Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/bjd.19335 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Clinical benefit with tebentafusp in a patient with GNAQ mutant metastatic blue nevus-associated melanoma.
J Immunother Cancer
November 2024
Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA
Melanoma arising in association with a blue nevus (BN) is rare but has molecular similarities to uveal melanoma (UM), including GNAQ/11 mutations. Tebentafusp was recently approved for UM based on improved overall survival in a phase 3 study. We hypothesized that tebentafusp may be active in BN-associated melanoma.
View Article and Find Full Text PDF[Uveal Melanoma: Molecular and Genetic Mechanisms of Development and Therapeutic Approaches].
Mol Biol (Mosk)
October 2024
Institute of Chemical Biology and Fundamental Medicine, Siberian Branch, Russian Academy of Sciences, Novosibirsk, 630090 Russia.
Article Synopsis
- * The cancer's molecular mechanisms are not well understood, but mutations in the GNAQ and GNA11 genes are prevalent, and a specific signaling pathway is crucial for tumor development.
- * Current therapies for metastatic uveal melanoma (MUM) are limited, though research is focused on targeted drugs and immunotherapies, with an emphasis on identifying genetic mutations for predicting metastasis risk and guiding treatment decisions.
EHMT2 promotes tumorigenesis in -mutant uveal melanoma ARHGAP29-mediated RhoA pathway.
Acta Pharm Sin B
March 2024
Department of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200001, China.
Article Synopsis
- Constitutive activation of GNAQ/11 is the primary oncogenic event in uveal melanoma (UM), but directly targeting these genes hasn't proven feasible due to their essential cellular functions.
- Research indicated that inhibiting EHMT2, a specific protein, significantly decreased cancer cell growth and movement, with higher levels of EHMT2 associated with worse patient outcomes in UM.
- The study suggests that targeting both EHMT2 and GNAQ/11 pathways could provide an effective therapeutic strategy for UM by disrupting their roles in cancer progression.
INPP5A phosphatase is a synthetic lethal target in GNAQ and GNA11-mutant melanomas.
Nat Cancer
March 2024
Oncology, Novartis Institute for Biomedical Research, Basel, Switzerland.
Activating mutations in GNAQ/GNA11 occur in over 90% of uveal melanomas (UMs), the most lethal melanoma subtype; however, targeting these oncogenes has proven challenging and inhibiting their downstream effectors show limited clinical efficacy. Here, we performed genome-scale CRISPR screens along with computational analyses of cancer dependency and gene expression datasets to identify the inositol-metabolizing phosphatase INPP5A as a selective dependency in GNAQ/11-mutant UM cells in vitro and in vivo. Mutant cells intrinsically produce high levels of the second messenger inositol 1,4,5 trisphosphate (IP3) that accumulate upon suppression of INPP5A, resulting in hyperactivation of IP3-receptor signaling, increased cytosolic calcium and p53-dependent apoptosis.
View Article and Find Full Text PDFMiR-181a-5p inhibits uveal melanoma development by targeting GNAQ and AKT3.
Am J Cancer Res
January 2023
Department of Pharmacology and Physiology, Université de Montréal Montréal, QC H3T 1C5, Canada.
Uveal melanoma (UM) is the most common primary intraocular malignant tumor type in adults. Even after the treatment of the ocular tumor, the prognosis of patients with metastasis remains poor. Hence, an urgent unmet need exists to identify novel approaches to treat advanced UM.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!