Molecular genetics and targeted therapies for cutaneous melanoma

2006 ◽  
Vol 1 (1) ◽  
pp. 59-64
Author(s):  
Keith T. Flaherty
2008 ◽  
Vol 3 (2) ◽  
pp. 81-87
Author(s):  
Keith Flaherty ◽  
Keiran S.M. Smalley

Author(s):  
Riccardo Marconcini ◽  
Gaetano Pezzicoli ◽  
Luigia Stefania Stucci ◽  
Maria Chiara Sergi ◽  
Lucia Lospalluti ◽  
...  

2016 ◽  
Vol 69 ◽  
pp. S74
Author(s):  
B. Montico ◽  
G. Giurato ◽  
M. Polano ◽  
A. Rizzo ◽  
J. Dal Col ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (20) ◽  
pp. 5219
Author(s):  
David Millán-Esteban ◽  
María Peña-Chilet ◽  
Zaida García-Casado ◽  
Esperanza Manrique-Silva ◽  
Celia Requena ◽  
...  

According to the divergent pathway model, cutaneous melanoma comprises a nevogenic group with a propensity to melanocyte proliferation and another one associated with cumulative solar damage (CSD). While characterized clinically and epidemiologically, the differences in the molecular profiles between the groups have remained primarily uninvestigated. This study has used a custom gene panel and bioinformatics tools to investigate the potential molecular differences in a thoroughly characterized cohort of 119 melanoma patients belonging to nevogenic and CSD groups. We found that the nevogenic melanomas had a restricted set of mutations, with the prominently mutated gene being BRAF. The CSD melanomas, in contrast, showed mutations in a diverse group of genes that included NF1, ROS1, GNA11, and RAC1. We thus provide evidence that nevogenic and CSD melanomas constitute different biological entities and highlight the need to explore new targeted therapies.


Author(s):  
Matthew S. Evans ◽  
SubbaRao V. Madhunapantula ◽  
Gavin P. Robertson ◽  
Joseph J. Drabick

2021 ◽  
Vol 26 (6) ◽  
pp. 541-555
Author(s):  
Sara D. A. Angione ◽  
Alemayehu Y. Akalu ◽  
Jessica Gartrell ◽  
Elimika Pfuma Fletcher ◽  
Gilbert J. Burckart ◽  
...  

Cancer remains the leading cause of death from disease in children. Historically, in contrast to their adult counterparts, the causes of pediatric malignancies have remained largely unknown, with most pediatric cancers displaying low mutational burdens. Research related to molecular genetics in pediatric cancers is advancing our understanding of potential drivers of tumorigenesis and opening new opportunities for targeted therapies. One such area is fusion oncoproteins, which are a product of chromosomal rearrangements resulting in the fusion of different genes. They have been identified as oncogenic drivers in several sarcomas and leukemias. Continued advancement in the understanding of the biology of fusion oncoproteins will contribute to the discovery and development of new therapies for childhood cancers. Here we review the current scientific knowledge on fusion oncoproteins, focusing on pediatric sarcomas and hematologic cancers, and highlight the challenges and current efforts in developing drugs to target fusion oncoproteins.


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