatment with metformin + TKIs, overall survival was improved significantly, and therefore it is important to evaluate LKB1 expression in addition to mutations which could be related with treatment response in patients given metformin plus antineoplastic agents. LKB1 can activate AMP-activated protein kinase (AMPK) signaling through specific phosphorylations at aminoacid residues. AMPK can regulate cell cycle, cell proliferation and cell survival in NSCLC. Recently, the loss of expression of LKB1 has been associated with a reduced activation in AMPK using in vivo models, and increase in tumor necrosis after treatment with bevacizumab. The expression of AMPK has also been evaluated in NSCLC, a study which included 99 samples concluded that increased AMPK expression was associated with worse overall survival. Nonetheless, the association between AMPK expression and metformin treatment has not been ascertained. Metformin is a biguanide used as treatment for type 2 diabetes. Additionally, several studies have identified a reduced incidence and mortality from diverse neoplasms in patients treated with metformin. In vitro studies have shown that metformin is cytotoxic in lung adenocarcinoma cells, producing a cell cycle arrest at G0 and G1, and it inhibits resistance to TKIs induced by Epithelial-Mesenchymal transition (EMT). Retrospective trials have also provided evidence as to the benefit of metformin in patients undergoing treatment for NSCLC. Several prospective trials have evaluated the concurrent use of metformin plus TKIs for patients with lung adenocarcinoma, though results have been controversial. This randomized, phase 3 study will evaluate the PFS in patients with NSCLC with EGFR mutations undergoing treatment with TKIs plus placebo vs. TKIs plus metformin.
This is a prospective, single arm study to investigate the efficacy and safety furmonertinib 80mg/d as adjuvant treatment for 3 years post surgery of stage IA with high-risk factors and stage IB non-small cell lung cancer. A total of 114 patients would be enrolled. The primary endpoint is the disease-free survival rate at 3 years.
This study is a randomized, active control, open-label, phase 2 trial. Erlotinib-treated NSCLC patients will be screened for Globo H, and only Globo H+ (H score ≥ 100) subjects are eligible for the study. Eligible subjects who have been treated with 3±1 months of first-line erlotinib and have achieved stable disease (SD) or partial response (PR) status will be randomized in the ratio of 1:1 to receive erlotinib alone or erlotinib plus OBI-833/OBI-821 therapy.