-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
-
Cosmetic Ingredient
- Water Treatment Chemical
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
Breast cancer is one of the most common malignancies in women worldwide, and family history is a strong risk factor for the disease
About 15-20% of the familial risk is due to related inherited, rare pathological variants in the BRCA1 and BRCA2 genes
The risk of breast cancer in BRCA1 pathological variant carriers is influenced by genetic factors
HMMR (hyaluronan-mediated motor receptor) interacts with BRCA1 and further regulates cell division and apical-basolateral polarization in mammary epithelial cells
In this study, by analyzing human germline cell and tumor-related data, and at the molecular and cellular levels in mouse models, we describe the relationship between molecular, cellular, and tissue microenvironmental changes in BRCA1-related breast cancer risk.
A number of different biological processes, including the interaction between BRCA1 and HMMR, influence the risk of this disease
This result correlates with micronucleation, activation of the cGAS-STING signaling pathway, and non-canonical NF-κB signaling pathway
In conclusion, the study revealed a series of molecular, cellular and tissue microenvironmental changes associated with increased breast cancer risk through analysis from mouse models to humans
Effects of HMMR overexpression on Brca1-mutated tumors, and these changes may contribute to the development of BRCA1-related breast cancer
Original source:
Original Source: Original Source:Mateo, F.
Mateo, F.
, He, Z.
, Mei, L.
et al.
Modification of BRCA1-associated breast cancer risk by HMMR overexpression.
Nat Commun 13, 1895 (07 April 2022).
https://doi.
org/10.
1038/ s41467-022-29335-z.
Leave a message here