scholarly journals Breast tumour angiogenesis

2007 ◽  
Vol 9 (6) ◽  
Author(s):  
Stephen B Fox ◽  
Daniele G Generali ◽  
Adrian L Harris
2010 ◽  
Vol 28 (4) ◽  
pp. 1264-1272 ◽  
Author(s):  
Funda Ustun ◽  
Gülay Durmus-Altun ◽  
Semsi Altaner ◽  
Nermin Tuncbilek ◽  
Cem Uzal ◽  
...  

2020 ◽  
Vol 114 ◽  
pp. 256-269 ◽  
Author(s):  
Maria K. Koch ◽  
Anna Jaeschke ◽  
Berline Murekatete ◽  
Akhilandeshwari Ravichandran ◽  
Mikhail Tsurkan ◽  
...  

1998 ◽  
Vol 77 (1) ◽  
pp. 51-56 ◽  
Author(s):  
KG Peters ◽  
A Coogan ◽  
D Berry ◽  
J Marks ◽  
JD Iglehart ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Shan Gao ◽  
Jingcheng Jiang ◽  
Pan Li ◽  
Huijuan Song ◽  
Weiwei Wang ◽  
...  

Metformin is one of the most widely prescribed antidiabetics for type 2 diabetes. A critical role of metformin against tumorigenesis has recently been implicated, although several studies also reported the lack of anticancer property of the antidiabetics. Given the controversies regarding the potential role of metformin against tumour progression, the effect of metformin against breast, cervical, and ovarian tumour cell lines was examined followed byin vivoassessment of metformin on tumour growth using xenograft breast cancer models. Significant inhibitory impact of metformin was observed in MCF-7, HeLa, and SKOV-3 cells, suggesting an antiproliferative property of metformin against breast, cervical, and ovarian tumour cells, respectively, with the breast tumour cells, MCF-7, being the most responsive.In vivoassessment was subsequently carried out, where mice with breast tumours were treated with metformin (20 mg/kg body weight) or sterile PBS solution for 15 consecutive days. No inhibition of breast tumour progression was detected. However, tumour necrosis was significantly increased in the metformin-treated group, accompanied by decreased capillary formation within the tumours. Thus, despite the lack of short-term benefit of metformin against tumour progression, a preventive role of metformin against breast cancer was implicated, which is at partially attributable to the attenuation of tumour angiogenesis.


Tumor Biology ◽  
2008 ◽  
Vol 29 (2) ◽  
pp. 130-136 ◽  
Author(s):  
Jaclyn K. Wright ◽  
Julia H. Botha ◽  
Strinivasen Naidoo

1994 ◽  
Vol 71 (05) ◽  
pp. 684-691 ◽  
Author(s):  
László Damjanovich ◽  
Csaba Turzó ◽  
Róza Ádány

SummaryThe plasminogen activation system is a delicately balanced assembly of enzymes which seems to have primary influence on tumour progression. The conversion of plasminogen into serine protease plasmin with fibrinolytic activity depends on the actual balance between plasminogen activators (urokinase type; u-PA and tissue type; t-PA) and their inhibitors (type 1 and 2 plasminogen activator inhibitors; PAI-1 and PAI-2). The purpose of this study was to determine the exact histological localization of all the major factors involved in plasminogen activation, and activation inhibition (plasmin system) in benign and malignant breast tumour samples. Our results show that factors of the plasmin system are present both in benign and malignant tumours. Cancer cells strongly labelled for both u-PA and t-PA, but epithelial cells of fibroadenoma samples were also stained for plasminogen activators at least as intensively as tumour cells in cancerous tissues. In fibroadenomas, all the epithelial cells were labelled for PAM. Staining became sporadic in malignant tumours, cells located at the periphery of tumour cell clusters regularly did not show reaction for PAI-1. In the benign tumour samples the perialveolar connective tissue stroma contained a lot of PAI-1 positive cells, showing characteristics of fibroblasts; but their number was strongly decreased in the stroma of malignant tumours. These findings indicate that the higher level of u-PA antigen, detected in malignant breast tumour samples by biochemical techniques, does not necessarily indicate increased u-PA production by tumour cells but it might be owing to the increased number of cells producing u-PA as well. In malignant tumours PAI-1 seems to be decreased in the frontage of malignant cell invasion; i.e. malignant cells at the host/tumour interface do not express PAI-1 in morphologically detectable quantity and in the peritumoural connective tissue the number of fibroblasts containing PAI-1 is also decreased.


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