scholarly journals In Vivo Bioluminescence Tomography for Monitoring Breast Tumor Growth and Metastatic Spreading: Comparative Study and Mathematical Modeling

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Séverine Mollard ◽  
Raphaelle Fanciullino ◽  
Sarah Giacometti ◽  
Cindy Serdjebi ◽  
Sebastien Benzekry ◽  
...  
Keyword(s):  
Mathematical Modeling ◽  
Tumor Growth ◽  
Comparative Study ◽  
Breast Tumor ◽  
Bioluminescence Tomography ◽  
Metastatic Spreading

scholarly journals Promising potential of [177Lu]Lu-DOTA-folate to enhance tumor response to immunotherapy—a preclinical study using a syngeneic breast cancer model

2020 ◽  
Author(s):  
Patrycja Guzik ◽  
Klaudia Siwowska ◽  
Hsin-Yu Fang ◽  
Susan Cohrs ◽  
Peter Bernhardt ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Survival Time ◽  
Tumor Cells ◽  
Median Survival ◽  
Breast Tumor ◽  
Median Survival Time ◽  
Therapy Outcome ◽  
Minor Effect

Abstract Purpose It was previously demonstrated that radiation effects can enhance the therapy outcome of immune checkpoint inhibitors. In this study, a syngeneic breast tumor mouse model was used to investigate the effect of [177Lu]Lu-DOTA-folate as an immune stimulus to enhance anti-CTLA-4 immunotherapy. Methods In vitro and in vivo studies were performed to characterize NF9006 breast tumor cells with regard to folate receptor (FR) expression and the possibility of tumor targeting using [177Lu]Lu-DOTA-folate. A preclinical therapy study was performed over 70 days with NF9006 tumor-bearing mice that received vehicle only (group A); [177Lu]Lu-DOTA-folate (5 MBq; 3.5 Gy absorbed tumor dose; group B); anti-CTLA-4 antibody (3 × 200 μg; group C), or both agents (group D). The mice were monitored regarding tumor growth over time and signs indicating adverse events of the treatment. Results [177Lu]Lu-DOTA-folate bound specifically to NF9006 tumor cells and tissue in vitro and accumulated in NF9006 tumors in vivo. The treatment with [177Lu]Lu-DOTA-folate or an anti-CTLA-4 antibody had only a minor effect on NF9006 tumor growth and did not substantially increase the median survival time of mice (23 day and 19 days, respectively) as compared with untreated controls (12 days). [177Lu]Lu-DOTA-folate sensitized, however, the tumors to anti-CTLA-4 immunotherapy, which became obvious by reduced tumor growth and, hence, a significantly improved median survival time of mice (> 70 days). No obvious signs of adverse effects were observed in treated mice as compared with untreated controls. Conclusion Application of [177Lu]Lu-DOTA-folate had a positive effect on the therapy outcome of anti-CTLA-4 immunotherapy. The results of this study may open new perspectives for future clinical translation of folate radioconjugates.

scholarly journals Nav1.5 regulates breast tumor growth and metastatic dissemination in vivo

Oncotarget ◽  
2015 ◽  
Vol 6 (32) ◽  
pp. 32914-32929 ◽  
Author(s):  
Michaela Nelson ◽  
Ming Yang ◽  
Rebecca Millican-Slater ◽  
William J. Brackenbury
Keyword(s):  
Tumor Growth ◽  
Breast Tumor ◽  
Metastatic Dissemination

scholarly journals Forkhead Box Transcription Factor (FOXO3a) mediates the cytotoxic effect of vernodalin in vitro and inhibits the breast tumor growth in vivo

2015 ◽  
Vol 34 (1) ◽  
Author(s):  
Suresh Kumar Ananda Sadagopan ◽  
Nooshin Mohebali ◽  
Chung Yeng Looi ◽  
Mohadeseh Hasanpourghadi ◽  
Ashok Kumar Pandurangan ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Tumor Growth ◽  
Breast Tumor ◽  
Cytotoxic Effect ◽  
Forkhead Box

scholarly journals Atovaquone Suppresses Triple-Negative Breast Tumor Growth by Reducing Immune-Suppressive Cells

2021 ◽  
Vol 22 (10) ◽  
pp. 5150
Author(s):  
Nehal Gupta ◽  
Shreyas Gaikwad ◽  
Itishree Kaushik ◽  
Stephen E. Wright ◽  
Maciej M. Markiewski ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Cancer Progression ◽  
Breast Tumor ◽  
Triple Negative ◽  
Immune Surveillance ◽  
Suppressor Cells ◽  
Myeloid Derived Suppressor Cells ◽  
In Vivo Models ◽  
Ribosomal Protein S19

A major contributing factor in triple-negative breast cancer progression is its ability to evade immune surveillance. One mechanism for this immunosuppression is through ribosomal protein S19 (RPS19), which facilitates myeloid-derived suppressor cells (MDSCs) recruitment in tumors, which generate cytokines TGF-β and IL-10 and induce regulatory T cells (Tregs), all of which are immunosuppressive and enhance tumor progression. Hence, enhancing the immune system in breast tumors could be a strategy for anticancer therapeutics. The present study evaluated the immune response of atovaquone, an antiprotozoal drug, in three independent breast-tumor models. Our results demonstrated that oral administration of atovaquone reduced HCC1806, CI66 and 4T1 paclitaxel-resistant (4T1-PR) breast-tumor growth by 45%, 70% and 42%, respectively. MDSCs, TGF-β, IL-10 and Tregs of blood and tumors were analyzed from all of these in vivo models. Our results demonstrated that atovaquone treatment in mice bearing HCC1806 tumors reduced MDSCs from tumor and blood by 70% and 30%, respectively. We also observed a 25% reduction in tumor MDSCs in atovaquone-treated mice bearing CI66 and 4T1-PR tumors. In addition, a decrease in TGF-β and IL-10 in tumor lysates was observed in atovaquone-treated mice with a reduction in tumor Tregs. Moreover, a significant reduction in the expression of RPS19 was found in tumors treated with atovaquone.

Estrogen receptor β represses breast tumor growth and angiogenesis in vivo

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 10101-10101
Author(s):  
J. Hartman ◽  
K. Lindberg ◽  
J. Inzunza ◽  
J. Wan ◽  
A. Ström ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Breast Tumor ◽  
Breast Cancer Cells ◽  
Cancer Cell Growth ◽  
Breast Cancer Cell Growth ◽  
Angiogenic Effect

10101 Background: Estrogens are well known stimulators of breast cancer cell growth in vitro as well as in vivo. Two different estrogen receptors exist, namely estrogen receptor (ER) α and β. ERα mediates the proliferative effect of estrogen in breast cancer cells and we have earlier shown that ERβ inhibits cell-cycle progression in vitro. Estrogens are well known stimulators of in vivo breast cancer cell growth as well as angiogenesis, and the effect is mediated through ERα. The function of ERβ in this context is not well understood. Methods: We have used ERα-positive T47D breast cancer cells stably transfected with a Tet/Off regulated ERβ expression vector system. The ERβ-inducible tumor cells are studied in vitro as well as in vivo. Results: By transplanting ERβ-inducible breast cancer cells into SCID-mice, we show that ERβ inhibits tumor growth and reduces the volume of established tumors. Furthermore, we show by immunohistochemistry, that the number of blood microvessels in the tumor periphery is decreased by ERβ expression, counteracting the well-known pro-angiogenic effect of ERα. By Western blot analysis on tumor extracts, we show that the concentration of the important pro-angiogenic growth factors VEGF and bFGF, normally expressed by breast tumor cells, is decreased in the ERβ-expressing tumors compared to the normal tumors. To exclude that the observed anti-angiogenic effect is just a result of reduced tumor growth, we incubated Tet/Off regulated ERβ expressing cells in vitro, during non-hypoxic conditions. We found that the expression of ERβ leads to decreased expression of VEGF and PDGFβ at the mRNA and protein-levels. In transient transfection assays, we found estrogen-ERα mediated up regulation of VEGF, PDGFβ and bFGF-promoter activities in T47D cells, and these activities were all suppressed following co-transfection with an ERβ-expression vector. Conclusions: We conclude that ERβ inhibits growth factor expression at transcriptional level in breast cancer cells; taken together, our data indicates that ERβ inhibits growth and angiogenesis of tumors formed by T47D breast cancer cells. This makes ERβ an interesting therapeutic target in breast cancer and perhaps treatment with the newly designed ERβ-selective ligands might work as a new anti-proliferative and anti-angiogenic therapy. No significant financial relationships to disclose.

Reduction-responsive core-crosslinked hyaluronic acid-b-poly(trimethylene carbonate-co-dithiolane trimethylene carbonate) micelles: synthesis and CD44-mediated potent delivery of docetaxel to triple negative breast tumor in vivo

2018 ◽  
Vol 6 (19) ◽  
pp. 3040-3047 ◽  
Author(s):  
Yaqin Zhu ◽  
Jian Zhang ◽  
Fenghua Meng ◽  
Liang Cheng ◽  
Jan Feijen ◽  
...  
Keyword(s):  
Hyaluronic Acid ◽  
Tumor Growth ◽  
Breast Tumor ◽  
Triple Negative ◽  
Trimethylene Carbonate ◽  
Inhibit Tumor Growth

Docetaxel-loaded core crosslinked HA-P(TMC-DTC) micelles show high targetability to CD44-overexpressing MDA-MB-231 breast tumor and effectively inhibit tumor growth.

Deoxyelephantopin exhibits potent effects against breast tumor growth and metastasis in vitro and in vivo

Planta Medica ◽  
2007 ◽  
Vol 73 (09) ◽  
Author(s):  
CC Huang ◽  
CP Lo ◽  
CY Chiu ◽  
MC Hsieh ◽  
LF Shyur
Keyword(s):  
Tumor Growth ◽  
Breast Tumor ◽  
Tumor Growth And Metastasis

scholarly journals Fucoidan from Fucus vesiculosus inhibits new blood vessel formation and breast tumor growth in vivo

2019 ◽  
Vol 223 ◽  
pp. 115034 ◽  
Author(s):  
Catarina Oliveira ◽  
Sara Granja ◽  
Nuno M Neves ◽  
Rui L Reis ◽  
Fátima Baltazar ◽  
...  
Keyword(s):  
Blood Vessel ◽  
Tumor Growth ◽  
Breast Tumor ◽  
Fucus Vesiculosus ◽  
Blood Vessel Formation ◽  
Vessel Formation

mTORC1 is a target of nordihydroguaiaretic acid to prevent breast tumor growth in vitro and in vivo

2012 ◽  
Vol 136 (2) ◽  
pp. 379-388 ◽  
Author(s):  
Yue Zhang ◽  
Song Xu ◽  
Jun Lin ◽  
Guangyu Yao ◽  
Zelong Han ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Breast Tumor ◽  
Nordihydroguaiaretic Acid
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