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A plain language summary of the 7-year update from part 1 of the COLUMBUS study: encorafenib and binimetinib for people with BRAF V600-mutant melanoma.
Future Oncol
January 2025
tMelanoma,Cancer Immunotherapy and Innovative Therapies Unit, Istituto Nazionale Tumori IRCCS Fondazione Pascale, Napoli, Italy.
Impact of BRAF and MEK Inhibitors on Gingival Hyperplasia in Melanoma Patients-A Case Report.
J Clin Med
December 2024
Department of Dental Medicine, Faculty of Medicine, University of Novi Sad, 21000 Novi Sad, Serbia.
: Although BRAF inhibitors, such as vemurafenib, produce a marked response in patients with advanced melanoma with a BRAF V600 mutation, they eventually develop resistance to this treatment. To address this issue, vemurafenib is increasingly combined with the MEK inhibitor cobimetinib, leading to improved response rates and enhanced survival. However, this treatment modality is associated with numerous side effects.
View Article and Find Full Text PDFDiclofenac Enhances the Response of BRAF Inhibitor to Melanoma Through ROS/p38/p53 Signaling.
Clin Exp Pharmacol Physiol
March 2025
Department of Dermatology, Fudan University Huashan Hospital, Shanghai, China.
BRAF inhibitors (BRAFi) represent a cornerstone in melanoma therapy due to their high efficacy. However, the emergence of resistance causes a significant challenge to their clinical utility. This study aims to investigate the potential of diclofenac as a sensitizer for BRAFi therapy in melanoma and to elucidate its underlying mechanism.
View Article and Find Full Text PDFInhibition of glutaminase elicits senolysis in therapy-induced senescent melanoma cells.
Cell Death Dis
December 2024
Department of Dermatology, Case Western Reserve University and University Hospitals Cleveland Medical Center, Cleveland, OH, 44106, USA.
The cyclin D1-Cyclin-Dependent Kinases 4 and 6 (CDK4/6) complex is crucial for the development of melanoma. We previously demonstrated that targeting CDK4/6 using small molecule inhibitors (CDK4/6i) suppresses Braf melanoma growth in vitro and in vivo through induction of cellular senescence. However, clinical trials investigating CDK4/6i in melanoma have not yielded successful outcomes, underscoring the necessity to enhance the therapeutic efficacy of CDK4/6i.
View Article and Find Full Text PDFInterfering Nuclear Protein Laminb1 Induces DNA Damage and Reduces Vemurafenib Resistance in Melanoma Cells In Vitro.
Cancers (Basel)
December 2024
Bioinspired Engineering and Biomechanics Center (BEBC), Xi'an Jiaotong University, Xi'an 710049, China.
Background/objectives: Drug resistance poses a substantial clinical challenge in melanoma treatment, yet the underlying mechanism remains elusive. Here, we report the novel role of laminB1, a nuclear structure protein, in regulating the response of BRAF-mutated melanoma cells to vemurafenib.
Results: Our analysis of clinical samples and existing databases highlights the tight correlation between the laminB1 expression level and melanoma progression and prognosis.
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