Immunohistochemical Expression of RhoJ Protein in Breast Carcinoma
- 1CurePath Laboratory (Chirec Institute-Brussels, CHU Tivoli-La Louvière)
- 2Department of Pathology, Brussels University Hospital, Anderlecht, Belgium
- 3CMMI, Charleroi
Abstract
Background:: Breast cancer is the most common form of cancer diagnosed in women. Breast cancer cells gain the expression of mesenchymal-specific genes in a process known as epithelial-mesenchymal transition (EMT). RhoJ, a small Rho GTPase, is a key regulator that promotes resistance to a wide range of chemotherapeutic agents in epithelial-mesenchymal transition tumor cells.
Methods:: Sixty-three cases of invasive breast carcinoma and 10 cases of normal breast tissue were collected to examine the protein’s expression of RhoJ in epithelial and stromal cells. Two pathologists performed the H-Score in a blinded fashion.
Results:: Normal ductal cells expressed RhoJ moderately to sometimes intensely. Normal breast stroma showed low to moderate expression in 95% of cases. All malignant ductal cells, except for 2 cases of metaplastic carcinoma, showed diffuse and intense expression. Stromal cells in invasive areas showed low to moderate expression. We found no statistically significant difference in RhoJ expression between carcinoma and normal breast tissue or between carcinoma subtypes (no special type vs. lobular; triple negative vs. luminal). Interestingly, we found a lower expression of RhoJ in metaplastic carcinomas (2 cases of spindle cell variants).
Conclusions:: High levels of RhoJ expression in most breast carcinomas suggest it could be a valuable therapeutic target. However, further studies involving a larger patient cohort are necessary to validate these findings.
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BibTeX
@article{catteau2026immunohistochemical,
title = {{Immunohistochemical Expression of RhoJ Protein in Breast Carcinoma}},
author = {Xavier Catteau and Manon Charry and Justine Allard and Sandrine Rorive and Isabelle Salmon and Jean-Christophe Noël},
journal = {Applied Immunohistochemistry \& Molecular Morphology},
year = {2026},
month = aug,
doi = {10.1097/pai.0000000000001330},
url = {https://doi.org/10.1097/pai.0000000000001330},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Immunohistochemical Expression of RhoJ Protein in Breast Carcinoma
AU - Xavier Catteau
AU - Manon Charry
AU - Justine Allard
AU - Sandrine Rorive
AU - Isabelle Salmon
AU - Jean-Christophe Noël
PY - 2026
DA - 2026/08/05
JO - Applied Immunohistochemistry & Molecular Morphology
DO - 10.1097/pai.0000000000001330
UR - https://doi.org/10.1097/pai.0000000000001330
AB - Background:: Breast cancer is the most common form of cancer diagnosed in women. Breast cancer cells gain the expression of mesenchymal-specific genes in a process known as epithelial-mesenchymal transition (EMT). RhoJ, a small Rho GTPase, is a key regulator that promotes resistance to a wide range of chemotherapeutic agents in epithelial-mesenchymal transition tumor cells. Methods:: Sixty-three cases of invasive breast carcinoma and 10 cases of normal breast tissue were collected to examine the protein’s expression of RhoJ in epithelial and stromal cells. Two pathologists performed the H-Score in a blinded fashion. Results:: Normal ductal cells expressed RhoJ moderately to sometimes intensely. Normal breast stroma showed low to moderate expression in 95% of cases. All malignant ductal cells, except for 2 cases of metaplastic carcinoma, showed diffuse and intense expression. Stromal cells in invasive areas showed low to moderate expression. We found no statistically significant difference in RhoJ expression between carcinoma and normal breast tissue or between carcinoma subtypes (no special type vs. lobular; triple negative vs. luminal). Interestingly, we found a lower expression of RhoJ in metaplastic carcinomas (2 cases of spindle cell variants). Conclusions:: High levels of RhoJ expression in most breast carcinomas suggest it could be a valuable therapeutic target. However, further studies involving a larger patient cohort are necessary to validate these findings.
SN - 1541-2016
SN - 1533-4058
ER -