Sunitinib treatment reduces tumor growth and limits changes in microvascular properties after minor surgical intervention in an in vivo model of secondary breast cancer growth in bone

2016 ◽  
Vol 113 (5) ◽  
pp. 515-521 ◽  
Author(s):  
Malte Schroeder ◽  
Lennart Viezens ◽  
Jasmin Wellbrock ◽  
Walter Fiedler ◽  
Wolfgang Rüther ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Surgical Intervention ◽  
Cancer Growth ◽  
In Vivo Model ◽  
Sunitinib Treatment ◽  
Breast Cancer Growth ◽  
Secondary Breast Cancer

scholarly journals IL-1 drives breast cancer growth and bone metastasis in vivo

Oncotarget ◽  
2016 ◽  
Vol 7 (46) ◽  
pp. 75571-75584 ◽  
Author(s):  
Ingunn Holen ◽  
Diane V. Lefley ◽  
Sheila E. Francis ◽  
Sarah Rennicks ◽  
Steven Bradbury ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Bone Metastasis ◽  
Cancer Growth ◽  
Breast Cancer Growth

scholarly journals Estrogen Deprivation and Inhibition of Breast Cancer Growth in Vivo through Activation of the Orphan Nuclear Receptor Liver X Receptor

2007 ◽  
Vol 21 (8) ◽  
pp. 1781-1790 ◽  
Author(s):  
Haibiao Gong ◽  
Ping Guo ◽  
Yonggong Zhai ◽  
Jie Zhou ◽  
Hirdesh Uppal ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Liver X Receptor ◽  
Cancer Growth ◽  
Estrogen Metabolism ◽  
Endocrine Disorders ◽  
Estrogen Deprivation ◽  
Uterine Epithelial Cell ◽  
Hepatic Expression ◽  
Breast Cancer Growth

Abstract Estrogen plays an important role in normal physiology. It is also a risk factor for breast cancer, and antiestrogen therapies have been shown to be effective in the treatment and prevention of breast cancers. The liver is important for estrogen metabolism, and a compromised liver function has been linked to hyperestrogenism in patients. In this report, we showed that the liver X receptor (LXR) controls estrogen homeostasis by regulating the basal and inducible hepatic expression of estrogen sulfotransferase (Est, or Sult1e1), an enzyme critical for metabolic estrogen deactivation. Genetic or pharmacological activation of LXR resulted in Est induction, which in turn inhibited estrogen-dependent uterine epithelial cell proliferation and gene expression, as well as breast cancer growth in a nude mouse model of tumorigenicity. We further established that Est is a transcriptional target of LXR, and deletion of the Est gene in mice abolished the LXR effect on estrogen deprivation. Interestingly, Est regulation by LXR appeared to be liver specific, further underscoring the role of liver in estrogen metabolism. Activation of LXR failed to induce other major estrogen-metabolizing enzymes, suggesting that the LXR effect on estrogen metabolism is Est specific. In summary, our results have revealed a novel mechanism controlling estrogen homeostasis in vivo and may have implications for drug development in the treatment of breast cancer and other estrogen-related cancerous endocrine disorders.

scholarly journals Small molecule STAT3 inhibitor, 6Br-6a suppresses breast cancer growth in vitro and in vivo

2020 ◽  
Vol 121 ◽  
pp. 109502 ◽  
Author(s):  
Zhe Liu ◽  
Xianmin Ge ◽  
Yuchen Gu ◽  
Yingying Huang ◽  
Hao Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Small Molecule ◽  
Cancer Growth ◽  
Breast Cancer Growth

Photodynamic acidification therapy to reduce triple negative breast cancer growth in vivo.

2016 ◽  
Vol 34 (15_suppl) ◽  
pp. e12574-e12574 ◽  
Author(s):  
Nuha Buchanan Kadri ◽  
Matthew Gdovin ◽  
Nizar Alyassin ◽  
Justin Avila ◽  
Aryana Cruz ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Cancer Growth ◽  
Breast Cancer Growth

scholarly journals Locally advanced breast cancer as a model for biomarkers research

2003 ◽  
Vol 11 (3) ◽  
pp. 135-138
Author(s):  
Dragica Nikolic-Vukosavljevic
Keyword(s):  
Breast Cancer ◽  
Advanced Breast Cancer ◽  
Locally Advanced Breast Cancer ◽  
Locally Advanced ◽  
Molecular Biomarkers ◽  
Advanced Breast ◽  
In Vivo Model ◽  
Breast Cancer Growth ◽  
Er Alpha

The presence of the tumor in locally advanced breast cancer as an in vivo model offers the possibility of studying the effect of primary anticancer therapy on biological parameters. The hypothesis is that changes in certain molecular biomarkers, particular determinants of tumor growth such as proliferation or apoptosis, or molecular biomarkers of angiogenesis modulation, may predict clinical outcome. In this review, numerous molecular biomarkers of proliferation (ER alpha and ER beta, PR, EGF-R family) and apoptosis (p53, Bcl-2 family), as well as molecular biomarkers of angiogenesis (FGF, VEGF) are discussed for their possible role in locally advanced breast cancer growth.

Specific endothelin-A-receptor antagonist ZD4054 inhibits breast cancer growth in vitro and in vivo

2008 ◽  
Vol 68 (S 01) ◽  
Author(s):  
M Smollich ◽  
M Götte ◽  
J Fischgräbe ◽  
I Radke ◽  
L Macedo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Receptor Antagonist ◽  
Cancer Growth ◽  
Endothelin A Receptor ◽  
Endothelin A ◽  
Breast Cancer Growth

Prediction of breast cancer growth rate In vivo and its clinical implications.

2018 ◽  
Vol 36 (15_suppl) ◽  
pp. e12581-e12581
Author(s):  
Shristi Bhattarai ◽  
Sergey Klimov ◽  
Mohammed A. Aleskandarany ◽  
Helen Burrell ◽  
Anthony Wormall ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Rate ◽  
Cancer Growth ◽  
Clinical Implications ◽  
Breast Cancer Growth
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