Prospective study on the role of glucose metabolism in breast cancer occurrence

2011 ◽  
Vol 130 (4) ◽  
pp. 921-929 ◽  
Author(s):  
Sabina Sieri ◽  
Paola Muti ◽  
Agnoli Claudia ◽  
Franco Berrino ◽  
Valeria Pala ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Glucose Metabolism ◽  
Prospective Study ◽  
Cancer Occurrence

Russia (St.-Petersburg)/WHO randomized prospective study of the role of BSE in reduction of breast cancer mortality

1998 ◽  
Vol 34 ◽  
pp. S92
Author(s):  
V. Semiglazov ◽  
V. Moiseyenko ◽  
C. Protsenko ◽  
R. Kharikova ◽  
A. Manihas
Keyword(s):  
Breast Cancer ◽  
Prospective Study ◽  
Cancer Mortality ◽  
Breast Cancer Mortality

scholarly journals Glucose Transporter 3 Is Essential for the Survival of Breast Cancer Cells in the Brain

Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1568 ◽  
Author(s):  
Min-Hsun Kuo ◽  
Wen-Wei Chang ◽  
Bi-Wen Yeh ◽  
Yeh-Shiu Chu ◽  
Yueh-Chun Lee ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Glucose Metabolism ◽  
Brain Metastasis ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Glucose Transporter ◽  
Metastatic Breast ◽  
Breast Cancer Brain Metastasis ◽  
The Brain

Breast cancer brain metastasis commonly occurs in one-fourth of breast cancer patients and is associated with poor prognosis. Abnormal glucose metabolism is found to promote cancer metastasis. Moreover, the tumor microenvironment is crucial and plays an active role in the metabolic adaptations and survival of cancer cells. Glucose transporters are overexpressed in cancer cells to increase glucose uptake. The glucose transporter 3 (GLUT3) is a high-affinity glucose transporter that is highly expressed in mammalian neurons. GLUT3 is also overexpressed in several malignant brain tumors. However, the role of GLUT3 in breast cancer brain metastasis remains unknown. The results of the present study demonstrated that GLUT3 is highly overexpressed in brain metastatic breast cancers and mediates glucose metabolic reprogramming. Furthermore, knockdown of cAMP-response element binding protein (CREB) could directly regulate GLUT3 expression in brain metastatic breast cancer cells. Notably, we verified and provided a novel role of GLUT3 in mediating glucose metabolism and assisting breast cancer cells to survive in the brain to promote brain metastasis.

242. The role of core biopsy in the preoperative classification of breast cancer according to the prognostic factors: A prospective study

2016 ◽  
Vol 42 (9) ◽  
pp. S133
Author(s):  
S. Lanitis ◽  
P. Zafeiriadou ◽  
N. Arkadopoulos ◽  
S. Peristeraki ◽  
A. Kouloura ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Prognostic Factors ◽  
Prospective Study ◽  
Core Biopsy ◽  
A Prospective Study

scholarly journals Microcalcifications Drive Breast Cancer Occurrence and Development by Macrophage-Mediated Epithelial to Mesenchymal Transition

2019 ◽  
Vol 20 (22) ◽  
pp. 5633 ◽  
Author(s):  
Manuel Scimeca ◽  
Rita Bonfiglio ◽  
Erika Menichini ◽  
Loredana Albonici ◽  
Nicoletta Urbano ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Calcium Oxalate ◽  
Epithelial To Mesenchymal Transition ◽  
Benign Lesions ◽  
Mesenchymal Transition ◽  
Cancer Occurrence ◽  
Vitro Data ◽  
In Vitro Data

Background: This study aims to investigate: (a) the putative association between the presence of microcalcifications and the expression of both epithelial-to-mesenchymal transition and bone biomarkers, (b) the role of microcalcifications in the breast osteoblast-like cells (BOLCs) formation, and (c) the association between microcalcification composition and breast cancer progression. Methods: We collected 174 biopsies on which we performed immunohistochemical and ultrastructural analysis. In vitro experiments were performed to demonstrate the relationship among microcalcification, BOLCs development, and breast cancer occurrence. Ex vivo investigations demonstrated the significant increase of breast osteoblast-like cells in breast lesions with microcalcifications with respect to those without microcalcifications. Results: In vitro data displayed that in the presence of calcium oxalate and activated monocytes, breast cancer cells undergo epithelial to mesenchymal transition. Also, in this condition, cells acquired an osteoblast phenotype, thus producing hydroxyapatite. To further confirm in vitro data, we studied 15 benign lesions with microcalcification from patients that developed a malignant condition in the same breast quadrant. Immunohistochemical analysis showed macrophages’ polarization in benign lesions with calcium oxalate. Conclusions: Altogether, our data shed new light about the role of microcalcifications in breast cancer occurrence and progression.

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