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Browse 1,292 clinical trials for melanoma. Find studies that match your criteria and connect with research centers.
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NCT06337617
This was a multi-center, observational, retrospective cohort study to evaluate the effectiveness and safety of dabrafenib in combination with trametinib in Chinese patients with unresectable or metastatic BRAF V600 mutation positive melanoma, for mucosal melanoma patients (Cohort A) and non-mucosal melanoma patients (Cohort B, cutaneous and acral melanoma), separately. Study population was identified as patients initiating dabrafenib plus trametinib from 01 May 2020 to 31 July 2022 who fulfilled the inclusion/exclusion criteria. The follow-up period ended at the earliest of the following: end of study observation period (i.e., 31 December 2022), death, upon withdrawal of consent or the last available record.
NCT03932253
Melanoma is one of the most common cutaneous cancers worldwide. Activating mutations in RAS oncogenes are found in a third of all human cancers and NRAS mutations are found in 15%-20% of melanomas. Acquisition of a functional mutation in NRAS results in activation of the Ras / Raf / MEK / ERK signaling pathway leading to unconstrained cell growth and cell transformation. NRAS mutation status was identified as an independent poor prognostic factor in stage IV melanoma. No drug was approved to treat melanoma patients with NRAS mutation or amplification until now. FCN-159, an oral and potent MEK1/2 inhibitor, has more than 10 folds higher selectivity against activated MEK1 and MEK2 compared with trametinib, and has demonstrated significant antitumor growth inhibition in two patient-derived xenograft (PDX) models with NRAS mutation. Approximately 10%-15% of melanomas is reported to be NF1-mutant. NF1 gene is located in chromosome 17 q11.2 and encodes neurofibromin 1. Neurofibromin 1 is a RAS-specific GTP enzyme-activated protein that converts RAS from the active guanosine triphosphate (GTP) binding state to the inactivated guanosine diphosphate (GDP) binding state and acts as a negative regulatory factor for RAS and its downstream MAPK and PI3K-Akt pathways. Recent treatments of NF1 mutation focus on the downstream of the MAPK pathway, such as MEK kinase. Blocking the MEK kinase can reduce neurofibroma in mice with NF1 mutation and prolong the survival time of mice with malignant peripheral nerve sheath tumor (MPNST) xenograft. In the NF1 mutant monocytic leukemia mouse model, the use of MEK inhibitors can improve mouse survival rate. This is the first in human study to evaluate the safety and anti-tumor activity in patients.