M
Matthew P. Vivero
Researcher at Boston Children's Hospital
Publications - 19
Citations - 783
Matthew P. Vivero is an academic researcher from Boston Children's Hospital. The author has contributed to research in topics: Biology & Medicine. The author has an hindex of 8, co-authored 12 publications receiving 599 citations. Previous affiliations of Matthew P. Vivero include Brigham and Women's Hospital & Columbia University.
Papers
More filters
Journal ArticleDOI
Lymphatic and Other Vascular Malformative/Overgrowth Disorders Are Caused by Somatic Mutations in PIK3CA
Valerie L. Luks,Nolan Kamitaki,Matthew P. Vivero,Wibke Uller,Rashed Rab,Judith V.M.G. Bovée,Kristy L. Rialon,Carlos J. Guevara,Ahmad I. Alomari,Arin K. Greene,Steven J. Fishman,Harry P.W. Kozakewich,Reid A. Maclellan,John B. Mulliken,Reza Rahbar,Samantha A. Spencer,Cameron C. Trenor,Joseph Upton,David Zurakowski,Jonathan A. Perkins,Andrew L Kirsh,James T. Bennett,William B. Dobyns,Kyle C. Kurek,Matthew L. Warman,Matthew L. Warman,Matthew L. Warman,Steven A. McCarroll,Rudy Murillo +28 more
TL;DR: Most individuals from Boston Children's Hospital who had isolated LM or LM as part of a syndrome were somatic mosaic for PIK3CA mutations, with 5 specific PIK 3CA mutations accounting for ∼ 80% of cases.
Journal ArticleDOI
A Somatic MAP3K3 Mutation Is Associated with Verrucous Venous Malformation
Javier A. Couto,Matthew P. Vivero,Harry P.W. Kozakewich,Amir H. Taghinia,John B. Mulliken,Matthew L. Warman,Arin K. Greene +6 more
TL;DR: The hypothesis that VVM lesions arise as a consequence of a somatic mutation is tested by whole-exome sequencing on VVM tissue from six unrelated individuals and looking for somatic mutations affecting the same gene in specimens from multiple persons.
Journal ArticleDOI
Endothelial Cells from Capillary Malformations Are Enriched for Somatic GNAQ Mutations.
Javier A. Couto,Lan Huang,Matthew P. Vivero,Nolan Kamitaki,Reid A. Maclellan,John B. Mulliken,Joyce Bischoff,Matthew L. Warman,Arin K. Greene +8 more
TL;DR: Endothelial cells in capillary malformations are enriched for GNAQ mutations and are likely responsible for the pathophysiology underlying capillarymalformation.
Journal ArticleDOI
PIK3CA activating mutations in facial infiltrating lipomatosis.
Reid A. Maclellan,Valerie L. Luks,Matthew P. Vivero,John B. Mulliken,David Zurakowski,Bonnie L. Padwa,Matthew L. Warman,Arin K. Greene,Kyle C. Kurek +8 more
TL;DR: Because PIK3CA encodes a catalytic subunit of PI3K, and in vitro studies have shown that the overgrowth-associated mutations increase this enzyme’s activity,PI3K inhibitors currently in clinical trials for patients with cancer may have a therapeutic role in patients with facial infiltrating lipomatosis.
Journal ArticleDOI
Spry1 and Spry2 Are Essential for Development of the Temporomandibular Joint
TL;DR: The importance of regulated RTK signaling during TMJ development is demonstrated and multiple skeletal origins for the fossa are suggested, providing the evidence that the TMJ condyle and disc develop independently of the mandibular fossa.