Modification of BRCA1-associated breast cancer risk by HMMR overexpression

Francesca Mateo
ProCURE
March 15, 2022
Nat Commun
https://pubmed.ncbi.nlm.nih.gov/35393420

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/35393420

Research summary

This study examines how overexpression of human HMMR modifies breast cancer risk in BRCA1-deficient contexts. Using a mouse model with human HMMR inserted into Rosa26 under Blg-Cre control, the authors show that HMMR enhances tumorigenesis through mitotic instability, AURKA activation, NF-κB pathway activation, and macrophage recruitment.

Key outcome of the study

Human HMMR overexpression accelerates tumor development in BRCA1-deficient tissue via genomic instability and inflammatory signaling, identifying it as a breast cancer risk modifier.

Mouse model

Rosa26 Knockin of human HMMR gene with loxP-STOP-loxP cassette; Cre-inducible expression driven by Blg-Cre in mammary epithelial cells, combined with Brca1 and Trp53 mutations.

TARGET:
HMMR, Brca1, Trp53
HMMR: RHAMM; Brca1: Breast cancer 1; Trp53: Tumor protein p53

Keywords

BRCA1-associated breast cancer, Inflammation, Tumor progression, Risk modifier genes

Technical specifications

Human gene Knockin, Rosa26 locus, Cre-loxP, Conditional overexpression, Mammary-specific Blg-Cre

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