Zobrazeno 1 - 4
of 4
pro vyhledávání: '"Madison Chacon"'
Autor:
Michelle Boisvert, Ashwyn A Perera, Alexandra L Condurat, John Jeang, Jessica W Tsai, Dana Novikov, Kevin Zhou, Madison Chacon, Jeromy DiGiacomo, Rushil Kumbhani, Dayle Wang, Michael D Taylor, Jordan R Hansford, Louise Ludlow, Nada Jabado, Keith L Ligon, Rameen Beroukhim, Pratiti Bandopadhayay, David T W Jones
Publikováno v:
Neuro-Oncology. 24:i101-i102
Pediatric low-grade gliomas (pLGGs) are the most frequent brain tumors in children and comprise a heterogeneous group of tumors with different locations, histologic subtypes, ages at presentation, and clinical behavior. Tumors frequently respond to t
Autor:
Leslie Lupien, Adam Boynton, Madison Chacon, Rushil Kumbhani, Gabrielle Gionet, Amy Goodale, David Root, Hasmik Keshishian, Margaret Robinson, Steven Carr, Pratiti Bandopadhayay
Publikováno v:
Neuro-Oncology. 24:i123-i123
MYC-driven medulloblastomas are a particularly devastating group of pediatric brain tumors that exhibit resistance and continued progression despite standard of care treatments. Our preclinical work identified BET-bromodomain inhibitors as a potentia
Autor:
Adam Boynton, Leslie Lupien, Rushil Kumbhani, Gabrielle Gionet, Madison Chacon, Amy Goodale, David Root, Hasmik Keshishian, Margaret Robinson, Steven Carr, Pratiti Bandopadhayay
Publikováno v:
Neuro-Oncology. 24:i126-i126
BET-bromodomain inhibition (BETi) is a promising therapeutic strategy to target MYC-driven cancers, including Group 3 medulloblastoma, a deadly childhood brain tumor. We have shown that BET inhibitors exhibit preclinical efficacy against MYC¬-amplif
Autor:
Leslie Lupien, Veronica Rendo, Eric Morin, Nicholas Khuu, Jeromy DiGiacomo, Prasidda Khadka, Madison Chacon, Sophie Lu, Kristine Pelton, Lara Elcavage, Jaldeep Langhnoja, Keith Ligon, Rameen Beroukhim, Timothy Phoenix, Pratiti Bandopadhayay
Publikováno v:
Neuro-Oncology. 24:i31-i31
TP53 is the most frequently mutated tumor suppressor with somatic alterations found in approximately 50% of all human cancers. In the remaining TP53 wild-type (WT) tumors, functional inactivation of the p53 pathway may be achieved through a variety o