J
John B. Mulliken
Researcher at Boston Children's Hospital
Publications - 567
Citations - 50267
John B. Mulliken is an academic researcher from Boston Children's Hospital. The author has contributed to research in topics: Hemangioma & Hemifacial microsomia. The author has an hindex of 114, co-authored 565 publications receiving 46602 citations. Previous affiliations of John B. Mulliken include Brown University & Shriners Hospitals for Children.
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Journal ArticleDOI
Hemangiomas and vascular malformations in infants and children: a classification based on endothelial characteristics.
John B. Mulliken,Julie Glowacki +1 more
TL;DR: … Those difficulties which have hitherto amused philosophers, and blocked up the way to knowledge, are entirely owing to ourselves.
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Mutations Involving the Transcription Factor CBFA1 Cause Cleidocranial Dysplasia
Stefan Mundlos,Stefan Mundlos,Florian Otto,C Mundlos,C Mundlos,John B. Mulliken,Arthur S. Aylsworth,S Albright,Dick Lindhout,William G. Cole,W Henn,Joan H.M. Knoll,Joan H.M. Knoll,Michael John Owen,Roland Mertelsmann,Bernhard Zabel,Bjorn R. Olsen,Bjorn R. Olsen +17 more
TL;DR: It is concluded that CBFA1 mutations cause Cleidocranial dysplasia and that heterozygous loss of function is sufficient to produce the disorder.
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Interferon Alfa-2a Therapy for Life-Threatening Hemangiomas of Infancy
TL;DR: Evaluated the effects of daily subcutaneous injections of interferon alfa-2a in 20 neonates and infants with life-threatening or vision-threatening hemangiomas that failed to respond to corticosteroid therapy, finding no safe and effective treatment.
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Grafting of burns with cultured epithelium prepared from autologous epidermal cells
TL;DR: The cells from a small piece of epidermis can be grown into a large number of cultured epithelia, which were grafted onto full-thickness burn wounds in two patients, and survived for the period of observation.
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Vascular Dysmorphogenesis Caused by an Activating Mutation in the Receptor Tyrosine Kinase TIE2
Miikka Vikkula,Laurence M. Boon,Kermit L. Carraway,Jennifer T. Calvert,A. John Diamonti,Boyan C. Goumnerov,Krystyna A. Pasyk,Douglas A. Marchuk,Matthew L. Warman,Lewis C. Cantley,John B. Mulliken,Bjorn R. Olsen +11 more
TL;DR: It is concluded that an activating mutation in TIE2 causes inherited VMs in the two families and that the TIE1 signaling pathway is critical for endothelial cell-smooth muscle cell communication in venous morphogenesis.