Asset Details
Do you wish to reserve the book?
Gain‐of‐function mutations and copy number increases of Notch2 in diffuse large B‐cell lymphoma
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Gain‐of‐function mutations and copy number increases of Notch2 in diffuse large B‐cell lymphoma
Do you wish to request the book?
Gain‐of‐function mutations and copy number increases of Notch2 in diffuse large B‐cell lymphoma
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Gain‐of‐function mutations and copy number increases of Notch2 in diffuse large B‐cell lymphoma
2009
Overview
Signaling through the Notch1 receptor has a pivotal role in early thymocyte development. Gain of Notch1 function results in the development of T‐cell acute lymphoblastic leukemia in a number of mouse experimental models, and activating Notch1 mutations deregulate Notch1 signaling in the majority of human T‐cell acute lymphoblastic leukemias. Notch2, another member of the Notch gene family, is preferentially expressed in mature B cells and is essential for marginal zone B‐cell generation. Here, we report that 5 of 63 (~8%) diffuse large B‐cell lymphomas, a subtype of mature B‐cell lymphomas, have Notch2 mutations. These mutations lead to partial or complete deletion of the proline‐, glutamic acid‐, serine‐ and threonine‐rich (PEST) domain, or a single amino acid substitution at the C‐terminus of Notch2 protein. Furthermore, high‐density oligonucleotide microarray analysis revealed that some diffuse large B‐cell lymphoma cases also have increased copies of the mutated Notch2 allele. In the Notch activation‐sensitive luciferase reporter assay in vitro, mutant Notch2 receptors show increased activity compared with wild‐type Notch2. These findings implicate Notch2 gain‐of‐function mutations in the pathogenesis of a subset of B‐cell lymphomas, and suggest broader roles for Notch gene mutations in human cancers. (Cancer Sci 2009; 100: 920–926)
Publisher
Blackwell Publishing Asia,Blackwell
Subject
/ Alleles
/ Biological and medical sciences
/ DNA, Complementary - genetics
/ DNA-Binding Proteins - metabolism
/ Female
/ Gene Expression Regulation, Neoplastic - genetics
/ Hematologic and hematopoietic diseases
/ Humans
/ Interferon Regulatory Factors - metabolism
/ Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis
/ Lymphoma, Large B-Cell, Diffuse - genetics
/ Lymphoma, Large B-Cell, Diffuse - metabolism
/ Male
/ Original
/ Proto-Oncogene Proteins c-bcl-6
/ Receptor, Notch2 - metabolism
/ Tumors
