Over-expression of Smad7 in osteosarcoma cells inhibits primary tumor growth, the associated bone osteolysis and the development of lung metastasis in murine xenograft model

2013 ◽  
Author(s):  
Audrey Lamora ◽  
Julie Talbot ◽  
Berengere Gobin ◽  
Marion Leduc ◽  
Julien Taurelle ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Lung Metastasis ◽  
Primary Tumor ◽  
Xenograft Model ◽  
Primary Tumor Growth ◽  
Osteosarcoma Cells ◽  
Over Expression ◽  
Murine Xenograft Model

scholarly journals Cancer-associated fibroblasts stimulate primary tumor growth and metastatic spread in an orthotopic prostate cancer xenograft model

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Johannes Linxweiler ◽  
Turkan Hajili ◽  
Christina Körbel ◽  
Carolina Berchem ◽  
Philip Zeuschner ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Growth ◽  
Primary Tumor ◽  
Xenograft Model ◽  
Metastatic Spread ◽  
Cancer Associated Fibroblasts ◽  
Primary Tumor Growth

scholarly journals Host deficiency in ephrin-A1 inhibits breast cancer metastasis

F1000Research ◽  
2020 ◽  
Vol 9 ◽  
pp. 217 ◽  
Author(s):  
Eileen Shiuan ◽  
Ashwin Inala ◽  
Shan Wang ◽  
Wenqiang Song ◽  
Victoria Youngblood ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Cancer Cell ◽  
Lung Metastasis ◽  
Primary Tumor ◽  
Tumor Recurrence ◽  
Cancer Metastasis ◽  
Primary Tumor Growth ◽  
Primary Tumors ◽  
4T1 Cells

Background: The conventional dogma of treating cancer by focusing on the elimination of tumor cells has been recently refined to include consideration of the tumor microenvironment, which includes host stromal cells. Ephrin-A1, a cell surface protein involved in adhesion and migration, has been shown to be tumor suppressive in the context of the cancer cell. However, its role in the host has not been fully investigated. Here, we examine how ephrin-A1 host deficiency affects cancer growth and metastasis in a murine model of breast cancer. Methods: 4T1 cells were orthotopically implanted into the mammary fat pads or injected into the tail veins of ephrin-A1 wild-type (Efna1+/+), heterozygous (Efna1+/-), or knockout (Efna1-/-) mice. Tumor growth, lung metastasis, and tumor recurrence after surgical resection were measured. Flow cytometry and immunohistochemistry (IHC) were used to analyze various cell populations in primary tumors and tumor-bearing lungs. Results: While primary tumor growth did not differ between Efna1+/+, Efna1+/-, and Efna1-/- mice, lung metastasis and primary tumor recurrence were significantly decreased in knockout mice. Efna1-/- mice had reduced lung colonization of 4T1 cells compared to Efna1+/+ littermate controls as early as 24 hours after tail vein injection. Furthermore, established lung lesions in Efna1-/- mice had reduced proliferation compared to those in Efna1+/+ controls. Conclusions: Our studies demonstrate that host deficiency of ephrin-A1 does not impact primary tumor growth but does affect metastasis by providing a less favorable metastatic niche for cancer cell colonization and growth. Elucidating the mechanisms by which host ephrin-A1 impacts cancer relapse and metastasis may shed new light on novel therapeutic strategies.

Abstract B78: Rebastinib, a small molecule TIE2 kinase inhibitor, prevents primary tumor growth and lung metastasis in the PyMT breast cancer model

2013 ◽  
Author(s):  
Bryan D. Smith ◽  
Molly M. Hood ◽  
Michael D. Kaufman ◽  
Mark Berger ◽  
Daniel L. Flynn ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Lung Metastasis ◽  
Small Molecule ◽  
Primary Tumor ◽  
Kinase Inhibitor ◽  
Primary Tumor Growth ◽  
Cancer Model ◽  
Breast Cancer Model

scholarly journals P2.04-027 Targeting Adenosine A2B Receptor for Modulation of Tumor Microenvironment, Primary Tumor Growth, and Lung Metastasis

2017 ◽  
Vol 12 (1) ◽  
pp. S1013
Author(s):  
Jason Evans ◽  
Andrey Bobko ◽  
Stephanie Lewis ◽  
Charles Martin ◽  
Mohammed Rahman ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Tumor Growth ◽  
Lung Metastasis ◽  
Primary Tumor ◽  
Primary Tumor Growth ◽  
Adenosine A2b Receptor ◽  
A2b Receptor ◽  
Adenosine A2b

scholarly journals Host deficiency in ephrin-A1 inhibits breast cancer metastasis

F1000Research ◽  
2020 ◽  
Vol 9 ◽  
pp. 217
Author(s):  
Eileen Shiuan ◽  
Ashwin Inala ◽  
Shan Wang ◽  
Wenqiang Song ◽  
Victoria Youngblood ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Cancer Cell ◽  
Lung Metastasis ◽  
Primary Tumor ◽  
Tumor Recurrence ◽  
Cancer Metastasis ◽  
Primary Tumor Growth ◽  
Primary Tumors ◽  
4T1 Cells

Background: The conventional dogma of treating cancer by focusing on the elimination of tumor cells has been recently refined to include consideration of the tumor microenvironment, which includes host stromal cells. Ephrin-A1, a cell surface protein involved in adhesion and migration, has been shown to be tumor suppressive in the context of the cancer cell. However, its role in the host has not been fully investigated. Here, we examine how ephrin-A1 host deficiency affects cancer growth and metastasis in a murine model of breast cancer. Methods: 4T1 cells were orthotopically implanted into the mammary fat pads or injected into the tail veins of ephrin-A1 wild-type (Efna1+/+), heterozygous (Efna1+/-), or knockout (Efna1-/-) mice. Tumor growth, lung metastasis, and tumor recurrence after surgical resection were measured. Flow cytometry and immunohistochemistry (IHC) were used to analyze various cell populations in primary tumors and tumor-bearing lungs. Results: While primary tumor growth did not differ between Efna1+/+, Efna1+/-, and Efna1-/- mice, lung metastasis and primary tumor recurrence were significantly decreased in knockout mice. Efna1-/- mice had reduced lung colonization of 4T1 cells compared to Efna1+/+ littermate controls as early as 24 hours after tail vein injection. Furthermore, established lung lesions in Efna1-/- mice had reduced proliferation compared to those in Efna1+/+ controls. Conclusions: Our studies demonstrate that host deficiency of ephrin-A1 does not impact primary tumor growth but does affect metastasis by providing a less favorable metastatic niche for cancer cell colonization and growth. Elucidating the mechanisms by which host ephrin-A1 impacts cancer relapse and metastasis may shed new light on novel therapeutic strategies.

scholarly journals Overexpression of Smad7 Blocks Primary Tumor Growth and Lung Metastasis Development in Osteosarcoma

2014 ◽  
Vol 20 (19) ◽  
pp. 5097-5112 ◽  
Author(s):  
Audrey Lamora ◽  
Julie Talbot ◽  
Gwenola Bougras ◽  
Jérôme Amiaud ◽  
Marion Leduc ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Lung Metastasis ◽  
Primary Tumor ◽  
Primary Tumor Growth ◽  
Metastasis Development

scholarly journals TLR9 agonist enhances radiofrequency ablation-induced CTL responses, leading to the potent inhibition of primary tumor growth and lung metastasis 

2018 ◽  
Vol 16 (10) ◽  
pp. 820-832 ◽  
Author(s):  
Aizhang Xu ◽  
Lifeng Zhang ◽  
Jingying Yuan ◽  
Fatma Babikr ◽  
Andrew Freywald ◽  
...  
Keyword(s):  
Radiofrequency Ablation ◽  
Tumor Growth ◽  
Lung Metastasis ◽  
Primary Tumor ◽  
Primary Tumor Growth ◽  
Tlr9 Agonist ◽  
Potent Inhibition ◽  
Ctl Responses

Inhibition of tumor growth of cervical cancer cell line in a murine xenograft model by thalidomide

2006 ◽  
Vol 66 (S 01) ◽  
Author(s):  
LC Horn ◽  
M Hermes ◽  
M Wobus ◽  
J Schwock ◽  
M Brulport ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Tumor Growth ◽  
Cell Line ◽  
Cancer Cell ◽  
Xenograft Model ◽  
Cancer Cell Line ◽  
Cervical Cancer Cell ◽  
Cervical Cancer Cell Line ◽  
Murine Xenograft Model ◽  
Inhibition Of Tumor Growth

scholarly journals Intratumoral Canine Distemper Virus Infection Inhibits Tumor Growth by Modulation of the Tumor Microenvironment in a Murine Xenograft Model of Canine Histiocytic Sarcoma

2021 ◽  
Vol 22 (7) ◽  
pp. 3578
Author(s):  
Federico Armando ◽  
Adnan Fayyad ◽  
Stefanie Arms ◽  
Yvonne Barthel ◽  
Dirk Schaudien ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Virus Infection ◽  
Tumor Growth ◽  
Canine Distemper Virus ◽  
Xenograft Model ◽  
Histiocytic Sarcoma ◽  
Oncolytic Viruses ◽  
Canine Distemper ◽  
Murine Xenograft Model ◽  
The Impact

Histiocytic sarcomas refer to highly aggressive tumors with a poor prognosis that respond poorly to conventional treatment approaches. Oncolytic viruses, which have gained significant traction as a cancer therapy in recent decades, represent a promising option for treating histiocytic sarcomas through their replication and/or by modulating the tumor microenvironment. The live attenuated canine distemper virus (CDV) vaccine strain Onderstepoort represents an attractive candidate for oncolytic viral therapy. In the present study, oncolytic virotherapy with CDV was used to investigate the impact of this virus infection on tumor cell growth through direct oncolytic effects or by virus-mediated modulation of the tumor microenvironment with special emphasis on angiogenesis, expression of selected MMPs and TIMP-1 and tumor-associated macrophages in a murine xenograft model of canine histiocytic sarcoma. Treatment of mice with xenotransplanted canine histiocytic sarcomas using CDV induced overt retardation in tumor progression accompanied by necrosis of neoplastic cells, increased numbers of intratumoral macrophages, reduced angiogenesis and modulation of the expression of MMPs and TIMP-1. The present data suggest that CDV inhibits tumor growth in a multifactorial way, including direct cell lysis and reduction of angiogenesis and modulation of MMPs and their inhibitor TIMP-1, providing further support for the concept of its role in oncolytic therapies.

Variability and Discontinuity of the Pathognomonic Systemic Effects Caused by Walker 256 Tumor Progression in Rats

1995 ◽  
Vol 81 (5) ◽  
pp. 370-377 ◽  
Author(s):  
Ovidio Rettori ◽  
Ana Neuza Vieira-Matos ◽  
Quivo S. Tahin
Keyword(s):  
Tumor Growth ◽  
Primary Tumor ◽  
Marked Reduction ◽  
Prognostic Indicator ◽  
Individual Variability ◽  
Systemic Effects ◽  
Primary Tumor Growth ◽  
Multifocal Tumor ◽  
Walker 256 ◽  
Walker 256 Tumor

Cancer pathognomonic systemic effects (PSE) have high individual variability. For this reason present data were collected daily and synchronized considering four main points: inoculation day, onset of PSE, aggravation and death. The subclinical period free of PSE ranged between 15.7±2.2 days, the clinical period was less variable, 8.9±0.5 days, divided in a moderate and a grave phase of nearly the same length. PSE involved disturbances of fundamental homeostatic regulations: appetite, sodium, water, immune, etc. PSE triggering correlated highly with survival (r2=0.95, P<0.01), but poorly with primary tumor growth, and it was anticipated by metastases from 20.5±2.6 to 10.6±1.1 days (P<0.01). After multifocal simultaneous inoculations, PSE triggering was anticipated to 4.2±0.2 days (marked reduction of individual variability), in the presence of small total-tumor masses, absence of macroscopic metastases, and without changes in the following clinical period features. PSE triggering seems to be a major prognostic indicator probably related to multifocal tumor growth.

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