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Category :
Languages : en
Pages : 57
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Book Description
The most prevalent site of breast cancer metastasis is bone. We will begin to elucidate the molecular mechanisms involved in bone metastasis. We propose to develop and utilize green (GFP) and/or red (dsRed) fluorescent protein-tagged breast carcinoma xenografts to measure bone metastasis following intracardiac injection. Cell lines developed will be used to test whether a metastasis suppressor (BRMSl) and a gene it down-regulates (osteopontin) alter the efficiency of bone colonization. Concomitantly, we will test the impact of changed gene expression on the ability of tumor cells to adhere to human osteoblast cell cultures or human bone marrow endothelium.
Author:
Publisher:
ISBN:
Category :
Languages : en
Pages : 57
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Book Description
The most prevalent site of breast cancer metastasis is bone. We will begin to elucidate the molecular mechanisms involved in bone metastasis. We propose to develop and utilize green (GFP) and/or red (dsRed) fluorescent protein-tagged breast carcinoma xenografts to measure bone metastasis following intracardiac injection. Cell lines developed will be used to test whether a metastasis suppressor (BRMSl) and a gene it down-regulates (osteopontin) alter the efficiency of bone colonization. Concomitantly, we will test the impact of changed gene expression on the ability of tumor cells to adhere to human osteoblast cell cultures or human bone marrow endothelium.
Author: R.E. Mansel
Publisher: Springer Science & Business Media
ISBN: 1402058667
Category : Health & Fitness
Languages : en
Pages : 439
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Book Description
Written by experts in the subject area, the book covers a broad range of topics in the metastasis of breast cancer, from genetics, biology to clinical management. Main topics include genetic control, biology, growth factors, cell adhesion, cell motility and invasion, natures of bone metastasis, sentinel node therapies, hormonal links, new biomarkers and detection of micrometastasis and diagnosis. This timely book also covers the current treatment options.
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Category :
Languages : en
Pages : 9
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Bone metastasis is one of the major causes of morbidity and mortality in breast cancer (BC) patients. However, only a few human BC cell lines can efficiently metastasize to bone whereas most BC cell lines cannot. Recently, it was shown that systemic administration of the conditioned medium by a melanoma cell line redirected the metastatic dissemination of a weakly metastatic lung carcinoma cell line to the organ sites that were metastasized by the melanoma cell due to the formation of metastasis-permissive niches by bone marrow-derived cells (BMDCs) in these organ sites. The current project was proposed to test the hypothesis that factors secreted by metastasis-competent BC cells may condition bone marrow for the successful homing and skeletal remodeling of circulating BC cells. Athymic nude mice were treated with media conditioned by metastasis-competent BC cells and then inoculated with nonmetastatic BC cells in arterial circulation. The treatment induced limited bone metastasis. Bone histology analysis is currently being performed.
Author: Seema Sethi
Publisher: Springer
ISBN: 3319081624
Category : Medical
Languages : en
Pages : 83
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Book Description
This SpringerBrief gives the latest research on the role of miRNAs in breast cancer metastasis. MicroRNAs (miRNAs) are recently described small endogenous noncoding RNAs implicated in the posttranscriptional control of gene expression. These tiny molecules are involved in developmental, physiologic phenomenon as well as pathologic processes including cancers. In fact, miRNAs have emerged as critical regulators of cancer progression, invasion and metastasis. This is mainly because a single miRNA can affect several downstream genes and signaling pathways with oncogenic or tumor suppressor actions depending on the target genes affected. Due to this multimodal downstream signaling effects, these small endogenous molecules hold great promise in metastasis prevention and treatment. Modulating the activity of miRNAs can provide opportunities for novel cancer interventions. Targeting miRNAs could become a novel prognostic and therapeutic strategy to prevent the future development of metastasis. Thus, miRNAs could also serve as a potential targets for anti-metastatic therapy. The book explores how the expression of miRNAs in the primary tumor could be silenced using antagomirs (chemically modified anti-miRNA oligonucleotides), which could prevent the development of metastasis; whereas once metastasis develops then it could be treated with miRNA mimics for inducing its expression for the treatment. Therefore, development of miRNA-based prophylactic therapies could serve as precision and personalized medicine against future development of metastasis of breast and other cancers.
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Category :
Languages : en
Pages : 62
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Book Description
We have developed and characterised a model of breast cancer metastasis to bone that overcomes the deficiencies of earlier models. It utilises clones of a spontaneous mammary carcinoma that, after orthotopic injection of the tumor cells into the mammary gland, metastasise to bone and cause hypercalcemia. In addition, metastases are detected in some other organs, mainly lungs and liver. Other clones derived from the same primary tumor either do not metastasise, or metastasise only to lungs. In the past year, we have made substantial progress in two areas. One is in a study of the role of a gene, parathyroid hormone related protein (PTHrP), believed to be important in metastasis to bone. We have found that expression of PTHrP is not required for metastasis to bone, but once in the bone environment, high levels of PTHrP enhance tumor growth. This is consistent with a recent clinical study of the link between PTHrP and bone metastasis. Our genome wide screening for genes required for metastasis to bone has revealed several candidates, all but one of which have not been implicated previously in metastasis. They are caveolin- 1, bone morphometric protein-4, osteopontin, protease nexin-l and (33 integrin. Functional studies are underway with these genes.
Author: Chandi C. Mandal
Publisher: Frontiers Media SA
ISBN: 2889634086
Category :
Languages : en
Pages : 116
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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact.
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Category :
Languages : en
Pages : 21
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In order to study the role of MMP-8 on inhibition of cancer growth and progression, we initiated our work to clone the human MMP-8 cDNA and express it in vitro. The pcDNA3.1 contains the following elements: human cytomegalovirus (CMV) immediate-early promoter/enhancer that permits efficient, high-level expression of recombinant protein and V5 epitope that allows detection of recombinant protein with anti-V5 antibody. The MMP-8 cDNA with a V5-epitope tag was cloned downstream into the CMV promoter sequence. The construct pCMV-MMP-1-V5 was sequenced to verify cloning of the MMP-8 cDNA insert in frame. The molecular mechanisms of how TGF-beta1 mediates stimulation of invasion and formation of bone metastases have yet to be completely determined. In my laboratory, we have found that ATF-3 (activating transcription factor- 3) is strongly stimulated and its level is sustained by TGF-beta1 in highly invasive and bone metastatic human breast cancer cells. A defect in repression of ATF-3 expression in breast cancer cells could lead to activation of genes that participate in multi-step breast cancer progression.
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Category :
Languages : en
Pages : 26
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A clinically relevant syngeneic model of breast cancer metastasis has been used to determine gene expression alterations that occur both between primary breast cancers with varying metastatic potential and between matched primary and bone metastases. We have immunopurified epithelial and endothelial cell populations and profiled them separately to identify differentially expressed genes, some of which have not previously been associated with breast cancer metastasis. Expression profiles of vascular endothelium derived from primary tumors of varying metastatic potential identified aberrant expression of genes involved in angiogenesis, cell cycle progression, cytoskeletal structure and tumor suppression. Those altered in the primary tumor epithelium included developmental genes, metastasis suppressors and genes involved in cytoskeletal organization, cell cycle progression, apoptosis and transformation. The microarray data was confirmed by quantitative RT-QPCR. Further analysis of epithelium from matched spine metastases revealed some genes that were upregulated further at the metastatic site. These included stefin Al (inhibitor of cathepsin S) that was upregulated in highly metastatic primary epithelium and increased a further 9-fold in matched bone metastases. The expression in spine metastases was verified by in situ hybridization whilst the expression of stefin Al in subsets of tumor cells in invasive human breast cancer was confirmed by immunohistochemistry.
Author: Milica Pavlovic
Publisher:
ISBN:
Category :
Languages : en
Pages : 195
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El objetivo de esta tesis era identificar determinantes genéticos de cáncer de mama con metástasis óseas. Para ello se utilizó un enfoque integral que se sustenta en células humanas de cáncer de mama, modelos experimentales de ratón y datos clínicos. En primer lugar, nos centramos en los genes específicamente adquiridos para la metástasis ósea, altamente expresados en las lesiones de metástasis óseas, pero no enriquecidos en los tumores primarios de mama que recaen en el hueso. Entre estos genes, el factor secretado NOG destaca como altamente expresado en células de cáncer de mama, principalmente ER-negativas, con alta capacidad de desarrollar metástasis ósea en modelos de ratón. La expresión de NOG aumenta la diferenciación de los osteoclastos y la capacidad de auto-renovación de las células tumorales de mama, estimulando el crecimiento de metástasis óseas. Por otra parte, también nos centramos en las alteraciones genómicas que se asocian significativamente con la recurrencia ósea en tumores primarios de mama. Hemos podido identificar que determinadas alteraciones genéticas fueron adquiridas en derivados altamente metastáticos a hueso comparado con las células parentales. Curiosamente, se seleccionó una ganancia del número de copias en muestras de tumor primario de cáncer de mama con elevado riesgo de recahída en el hueso. En consecuencia, la expresión del gen metastático, que se encuentra dentro de la región genómica, se incrementó en tumores primarios y se asoció con la recurencia al hueso. Dicho gen se perfila como posible mediador de la metástasis ósea del cáncer de mama.
Author: D.R. Welch
Publisher: Springer Science & Business Media
ISBN: 0306478218
Category : Medical
Languages : en
Pages : 275
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Book Description
Being diagnosed with cancer is devastating. But when the cancer cells have to spread to form secondary colonies, the prognosis for the patient is worse. If meaningful improvements in survival are to occur, then control of metastasis will be a foundation. Relatively little is known about the control of the metastatic process at the molecular level. This volume begins to explore our current knowledge regarding the underlying molecular and biochemical mechanisms controlling the metastatic phenotype. While all of the authors attempted to put their findings into a context for translation to the clinical situation, the state-of-the-art does not fully allow this. Nonetheless, we write these summaries of our work as an early effort toward that end. I am grateful to all of the authors who have contributed generously of their time and energies to make this volume a reality. To metastasize, neoplastic cells dissociate from the primary tumor, enter a circulatory compartment (typically lymphatics or blood vasculature), survive transport, arrest, exit the circulation and finally proliferate at a discontinuous site in response to local growth factors. Unless cells accomplish every step of the metastatic cascade, metastases cannot develop. The process is highly inefficient, i. e. ,
