Anti-Estrogen Regulation of Macrophage Products That Influence Breast Cancer Cell Proliferation and Susceptibility to Apoptosis PDF Download
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Languages : en
Pages : 23
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Macrophage function can be regulated by breast cancer cells to sustain an inflammatory microenvironment that promotes cancer cell proliferation and survival. MCF-7 cells suppress IL-10 expression by co-cultured macrophages. Activated and resting THP-1 macrophages were able to induce SNAIL expression in MCF-7 cells. SNAIL has been implicated in the epithelial-mesenchymal transition which precedes metastasis. These observations suggest that tumor-associated macrophages may promote progression-related gene expression at discrete steps in the progression cascade. Both Faslodex(TradeMark) and tamoxifen were effective in up-regulating pigment epithelium-derived factor, a potent anti-angiogenic cytokine, and in down-regulating SNAIL in MCF-7 cells.
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Category :
Languages : en
Pages : 23
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Book Description
Macrophage function can be regulated by breast cancer cells to sustain an inflammatory microenvironment that promotes cancer cell proliferation and survival. MCF-7 cells suppress IL-10 expression by co-cultured macrophages. Activated and resting THP-1 macrophages were able to induce SNAIL expression in MCF-7 cells. SNAIL has been implicated in the epithelial-mesenchymal transition which precedes metastasis. These observations suggest that tumor-associated macrophages may promote progression-related gene expression at discrete steps in the progression cascade. Both Faslodex(TradeMark) and tamoxifen were effective in up-regulating pigment epithelium-derived factor, a potent anti-angiogenic cytokine, and in down-regulating SNAIL in MCF-7 cells.
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Category :
Languages : en
Pages : 8
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Book Description
In June 2006, I applied for a final no-cost extension to complete Task 2c of the project which required more time than previously anticipated. Program was slow owing to difficulty in recruiting a qualified laboratory technician for a single year. During the spring and summer (2006). I trained an undergraduate student, Ms. Giaelle Burnett, who is now assisting me with cell culture, western blotting and RT-PCR. The project will be completed in the current year (06/07).
Author: Shyam Narayan Sundar
Publisher:
ISBN:
Category :
Languages : en
Pages : 438
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Author: Shun-Yuan Jiang
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Category :
Languages : en
Pages : 346
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Author: Shunyuan Jiang
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Category :
Languages : en
Pages : 382
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Languages : en
Pages : 0
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This grant addresses the molecular mechanisms of resistance to the anti-estrogen, Tamoxifen, in breast cancers. Both estrogens and antiestrogens influence the cell cycle during the GI phase. In breast tumors, loss of the cdk inhibitor, p27, is associated with a poor prognosis and with steroid resistance. We postulate that altered p27 degradation in breast cancer may contribute to resistance to antiestrogen therapy. In the last year, we have assayed cell cycle effects of estradiol in the ER+ breast cancer cell line, MCF-7. MCF-7 arrests in G1 upon removal of estradiol or on addition of Tamoxifen. Upon re-addition of estradiol, cells re-enter the cell cycle with onset of S phase by 12 hours and loss of both p21 and p27 proteins. Cyclin D1 associated kinase activity rose transiently in early G1. Activation of cyclin E/cdk2 kinase in mid-late G1 was accompanied by loss of cyclin E-associated p21 and p27. The requirement for p27 in the quiescence induced by estradiol depletion was investigated using antisense p27 oligonucleotides. Introduction of the antisense oligonucleotides into quiescent estradiol depleted MCF-7 cells reduced p27 levels five fold. Despite the continued absence of estradiol, the p27 antisense treated group entered into S phase, with an S phase fraction of 28 % at 34 hours post-transfection, while control cells remained arrested. Thus, the loss of p27 was sufficient to mimic the effect of estradiol on G1-to-S phase progression in MCF-7 cells. These data suggest that loss of p27 is critical for estradiol dependant stimulation of breast cancer proliferation and an increase in p27 is essential for cell cycle arrest following an inhibition of estradiol signaling. Ongoing studies address how these effects are altered in steroid resistant breast cancer.
Author: Virginia A. Spencer
Publisher:
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Category :
Languages : en
Pages : 15
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Estrogen affects both the cytoskeletal and chromatin structure of breast cancer cells. The treatment of breast cancer cells with 10 nM estradiol causes the estrogen receptor to recruit histone acetyltransferases to the promoter of the estrogen-responsive PS2 gene within 60 min, while exposure to estrogen for 72 h increases the levels of DNA-associated cytokeratins. To determine the effect of estrogen on regions downstream of estrogen- responsive promoters, quantitative PCR was performed on DNA isolated from chromatin immunoprecipitations using anti-acetylated 113 and H4 antibodies. Treatment with 10 nM estradiol induced a transient state of 113 and 114 acetylation along the PS2 promoter, exon 2, and exon 3, that was maximal after 60-120 min. After three hours, this hyperacetylation decreased to levels above those observed along the PS2 gene in untreated MCF-7 cells. To determine how estrogen influences DNA-associated cytokeratins, the levels of total, intermediate filament-assembled and DNA-associated cytokeratins were determined by Western Blotting and two dimension gel electrophoresis. The level of DNA-associated cytokeratins increased after 2 h of 10 nM estradiol treatment, while the levels of total and filament cytokeratins remained the same. This suggests that early estrogen exposure (i.e. 2 h) promotes interactions between cytokeratins and DNA.
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Category :
Languages : en
Pages : 103
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While approximately 70% of breast cancers express the estrogen receptor (ER) at diagnosis, only two thirds of these will respond to antiestrogens such as Tamoxifen (TAM). Unfortunately, ER positive tumors that are initially responsive, invariably acquire resistance to hormonal therapies (reviewed in (1)).: TAM-resistant tumors usually show continued expression of the ER (2, 3). Estradiol regulates cell proliferation and development in the mammary gland. The elucidation of mechanisms whereby estradiol:ER influences cell cycle regulators and how these are blocked by Tamoxifen is highly relevant to the development of new treatments for steroid resistant breast cancer. Both estrogens and antiestrogens influence the cell cycle during the early Ol phase (4). The cell cycle is governed by a family of cyclin dependent kinases (cdks), whose activity is regulated by positive effectors, the cyclins, by phosphorylation and by negative regulators, the cdk inhibitors (reviewed in (5-7)). p27 or kinase inhibitor protein 1 (KIP 1) is strongly expressed in normal mammary epfthelial cells (8). That p27 protein levels are frequently reduced in primary breast cancers and this correlates with poor prognosis, suggests that p27 is an important negative regulator of the normal breast cell cycle (8-10) . The cellular abundance of p27 is importantly regulated by ubiquitin-mediated proteolysis (11). p27 protein decreases when quiescent MCF-7 breast cancer cells are stimulated to reenter the cell cycle with estradiol treatment and p27 increases when antiestrogens induce Gi arrest ((12, 13) and PNAS manuscript appended).
Author: Dil Afroze
Publisher: BoD – Books on Demand
ISBN: 1789239613
Category : Medical
Languages : en
Pages : 127
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Book Description
This book offers a comprehensive overview of recent developments in the field of breast cancer biology. It is a complete and descriptive reference on motioning pathways and new treatment options for the future transnational scientists and clinicians working on cancer research and treatment. We greatly appreciate the work of all the contributors to this book. They have brought with them tremendous diversity of perspectives and fields, which is truly reflective of the complexity of the topic, and they have come together in this project to serve as the node of multidisciplinary collaboration in this field. Finally, we must acknowledge the thousands of cancer patients who have participated in the studies, and who have inspired us to gather information to significantly progress knowledge in the field in recent years.
Author: Bharat B. Aggarwal
Publisher: Springer
ISBN: 3034808372
Category : Medical
Languages : en
Pages : 489
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Book Description
This volume examines in detail the role of chronic inflammatory processes in the development of several types of cancer. Leading experts describe the latest results of molecular and cellular research on infection, cancer-related inflammation and tumorigenesis. Further, the clinical significance of these findings in preventing cancer progression and approaches to treating the diseases are discussed. Individual chapters cover cancer of the lung, colon, breast, brain, head and neck, pancreas, prostate, bladder, kidney, liver, cervix and skin as well as gastric cancer, sarcoma, lymphoma, leukemia and multiple myeloma.
