Asset Details
Do you wish to reserve the book?
Brd4::Nutm1 fusion gene initiates NUT carcinoma in vivo
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?
Brd4::Nutm1 fusion gene initiates NUT carcinoma in vivo
Do you wish to request the book?
Brd4::Nutm1 fusion gene initiates NUT carcinoma in vivo
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
Brd4::Nutm1 fusion gene initiates NUT carcinoma in vivo
2024
Overview
NUT carcinoma (NC) is an aggressive cancer with no effective treatment. About 70% of NUT carcinoma is associated with chromosome translocation events that lead to the formation of a BRD4::NUTM1 fusion gene. Because the BRD4::NUTM1 gene is unequivocally cytotoxic when ectopically expressed in cell lines, questions remain on whether the fusion gene can initiate NC. Here, we report the first genetically engineered mouse model for NUT carcinoma that recapitulates the human t(15;19) chromosome translocation in mice. We demonstrated that the mouse t(2;17) syntenic chromosome translocation, forming the Brd4::Nutm1 fusion gene, could induce aggressive carcinomas in mice. The tumors present histopathological and molecular features similar to human NC, with enrichment of undifferentiated cells. Similar to the reports of human NC incidence, Brd4::Nutm1 can induce NC from a broad range of tissues with a strong phenotypical variability. The consistent induction of poorly differentiated carcinoma demonstrated a strong reprogramming activity of BRD4::NUTM1. The new mouse model provided a critical preclinical model for NC that will lead to better understanding and therapy development for NC.
Publisher
Life Science Alliance,Life Science Alliance LLC
Subject
/ Bromodomain Containing Proteins
/ Cancer
/ Cell Cycle Proteins - genetics
/ Cell Cycle Proteins - metabolism
/ Genes
/ Mice
/ Neoplasm Proteins - genetics
/ Neoplasm Proteins - metabolism
/ Nuclear Proteins - metabolism
/ Oncogene Proteins, Fusion - genetics
/ Proteins
/ Synteny
/ Transcription Factors - genetics
/ Transcription Factors - metabolism
/ Translocation, Genetic - genetics
/ Tumors
