Hexachlorobenzene promotes angiogenesis in vivo, in a breast cancer model and neovasculogenesis in vitro, in the human endothelial cell line HMEC-1

2014 ◽  
Vol 229 ◽  
pp. S153
Author(s):  
Carolina Pontillo ◽  
Alejandro Español ◽  
Florencia Chiappini ◽  
Noelia Miret ◽  
Claudia Cocca ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Endothelial Cell ◽  
Cell Line ◽  
Human Endothelial Cell ◽  
Cancer Model ◽  
Endothelial Cell Line ◽  
Breast Cancer Model ◽  
Human Endothelial Cell Line

Therapeutic monoclonal antibodies target phenotypically-differing human breast cancer

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 13510-13510
Author(s):  
S. E. Hahn ◽  
L. A. da Cruz ◽  
D. Sayegh ◽  
A. Ferry ◽  
K. O’Reilly ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
In Vivo Studies ◽  
Tumor Growth Inhibition ◽  
Cancer Model ◽  
Human Breast ◽  
Breast Cancer Model ◽  
Cancer Tissues

13510 Background: CD44 (an adhesion molecule and stem cell antigen), CD59 (a complement-inhibitory molecule), MCSP (an adhesion and cell-cell interactions), and Trop-2 (EpCam a related signaling molecule) represent a group of biologically-significant cancer proteins acting through distinct mechanisms. We have described Abs with in vitro and in vivo cancer suppressive activity to this group of targets. However, their effectiveness depends on the phenotype of malignant cells; cell response should correlate with expression of its Ag, and tumor cells represent a heterogeneous group of non-synchronous cells. The present study describes the efficacy of those antibodies in breast cancer models and the prevalence of their antigen targets in a survey of human breast cancer tissues. Methods: In vivo activity of antibodies ARH460–16–2 (anti-CD44), AR36A36.11.1 (anti-CD59), AR11BD-2E11–2 (anti-MCSP), and AR47A6.4.2 (anti-Trop-2) in estrogen-dependent and hormone sensitive xenograft models of human breast cancer was examined. In addition, distribution of the antigens in breast cancer was determined by immunohistochemistry using tumor tissue arrays of breast cancer sections from distinct patients. Results: Treatment of an established breast cancer model with ARH460–16–2 resulted in 51% median tumor xenograft suppression (p<0.05), as well as increased survival in an MDA-MB-231 (breast cancer) grafted model. 63% of human breast cancer sections expressed the CD44 antigen. Treatment with anti-CD59 antibody AR36A36.11.1 resulted in 68% xenograft tumor suppression (p<0.005). AR47A6.4.2 anti-Trop-2 antibody bound to 100% of human breast cancer sections tested, and showed efficacy in the estrogen- dependent MCF-7 breast cancer model. Anti-MCSP antibody AR11BD-2E11–2 demonstrated 80% tumor growth inhibition (p<0.001), increased survival in an estrogen-dependent model of breast cancer, and was found to stain 62% of breast cancer tissues examined. Conclusions: The heterogeneity of breast cancer cell phenotypes in in vitro and in vivo studies and variable composite cellular antigen targets is the basis for the therapeutic use of multiple antibodies, each with independent mechanisms of action, and offers a rationale for combined antibody therapy in selected patients. [Table: see text]

Human endothelial cell line from an angiosarcoma

1993 ◽  
Vol 29 (3) ◽  
pp. 199-202 ◽  
Author(s):  
Marie L. Hoover ◽  
Václav Větvička ◽  
John M. Hoffpauir ◽  
Carlo H. Tamburro
Keyword(s):  
Endothelial Cell ◽  
Cell Line ◽  
Human Endothelial Cell ◽  
Endothelial Cell Line ◽  
Human Endothelial Cell Line

Palmitic acid but not palmitoleic acid induces insulin resistance in a human endothelial cell line by decreasing SERCA pump expression

2016 ◽  
Vol 28 (1) ◽  
pp. 53-59 ◽  
Author(s):  
J. Gustavo Vazquez-Jimenez ◽  
Jesus Chavez-Reyes ◽  
Tatiana Romero-Garcia ◽  
Angel Zarain-Herzberg ◽  
Jesus Valdes-Flores ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Endothelial Cell ◽  
Palmitic Acid ◽  
Cell Line ◽  
Palmitoleic Acid ◽  
Human Endothelial Cell ◽  
Endothelial Cell Line ◽  
Human Endothelial Cell Line ◽  
Serca Pump

Structure-based discovery of a small non-peptidic Neuropilins antagonist exerting in vitro and in vivo anti-tumor activity on breast cancer model

2014 ◽  
Vol 349 (2) ◽  
pp. 120-127 ◽  
Author(s):  
Lucia Borriello ◽  
Matthieu Montès ◽  
Yves Lepelletier ◽  
Bertrand Leforban ◽  
Wang-Qing Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Model ◽  
Breast Cancer Model ◽  
Anti Tumor Activity

scholarly journals Gene Signatures Induced by Ionizing Radiation as Prognostic Tools in an In Vitro Experimental Breast Cancer Model

Cancers ◽  
2021 ◽  
Vol 13 (18) ◽  
pp. 4571
Author(s):  
Gloria M. Calaf ◽  
Leodan A. Crispin ◽  
Debasish Roy ◽  
Francisco Aguayo ◽  
Juan P. Muñoz ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cell Line ◽  
Cell Lines ◽  
Cancer Progression ◽  
Combined Treatment ◽  
Cancer Model ◽  
Altered Expression ◽  
Breast Cancer Model

This study aimed to analyze the expression of genes involved in radiation, using an Affymetrix system with an in vitro experimental breast cancer model developed by the combined treatment of low doses of high linear energy transfer (LET) radiation α particle radiation and estrogen yielding different stages in a malignantly transformed breast cancer cell model called Alpha model. Altered expression of different molecules was detected in the non-tumorigenic Alpha3, a malignant cell line transformed only by radiation and originally derived from the parental MCF-10F human cell line; that was compared with the Alpha 5 cell line, another cell line exposed to radiation and subsequently grown in the presence 17β-estradiol. This Alpha5, a tumorigenic cell line, originated the Tumor2 cell line. It can be summarized that the Alpha 3 cell line was characterized by greater gene expression of ATM and IL7R than control, Alpha5, and Tumor2 cell lines, it presented higher selenoprotein gene expression than control and Tumor2; epsin 3 gene expression was higher than control; stefin A gene expression was higher than Alpha5; and metallothionein was higher than control and Tumor2 cell line. Therefore, radiation, independently of estrogen, induced increased ATM, IL7R, selenoprotein, GABA receptor, epsin, stefin, and metallothioneins gene expression in comparison with the control. Results showed important findings of genes involved in cancers of the breast, lung, nervous system, and others. Most genes analyzed in these studies can be used for new prognostic tools and future therapies since they affect cancer progression and metastasis. Most of all, it was revealed that in the Alpha model, a breast cancer model developed by the authors, the cell line transformed only by radiation, independently of estrogen, was characterized by greater gene expression than other cell lines. Understanding the effect of radiotherapy in different cells will help us improve the clinical outcome of radiotherapies. Thus, gene signature has been demonstrated to be specific to tumor types, hence cell-dependency must be considered in future treatment planning. Molecular and clinical features affect the results of radiotherapy. Thus, using gene technology and molecular information is possible to improve therapies and reduction of side effects while providing new insights into breast cancer-related fields.

HIF-1 activation attenuates postischemic myocardial injury: role for heme oxygenase-1 in modulating microvascular chemokine generation

2005 ◽  
Vol 289 (2) ◽  
pp. H542-H548 ◽  
Author(s):  
Ramzi Ockaili ◽  
Ramesh Natarajan ◽  
Fadi Salloum ◽  
Bernard J. Fisher ◽  
Drew Jones ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Line ◽  
Heme Oxygenase ◽  
Ischemia Reperfusion ◽  
Microvascular Endothelial Cell ◽  
Endothelial Cell Line ◽  
Human Microvascular Endothelial Cell ◽  
Microvascular Endothelial

The CXC chemokine IL-8, which promotes adhesion, activation, and transmigration of polymorphonuclear neutrophils (PMN), has been associated with production of tissue injury in reperfused myocardium. Hypoxia-inducible factor-1 (HIF-1) is a heterodimeric peptide that is a key regulator of genes such as heme oxygenase (HO)-1 expressed under hypoxic conditions. We hypothesized that HO-1 plays an important role in regulating proinflammatory mediator production under conditions of ischemia-reperfusion. HIF-1 was activated in the human microvascular endothelial cell line (HMEC-1) with the prolyl hydroxylase inhibitor dimethyloxalylglycine (DMOG). DMOG significantly attenuated cytokine-induced IL-8 promoter activity and protein secretion and cytokine-induced PMN migration across human microvascular endothelial cell line HMEC-1 monolayers. In vivo studies in a rabbit model of myocardial ischemia-reperfusion showed that rabbits pretreated with a 20 mg/kg DMOG infusion ( n = 6) 24 h before study exhibited a 21.58 ± 1.76% infarct size compared with 35.25 ± 2.06% in saline-treated ischemia-reperfusion animals ( n = 6, change in reduction = 39%; P < 0.001). In DMOG-pretreated (20 mg/kg) animals, plasma IL-8 levels at 3 h after onset of reperfusion were 405 ± 40 pg/ml vs. 790 ± 40 pg/ml in saline-treated ischemia-reperfusion animals ( P < 0.001). DMOG pretreatment reduced myocardial myeloperoxidase activity, expressed as number of PMN per gram of myocardium, to 1.43 ± 0.59 vs. 4.86 ± 1.1 ( P = 0.012) in saline-treated ischemia-reperfused hearts. Both in vitro and in vivo DMOG-attenuated IL-8 production was associated with robust HO-1 expression. Thus our data show that HIF-1 activation induces substantial HO-1 expression that is associated with attenuated proinflammatory chemokine production by microvascular endothelium in vitro and in vivo.

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