Relevant bibliographies by topics / Fibrosarcoma cells

Academic literature on the topic 'Fibrosarcoma cells'

Author: Grafiati
Published: 18 May 2024

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Journal articles on the topic "Fibrosarcoma cells"

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Nikitovic, Dragana, Katerina Kouvidi, Nikos K. Karamanos, and George N. Tzanakakis. "The Roles of Hyaluronan/RHAMM/CD44 and Their Respective Interactions along the Insidious Pathways of Fibrosarcoma Progression." BioMed Research International 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/929531.

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Fibrosarcomas are rare malignant mesenchymal tumors originating from fibroblasts. Importantly, fibrosarcoma cells were shown to have a high content and turnover of extracellular matrix (ECM) components including hyaluronan (HA), proteoglycans, collagens, fibronectin, and laminin. ECMs are complicated structures that surround and support cells within tissues. During cancer progression, significant changes can be observed in the structural and mechanical properties of the ECM components. Importantly, hyaluronan deposition is usually higher in malignant tumors as compared to benign tissues, predicting tumor progression in some tumor types. Furthermore, activated stromal cells are able to produce tissue structure rich in hyaluronan in order to promote tumor growth. Key biological roles of HA result from its interactions with its specific CD44 and RHAMM (receptor for HA-mediated motility) cell-surface receptors. HA-receptor downstream signaling pathways regulate in turn cellular processes implicated in tumorigenesis. Growth factors, including PDGF-BB, TGFβ2, and FGF-2, enhanced hyaluronan deposition to ECM and modulated HA-receptor expression in fibrosarcoma cells. Indeed, FGF-2 through upregulation of specific HAS isoforms and hyaluronan synthesis regulated secretion and net hyaluronan deposition to the fibrosarcoma pericellular matrix modulating these cells’ migration capability. In this paper we discuss the involvement of hyaluronan/RHAMM/CD44 mediated signaling in the insidious pathways of fibrosarcoma progression.
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Valdèz, J. C., M. Rachid, N. Gobbato, and G. Perdigòn. "Apoptosis Study in Thymic Involution in Tumour-Bearing Mice." International Journal of Immunopathology and Pharmacology 11, no. 2 (May 1998): 49–55. http://dx.doi.org/10.1177/039463209801100201.

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By using a colorectal carcinoma induced by s.c. injection of 1,2-dimethylhydrazine and a transplantable fibrosarcoma developed in inbred BALB/c mice 6–8 weeks old we found that tumour development was accompanied by a remarkable thymic involution. Mice bearing small fibrosarcoma or carcinoma (0,05 cm3) had thymuses and spleens with the same weight as those of normal mice. Thymic atrophy and splenomegalia developed in mice bearing large fibrosarcoma (5,00 cm3) and large carcinoma (0,20 cm3). Thymic involution was not the result of an increase in spontaneous cellular apoptosis. However, an increased susceptibility to apoptosis induced by etoposide was observed in thymocytes from mice bearing large carcinomas or large fibrosarcomas, as compared to the same cells derived from normal or small tumour-bearing mice. Dexamethasone induced comparable levels of apoptosis in thymocytes from all groups (normal mice, mice bearing small and large carcinoma and mice bearing small and large fibrosarcoma); doxorrubicin had no significant effect in any group.
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VP, Vinodh, Rahmat Harun, Pulivendhan Sellamuthu, and Regunath Kandasamy. "Primary Central Nervous System Fibrosarcoma." Journal of Neurosciences in Rural Practice 08, S 01 (August 2017): S111—S113. http://dx.doi.org/10.4103/jnrp.jnrp_165_17.

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ABSTRACTWe report a rare case of a young female with primary brain fibrosarcoma, and to the best of our knowledge, we believe that only <50 cases have been reported or described worldwide so far. Fibrosarcoma is a malignant neoplasm, in which histologically the predominant cells are fibroblasts that divide excessively without cellular control and they can invade local tissues or metastasize. Primary central nervous system fibrosarcomas are very aggressive neoplasms and generally have a poor prognosis. This tumor is either from sarcomatous transformation of a meningioma or arises de novo within the brain parenchyma. Our patient, a 48-year-old woman, who presented with progressive speech disorder over the period of 4 months, showed a left temporoparietal lesion with surrounding edema and local mass effect. Total surgical resection was achieved. Histopathology revealed classical fibrosarcoma features and secondary screening revealed no other distant lesion as diagnosis of primary brain fibrosarcoma was established. This case is deemed to be extremely rare because most reports claim that recurrence is within 6 months with poor prognosis; however, this patient is currently recurrence-free at 3 years. This would suggest of the possibility for a relook into this disease's course and recurrence rate when complete excision is achieved. Due to extreme rarity of these tumors, more comparative studies will be needed to improve the disease outcome.
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Vysotskaya, O. V., A. I. Glukhov, Yu P. Semochkina, S. A. Gordeev, and E. Yu Moskaleva. "Telomerase activity, mTert gene expression and the telomere length in mouse mesenchymal stem cells in the late period after γ- and γ,n-irradiation and in the tumors developed from these cells." Biomeditsinskaya Khimiya 66, no. 3 (2020): 265–73. http://dx.doi.org/10.18097/pbmc20206603265.

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In proliferating normal and tumor cells, the telomere length (TL) is maintained by high telomerase activity (TA). In the absence of TA the TL maintenance involves a mechanism of alternative lengthening of telomeres (ALT). The aim of this study was to investigate the level of TA, the mTert expression and TL in cultured normal and transformed by γ- and γ,n-irradiation mesenchymal stem cells (MSCs) from mouse bone marrow, in sarcomas that developed after the transplantation of these cells into syngeneic mice, and in fibrosarcoma cell lines obtained from these tumors to find out the role of AT or ALT in maintaining TL in these cells. During prolonged cultivation of normal and transformed under the influence of γ- (1 Gy and 6 Gy) and γ,n-irradiation (0.05 Gy, 0.5 Gy, and 2 Gy) MSCs from mouse bone marrow, a decrease in TA was detected in irradiated cells. Even deeper decrease in TA was found in sarcomas developed after administration of transformed MSCs to syngeneic mice and in fibrosarcoma cell lines isolated from these tumors in which TA was either absent or was found to be at a very low level. TL in three of the four lines obtained was halved compared to the initial MSCs. With absent or low TA and reduced TL, the cells of all the obtained fibrosarcoma lines successfully proliferated without signs of a change in survival. The mechanism of telomere maintainance in fibrosarcoma cell lines in the absence of TA needs further investigation and it can be assumed that it is associated with the use of the ALT. The detected decrease or absence of TA in transformed under the action of irradiation MSCs with the preservation or even an increase in the telomerase gene expression may be associated with the formation of inactive splicing variants, and requires further study. The obtained lines of transformed MSCs and fibrosarcomas with TA and without the activity of this enzyme can be a useful model for studying the efficacy of TA and ALT inhibitors in vitro and in vivo.
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Annese, Tiziana, Roberto Ronca, Roberto Tamma, Arianna Giacomini, Simona Ruggieri, Elisabetta Grillo, Marco Presta, and Domenico Ribatti. "PTX3 Modulates Neovascularization and Immune Inflammatory Infiltrate in a Murine Model of Fibrosarcoma." International Journal of Molecular Sciences 20, no. 18 (September 17, 2019): 4599. http://dx.doi.org/10.3390/ijms20184599.

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Fibrosarcoma is an aggressive subtype of soft tissue sarcoma categorized in infantile/congenital-type and adult-type. Fibrosarcoma cells and its surrounding immune inflammatory infiltrates overexpress or induce the expression of fibroblast growth factor-2 (FGF-2) that have a crucial role in tumor progression and angiogenesis. The inflammation-associated long pentraxin 3 (PTX3) was found to reduce FGF-2-mediated angiogenesis, but its role on fibrosarcoma immune inflammatory infiltrate is still unknown. In this study, we have evaluated the PTX3 activity on immune infiltrating mast cells, macrophages and T-lymphocytes by immunohistochemistry on murine MC-TGS17-51 fibrosarcoma cells and on transgenic TgN(Tie2-hPTX3) mouse. In these fibrosarcoma models we found a reduced neovascularization and a significant decrease of inflammatory infiltrate. Indeed, we show that PTX3 reduces the level of complement 3 (C3) deposition reducing fibrosarcoma progression. In conclusion, we hypothesize that targeting fibrosarcoma microenvironment by FGF/FGFR inhibitors may improve treatment outcome.
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&NA;. "Modified fibrosarcoma cells induce immunity." Inpharma Weekly &NA;, no. 974 (February 1995): 11. http://dx.doi.org/10.2165/00128413-199509740-00024.

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Paddock, S. W., and G. A. Dunn. "Analysing collisions between fibroblasts and fibrosarcoma cells: fibrosarcoma cells show an active invasionary response." Journal of Cell Science 81, no. 1 (March 1, 1986): 163–87. http://dx.doi.org/10.1242/jcs.81.1.163.

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We describe a direct way of measuring contact inhibition of locomotion by analysing the changes in motion of pairs of colliding cells. This allows values to be assigned to each type of cell in mixed collisions and will enable certain hypotheses about the relationship between contact inhibition and invasion in culture to be tested critically. We find that fibrosarcoma (FS9) cells, on colliding with chick heart fibroblasts, show a reversed contact-inhibition response that we call contact promotion of locomotion. We also describe a measure of the lateral changes in motion that result from collisions between cells and show that this is dependent on the type of colliding cell but, unlike contact inhibition, it does not appear to be dependent on the type of cell with which it collides for the types studied here. Finally, we analyse how the total response is dependent on the dispositions and motions of the cells before collision and we find that FS9 cells, on colliding with fibroblasts, tend to turn towards the point of initial marginal contact. We conclude that the FS9 cells show a pronounced response on colliding with the fibroblasts, which is in contrast to the subjective impression that the FS9 cells do not respond much. These findings support the thesis of Abercrombie and colleagues, that the infiltration of a population of normal cells by a population of invasive cells in culture is dependent on the nature of the response of each cell type to collision with the other and that the invasive cells fail to show contact inhibition in these heterotypic collisions; but the findings further suggest that these invasive cells show an active invasionary response as opposed to merely failing to show contact inhibition.
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Bist, SS, Sarita Mishra, Vinish Agrawal, and Meena Harsh. "Soft Tissue Fibrosarcoma Neck Mimicking as Thyroid Swelling." An International Journal of Otorhinolaryngology Clinics 6, no. 1 (2014): 50–52. http://dx.doi.org/10.5005/jp-journals-10003-1150.

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ABSTRACT Fibrosarcomas are relatively uncommon tumors, commonly arise in the extremities; approximately 10% occur in the head and neck region, most commonly in the sinonasal tract and neck. We hereby report a case of fibrosarcoma in neck clinically mimicking as a thyroid swelling in a 14 years old boy. The patient reported with difficulty in breathing along with stridor at the time of presentation so endotracheal intubation was done to secure the airway. Subsequent ultrasonography guided fine needle aspiration cytology (FNAC) showed atypical cells suggestive of mesenchymal origin. Contrast-enhanced computed tomography scan showed a large heterogeneously enhancing mass lesion in right side of neck with retrosternal extension, while the right lobe of thyroid was displaced superiorly and left lobe was normal. We performed a complete surgical excision of the tumor and histopathological examination showed intermediate to high grade spindle cell sarcoma, favoring fibrosarcoma. Postoperative period was uneventful and the patient was referred to oncology unit for radiotherapy and chemotherapy, but the patient succumbed to the disease 5 weeks after surgery. How to cite this article Bist SS, Mishra S, Varshney S, Agrawal V, Harsh M. Soft Tissue Fibrosarcoma Neck Mimicking as Thyroid Swelling. Int J Otorhinolaryngol Clin 2014; 6(1):50-52.
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Eikelberg, Deborah Johanna, Lisa Allnoch, Pierre Grothmann, Julia Bohner, and Marion Hewicker-Trautwein. "Subcutaneous fibrosarcomas with pulmonary metastases in a white tiger (Panthera tigris) and a lion (Panthera leo)." Veterinary Record Case Reports 8, no. 2 (April 2020): e000960. http://dx.doi.org/10.1136/vetreccr-2019-000960.

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Two cases of recurrent subcutaneous fibrosarcomas in a white tiger and a lion were observed and the animals were euthanised humanely due to clinical deterioration. In both animals, postmortem examination revealed multinodular, white to fawn, firm to greasy, subcutaneous masses at the left side of the thorax infiltrating into the adjacent musculature. Furthermore, the tiger showed a single mass and the lion multiple masses in the lung. Histopathologically, the subcutaneous and pulmonary masses consisted of spindle-shaped neoplastic cells with necrotic areas, and infiltration with multinucleated giant cells and lymphocytes. Immunohistochemically, tumour cells labelled positive for vimentin and negative for desmin, factor VIII-related antigen, smooth muscle actin S100, CD31 and nerve growth factor receptor p75. Thus, the pulmonary tumours were diagnosed as metastases of subcutaneous fibrosarcomas. Like domestic cats, also large, non-domestic felids could be predisposed for metastasising fibrosarcoma, which may be associated with injections or trauma.
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Kaya, Mitsunori, Takuro Wada, Satoshi Nagoya, Satoshi Kawaguchi, Toshihiko Yamashita, Nobuyuki Yamamoto, Mitsunori Yoshimoto, Futoshi Okada, and Seiichi Ishii. "TNP-470 Suppresses the Tumorigenicity of HT1080 Fibrosarcoma Tumor Through the Inhibition of VEGF Secretion From the Tumor Cells." Sarcoma 5, no. 4 (2001): 197–202. http://dx.doi.org/10.1080/13577140120099182.

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Angiogenesis inhibitors are a novel class of promising therapeutic agents for treating cancer. TNP-470, a systemic analogue of fumagillin, is an angiogenesis inhibitor capable of suppressing the tumorigenicity in several animal models even though the mechanisms of action have not been completely clarified. In the current study, we investigated the effects of TNP-470 on human fibrosarcoma cellsin vivoandin vitro. The administration of TNP-470 could suppress the tumorigenicity of HT1080 fibrosarcoma tumor. The conditioned medium from HT1080 fibrosarcoma cells treated with TNP-470 inhibited the proliferation and migration of human endothelial cell line, HUVEC and ECV304. The concentration of VEGF in the conditioned medium from HT1080 cells treated with TNP-470 was lower than that of the cells without TNP-470 treatment, indicating that TNP-470 downregulates the secretion of VEGF from HT1080 cells. These findings strongly suggest that the direct action of TNP-470 on sarcoma cells inhibits angiogenesis through the downregulation of VEGF secretion and this angiogenesis suppression resulted in the inhibition of tumorigenicity of HT1080 fibrosarcoma tumo.
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Dissertations / Theses on the topic "Fibrosarcoma cells"

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Rai, Anuradha. "Activated natural killer cell mediated cyto toxicity of fibrosarcoma cells in mouse." Thesis, University of North Bengal, 1998. http://hdl.handle.net/123456789/926.

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Devlin, Selina Jane. "Induction of fibronectin matrix and growth effects on fibrosarcoma cells." Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334326.

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Alkarrawi, Mohammed. "2-Hydroxybenzoate analogue mediated apoptosis in human HT-1080 fibrosarcoma cells." Thesis, Cardiff University, 2005. http://orca.cf.ac.uk/56105/.

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The antitumour activities of 18 benzoic acid and 2-hydroxybenzoic acid analogues were investigated in HT-1080 fibrosarcoma cell line. Several approaches were used to identify the most effective apoptotic agents capable of inhibiting cell population expansion of HT-1080 cells mostly at a concentration of 0.4mM. Techniques used in this study included: cell viability assays (MTT, direct count and time-lapse tracking images), morphology (DAPI, haematoxylin-eosin, methyl green-pyronin y, and SEM), immunocytochemistry (Annexin V, caspase-3) and pharmacology (2-hydroxybenzoate uptake). The results indicated that most of these compounds showed antiproliferative activities at specific concentrations (range 0.025-8mM), with an incubation time of 2-180 hours. It is evident that zinc 2-hydroxybenzoate was the most effective antiproliferative agent at 0.3 and 0.4mM. Other analogues, mainly calcium, also showed antiproliferative activities but at higher concentrations (up to 8mM). The growth inhibitory effect on HT-1080 cells population after treatment with either calcium or zinc 2-hydroxybenzoates was identified as the occurrence of apoptosis. This was confirmed by the morphological techniques as well as by immunoassay including annexin V and caspase- 3, measured by flow cytometry. Although strong evidence has been presented here for apoptosis, the genetic mechanism remains uncertain. Neither the expression of the six proteins p53, p21, Bax, Bcl-2, histones and TNF-a, nor the cell cycle analysis was able to fully elucidate the mechanism of action of calcium and zinc 2-hydroxybenzoate on HT-1080 cells. Nonetheless, calcium and zinc 2-hydroxybenzoate-induced apoptosis clearly involved caspase-3 through Bax and p53/p21, respectively, and displayed the properties of potentially therapeutic compounds.
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Aabed, Tariq Ahmad. "Radiation effects on mesenchymal stem cells in a model of fibrosarcoma." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/22347/.

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Background: Radiotherapy is a mainstay of sarcoma treatment, but can cause fibrosis, characterized by production of extra-cellular matrix proteins such as collagen by cancer-associated fibroblasts (CAFs) in the cancer stroma and surrounding normal tissues, which makes tumours more aggressive and resistant to further treatment. Mesenchymal stem cells (MSCs) can be recruited to irradiated tumours and can differentiate into CAF-like cells but the mechanisms of these effects remain unclear. Aim: Determine the mechanisms of radiation effects on the recruitment of MSCs to tumours and their differentiation into CAF-like cells. Methods: Mouse MSCs were irradiated directly or exposed to irradiated mouse fibrosarcoma cells (FS120 or FS188) or their conditioned media (CM) and/or irradiated endothelial cells. Expression of CAF/fibrosis markers (collagen, fibronectin, PDGF receptor-β and α-SMA) by MSCs was assessed 3-4 days’ post radiation. Trans-well migration assays were also performed. Candidate proteins were investigated for their ability to stimulate migration and maturation of MSCs to CAF-like cells and for the ability of radiation to stimulate their production in fibrosarcoma cells. Irradiated FS120 and FS188 solid tumours were analysed for collagen, using Masson’s trichrome staining, and α-SMA using IHC and immunofluorescence. Results: Direct irradiation of MSCs had limited effects on their expression of CAF markers and migration, but exposure to irradiated tumour cells or CM and/or endothelial cells increased these effects. Candidate proteins TGF-β1, MCP-1, and SDF-1α all significantly enhanced the migration of MSCs, and radiation increased their production in fibrosarcoma cells. FS188 cells produced more MCP-1 than FS120 cells and FS188 and FS120 cells and their CM increased MSC migration in a radiation-dependent manner. Migration could be at least partially blocked by an MCP-1 blocking antibody. MSC expression of the MCP-1 receptor, CCR2, was increased after exposure to irradiated FS188 cells or their CM. In vivo, irradiated fibrosarcomas showed significant increases in collagen content, with more collagen in FS188 than in FS120 tumours. Conclusion: Results support the notion that MSCs play an important role in radiation-induced CAF activity and fibrosis in sarcoma. MCP-1 was identified as an important mediator of these effects. Moreover, endothelial cells were shown to play an important role in the recruitment of MSCs in response to radiation. In vitro results identifying FS188 cells as being more pro-fibrotic than FS120 cells were consistent with in vivo results. Further work to understand these processes should help to develop novel treatment strategies for combination with radiotherapy.
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Gillingham, Helen. "Role and regulation of aminopeptidase N (CD13) in HT1080 fibrosarcoma cells." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610322.

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Zong, Fang. "Studies on syndecan-1 in mesenchymal tumors." Stockholm : Department of Laboratory Medicine, Karolinska Institutet, 2010. http://diss.kib.ki.se/2010/978-91-7409-749-8/.

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Alfaro, Alejandro. "In situ hybridization of the feline major satellite DNA FA-SAT in feline fibrosarcoma cell lines and feline fibrosarcoma tissue sections." Giessen DVG Service, 2009. http://geb.uni-giessen.de/geb/volltexte/2009/7271/index.html.

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Alfaro, Alejandro [Verfasser]. "In situ hybridization of the feline major satellite DNA FA-SAT in feline fibrosarcoma cell lines and feline fibrosarcoma tissue sections / by Alfaro, Alejandro." Gießen : DVG-Service, 2009. http://d-nb.info/1000186083/34.

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McConnell, Michael James. "Cell-surface Tumoricidal Molecules and NF-kB in the Tumor-burdened Host." Thesis, Virginia Tech, 2002. http://hdl.handle.net/10919/9609.

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Tumor-distal immune suppression promotes tumor growth by preventing the recruitment of leukocytes to the tumor-proximal microenvironment. Tumor necrosis factor (TNF)-a is both secreted by and expressed on the cell-surface (mTNF-a) of macrophages. When stimulated with LPS, tumor-burdened host (TBH) macrophages secrete more TNF-a than normal host (NH) macrophages. In this study, I showed that mTNF-a is elevated both in freshly isolated and stimulated TBH macrophages. Additionally, I analyzed the expression of Fas and FasL on freshly isolated and LPS-stimulated macrophages and found no differences between TBH and NH macrophages. Fas and Fas ligand (FasL) cell-surface expression was analyzed on NH and TBH T-cells. While no difference was observed in freshly isolated cells, cell-surface expression of both proteins remained higher in TBH T-cells than NH T-cells after mitogenic stimulation. Fas and FasL analysis was also extended to the MethKDE fibrosarcoma and I found that these tumor cells express high levels of FasL. Because past observations show increased TNF-a mRNA expression in TBH macrophages relative to NH macrophages, I hypothesized that NF-kB activation may be increased as well. NF-kB is a transcription factor whose activation is required for TNF-a transcription. I observed increased NF-kB activation in both splenic and peritoneal TBH macrophages. Interestingly, electrophoretic mobility shift analysis (EMSA) suggests that different species of NF-kB were found in each distinct population of macrophages. Together, these data demonstrate that cell-surface tumoricidal molecules and NF-kB are dysregulated in the tumor-burdened host.
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Pecoraro, Matteo 1984. "The Role of p63 and the chromatin remodeler Lsh in senescence, tumor development and lymphangiogenesis." Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/326749.

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La senescencia celular es una detención irreversible del ciclo celular que tiene lugar en respuesta a diversos estímulos de estrés, actuando como un mecanismo supresor de tumores para impedir la proliferación de células con riesgo de transformación maligna. Así, mutaciones que interfieren con el proceso de la senescencia pueden favorecer la formación tumoral. De todas formas, cada vez hay más pruebas que sugieren que las células senescentes también pueden ejercer efectos pro-tumorigénicos en el tejido circundante mediante el fenotipo secretor asociado a senescencia (SASP). Así, descifrar los mediadores moleculares de la senescencia y el SASP es crítico para entender los estadios tempranos de la formación y progresión tumoral. Aquí mostramos que la isoforma ΔNα de p63, un factor de transcripción relacionado con p53, es un oncogén que promueve la iniciación tumoral en colaboración con Ras mediante la inhibición de la senescencia inducida por oncogenes (OIS). Efectivamente, el incremento en la expresión de ΔNp63α en queratinocitos primarios de ratón bloquea la OIS y directamente conduce a la formación de un carcinoma de células escamosas (SCC). También identificamos la Helicasa Específica Linfoide (Lsh), un miembro de la familia SNF2 de remodeladores de la cromatina, como nueva diana de p63 necesaria para la inhibición de la senescencia. Posteriormente, demostramos que Lsh es suficiente para iniciar la formación tumoral independientemente de p63, y que el aumento en su expresión conduce a un desarrollo tumoral más agresivo. Sorprendentemente, mostramos que Lsh tiene un papel en la inducción de la linfangiogénesis, un proceso característico de la progresión maligna y la metástasis. Es interesante notar que las pruebas apuntan hacia Lsh actuando sobre el SASP para dirigir la formación y la progresión tumoral. En conjunto, en este trabajo se identifican nuevos mediadores críticos de la senescencia y funciones de la desregulación de la senescencia durante la formación y la progresión tumoral.
Cellular senescence is an irreversible cell cycle arrest that occurs in response to various stresses, acting as a tumor-suppressive mechanism to impede the proliferation of cells at risk for malignant transformation. As such, mutations that interfere with the senescence process can favor tumor formation. However, increasing evidence suggests that senescent cells can also exert pro-tumorigenic effects on the surrounding tissue, through the senescence-associated secretory phenotype (SASP). As such, understanding the molecular mediators of senescence and the SASP is critical to unravel the early stages of tumor formation and progression. Here we show that the ΔNα isoform of p63, a p53-related transcription factor, is an oncogene that promotes tumor initiation in cooperation with Ras, through the inhibition of oncogene-induced senescence (OIS). Indeed, increased expression of Np63 in primary mouse keratinocytes blocks OIS and directly leads to the formation of squamous cell carcinoma (SCC). We also identify Lymphoid Specific Helicase (Lsh), a member of the SNF2 family of chromatin remodelers, as a novel target of p63, required for senescence bypass. Subsequently, we demonstrate that Lsh is sufficient to initiate tumor formation independently of p63, and that its increased expression leads to aggressive tumor development. Surprisingly, we show a role for Lsh in the induction of lymphangiogenesis, a hallmark of malignant progression and metastasis. Interestingly, the evidence points towards Lsh acting on the SASP to instruct tumor formation and progression. Together, this work identifies critical new mediators of senescence, and functional roles for senescence deregulation during tumor formation and progression.
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Books on the topic "Fibrosarcoma cells"

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Nelson, Cole S. Ia expression and suppressive activity of splenic adherent cells during growth of syngeneic murine fibrosarcomas. 1985.

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Book chapters on the topic "Fibrosarcoma cells"

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Wessels, J. M., W. Beisker, H. K. Seidlitz, and E. Unsöld. "Uptake Mechanism of Different Photosensitizers in Fibrosarcoma Cells, Fibroblasts and in Epithelial Cells." In Laser in der Medizin / Laser in Medicine, 108–11. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-50234-7_32.

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Ye, Jun, Hirofumi Nogami, Akira Hayashida, Kiichiro Teruya, Taichi Hara, Yoshinori Katakura, Kazumichi Otsubo, Shinkatsu Morisawa, and Sanetaka Shirahata. "The Inhibition of MMP-2 Expression in Human Fibrosarcoma HT1080 Cells by Electrolyzed-Reduced Water." In Animal Cell Technology: Basic & Applied Aspects, 317–21. Dordrecht: Springer Netherlands, 2003. http://dx.doi.org/10.1007/978-94-017-0726-8_55.

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Hensel, Karin, M. Siepmann, K. Haendschke, S. Emmelmann, A. Daigeler, J. Hauser, and G. Schmitz. "Monitoring of Insonicated Microbubble Behavior and their Effect on Sonoporation Supported Chemotherapy of Fibrosarcoma Cells." In IFMBE Proceedings, 1422–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-89208-3_337.

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Ye, Jun, Kiichiro Teruya, Yoshinori Katakura, Hiroshi Eto, and Sanetaka Shirahata. "Suppressive effect of fucoidan derived from mozuku on in vitro invasion of human fibrosarcoma HT1080 cells." In Animal Cell Technology: Basic & Applied Aspects, 409–15. Dordrecht: Springer Netherlands, 2006. http://dx.doi.org/10.1007/1-4020-4457-7_55.

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Maeda-Yamamoto, Mari, Kazuhiro Osada, Yuichi Yamaguchi, and Kenkou Tsuji. "Inhibitory Effects of Tea Catechins on Invasion of Human Fibrosarcoma HT1080 Cells to the Monolayer of Human Umbilical Vein Endothelial Cells." In Animal Cell Technology: Basic & Applied Aspects, 131–35. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5161-0_23.

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Rager-Zisman, B., J. Gopas, M. Bar-Eli, I. Har-Vardi, G. J. Hammerling, and S. Segal. "NK Sensitivity, H-2, c-K-ras Proto-Oncogene Expression and Metastases: Analysis of the Metastatic Potential of H-2 Gene Transfected Fibrosarcoma Cells." In Advances in Experimental Medicine and Biology, 151–60. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4899-5037-6_17.

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Wang, Kuan. "Titin." In Guidebook to the Cytoskeletal and Motor Proteins, 481–86. Oxford University PressOxford, 1999. http://dx.doi.org/10.1093/oso/9780198599579.003.00145.

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Abstract The name connectin was originally used in 1977 to designate a SOS-insoluble protein mixture from exhaustively extracted striated muscle. Subsequent isolation of titin from the ‘connectin’ fraction in 1981 led to the synonymous usage of titin and connectin in recent literature. An unrelated 70 kDa actin- and laminin-binding protein from fibrosarcoma cells is also called connectin.
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Goncu, Beyza. "Evaluation of Parathyroid Pathophysiology via Cell Distribution and Expression Patterns." In Parathyroid Glands [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106228.

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The parathyroid tissue is composed of the chief, oxyphil, and water-clear cells. The cell type in each parathyroid gland is highly heterogeneous between different pathologies. The parathyroid oxyphil cells are markedly increased in secondary hyperparathyroidism due to chronic kidney diseases. These cells include more eosinophil than oxyphil cells, but they are closer in size to the chief cells. Studies reported that the oxyphil cells are derived from chief cells, and this presents another cell type that occurs as “transitional oxyphilic cells.” As is known, calcium-sensing receptor (CaSR) is expressed abundantly in the chief cells. Expression of CaSR is elevated in disparate parathyroid tissues, which is possibly related to differential expression levels of parathyroid-specific transcription factors including GCM2 (Glial Cells Missing Transcription Factor 2), MAFB (V-maf musculoaponeurotic fibrosarcoma oncogene homolog B), GATA3 (GATA Binding Protein 3), RXR (The retinoid X receptor), and even VDR (Vitamin D Receptor). The pathways that connect CaSR to parathyroid cell proliferation are precisely not known yet. Evaluation of oxyphil and chief cells of parathyroid glands and their differential expression patterns are important to understand the parathyroid function and its behavioral changes due to related diseases. This chapter presents a summary of the current literature on the cell type distribution of parathyroid and pathophysiology by comparing the expression patterns.
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Bisogno, Gianni, and Hans Merks. "Soft-Tissue Sarcomas." In Oxford Textbook of Cancer in Children, 206–18. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198797210.003.0025.

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This chapter discusses soft-tissue sarcomas (STS) in children and adolescents, which comprise approximately 8% of all paediatric malignancies. It highlights the clinical, pathological, and biological characteristics of this heterogeneous group of tumors derived from mesenchymal cells, and it describes the current management and the treatment results. The first part of the chapter is dedicated to the most frequent paediatric STS, rhabdomyosarcomas (RMS), while the second part covers the diagnosis and treatment strategies for non-rhabdomyosarcoma STS (NRSTS) including synovial sarcomas (SS), adult-type NRSTS, and other histotypes (infantile fibrosarcoma (IFS), desmoplastic small round-cell tumour (DSRCT), and malignant rhabdoid tumour (MRT)).
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Chellaiah, A., A. Davis, and T. Mohanakumar. "Human Hdj2." In Guidebook to Molecular Chaperones and Protein-Folding Catalysts, 123. Oxford University PressOxford, 1997. http://dx.doi.org/10.1093/oso/9780198599494.003.0048.

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Abstract An hdj2 cDNA clone was originally isolated from a A-gt11 human umbilical vein endothelial cDNA library (HUVE) using a monoclonal antibody, SK2H10, which reacts specifically to human endothelial cells, monocytes (Schook et al., 1987; Wood et al., 1988). The cDNA clone consists of 1275 nucleotides (GenBank accession number L08063) with an open reading frame (ORF) of 1191 nucleotides (Chellaiah etal., 1993). BLAST comparison of nucleic sequences showed that Hdj2 is 99% homologous to another human cDNA, isolated from a human fibrosarcoma HT-1080 cDNA library, that encodes a homologue (HSDJ) of the DnaJ protein (Oh et al., 1993). Considering the utilization by the yeast Saccharomyces cerevisiae of multiple DnaJ-like proteins (see earlier entries in this section), it is not surprising to find three DnaJ homologues in humans (Cheetham et al., 1992; Chellaiah etal., 1993; Oh etal., 1993).
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Conference papers on the topic "Fibrosarcoma cells"

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Wessels, Jurina M., Wolfgang Beisker, and Harold K. Seidlitz. "Kinetic and localization properties of protoporphyrin dimethyl ester in fibrosarcoma cells." In Europto Biomedical Optics '93, edited by Giulio Jori, Johan Moan, and Willem M. Star. SPIE, 1994. http://dx.doi.org/10.1117/12.168676.

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Hua, Xin, and Han Chunshan. "The effects of tissue factor in the hematogenous metastasis of fibrosarcoma cells." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6029080.

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Yang, Difei, Dan J. Castro, Ivan H. El-Sayed, Mostafa A. El-Sayed, Romaine E. Saxton, and Nancy Y. Zhang. "Fourier-transform infrared spectroscopic comparison of cultured human fibroblast and fibrosarcoma cells." In Photonics West '95, edited by Britton Chance and Robert R. Alfano. SPIE, 1995. http://dx.doi.org/10.1117/12.210030.

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Petrenko, V. S., V. V. Vrublevskaya, M. A. Zhmurina, Yu Yu Skarga, and O. S. Morenkov. "ADAPTATION OF THE CHAPERONE MACHINE OF HUMAN FIBROSARCOMA HT1080 CELLS TO THE LOSS OF HSP90Α AS A RESULT OF THE KNOCKOUT OF THE HSP90AA1 GENE." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-356.

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Knockout of the HSP90AA1 gene encoding Hsp90α in HT1080 human fibrosarcoma cells was accompanied by adaptation of the cellular chaperone machine to Hsp90α loss. Adaptation included increased expression of Hsp90β, key Hsp90 co-chaperones, chaperones and co-chaperones of the Hsp70/Hsp40 complex, components of the TRiC/CCT complex, prefoldins, prefoldin-like PFDL, R2TP, and R2SP chaperone complexes, as well as key mitochondrial chaperones and chaperonins.
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Said, Georges, Marie Guilbert, Emilie Millerot-Serrurot, Laurence Schneider, Christine Terryn, Roselyne Garnotel, and Pierre Jeannesson. "Abstract 521: Impaired migration of human fibrosarcoma cells HT1080 on glycated collagen type I." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-521.

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Skriver, L., L. C. Petersen, L. R. Lund, L. S. Nielsen, and K. Danø. "SINGLE-CHAIN UROKINASE TYPE PLASMINOGEN ACTIVATOR (SCU-PA) FROM HT-1080 HUMAN FIBROSARCOMA CELLS IS A GENUINE PROENZYME." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644394.

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U-PA is released from many cells as a single polypeptide chain (scu-PA) that is converted into its active two-chain form (tcu-PA) by limited proteolysis with plasmin. There is general agreement that scu-PA has an extremely low amidolytic activity, but different oppinions exist, as to whether scu-PA itself can activate plasminogen. We have reinvestigated the plasminogen activating activity of our scu-PA preparations by means of a direct [125]I-plasminogen conversion assay and two amidolytic assays for plasmin and u-PA activity. In the [125]I-plasminogen conversion assay in the presence of bovine pancreatic trypsin inhibitor (BPTI) the subsequent plasmin catalyzed conversion of scu-PA is blocked while the plasminogen activation is unaffected. In this assay with 3oo nM Glu-plasminogen and 15 pM BPTI, 4o nM scu-PA caused a low but significant plasminogen conversion, which could be fully inhibited by pretreatment of scu-PA with diisopropylfluorophos-phate (DFP). DFP-treated scu-PA was convertible to fully active tcu-PA. Rates of plasminogen activation in this type of assay for scu-PA activity was at least 4oo fold slower than that measured for tcu-PA. A coupled amidolytic assay with Lys-plasminogen, scuPA or tcu-PA, BPTI, and the high affinity plasmin substrate H-D-Val-Phe-LyspNA (S2390) was performed under conditions that ensures a low steady state concentration of free plasmin. In this assay the initial rate of Lys-plasminogen activation by DFP-treated scu-PA was at least 25o fold slower than that measured for tcu-PA. Finally, u-PA activity was measured in an assay with the chromogenic substrate <Glu-Gly-ArgpNA (S2444) (o.8mM) in the presence of highly purified Glu-plasminogen (3oonM) and DFP-treated scu-PA (2nM) in the absence of BPTI. Within the initial 15 min of incubation no detectable hydrolysis of S2444 occurred. Addition of tcu-PA (2pM) or plasmin (o.lnM) to the scu-PA/Glu-plasminogen mixture caused a significant reduction of the lag period before onset of the cascade reaction leading to scu-PA conversion and subsequent hydrolysis of S2444. We conclude that the low rates of plasminogen activation measured in these assays by scu-PA might be accounted for by the presence of trace amounts of tcu-PA in the scu-PA preparations, and that scu-PA meets the requirements for a genuine proenzyme
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Ricetti, M. M., A. Samaden, V. Fregoni, M. Vigotti, F. Piovella, and E. Ascari. "TUMOR CELLS INTERACTIONS WITH SUBENDOTHELIAL EXTRACELLULAR MATRIX IN A PERFUSION SYSTEM: ROLE OF PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643197.

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It has been suggested that platelets may facilitate tumor metastasis by increasing tumour cell (TC) adhesion to vascular endothelium mainly through the formation of platelet/TC aggregates. In order to further investigate this we have utilized an in vitro model combining extracellular matrices (EM) from cultured vascular endothelial cells and two neoplastic clones from a mFS6 murine fibrosarcoma: one expressing high metastatic potency (M4) and one with low metastatic potential (M9). These two sublines express an in vitro platelet aggregating activity which has previously been characterized and which correlates with in vivo metastasizing capacity. To reproduce the in vivo flow conditions a flat perfusion chamber was used (*). Glass coverslips, carrying the EM were perfused for 10’ at a wall shear rate of 450 sec™1 with reconstituted heparinized human blood containing 3×10s/ml TC, with or without platelets. Coverage of the EM with adherent TC was evaluated by a morphometric method and expressed as percent TC coverage. M4 cells adhered to EM more than did M9 cells: 4.3% TC coverage for M4, versus 2.5% TC coverage for M9. In the presence of platelets, TC adherence was greatly increased, being 9.7% for M4 and 7.8% for M9. In the experiments performed in the presence of thrombocytes no platelet/TC thrombi were found onto the EM and no TC-induced platelet aggregation was detected in blood after perfusion. Our results confirm that platelets favour the occurrence of metastasis and suggest that other mechanisms than platelet/TC aggregates formation might be involved in this process.(*) K.S. Sakarlassen et al. J.Lab.Cl in.Med. 102:522, 1983
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Medcalf, R. L., E. van den Berg, and W.-D. Schleuning. "THE INFLUENCE OF GLUCOCORTICOID HORMONES ON THE GENE TRANSCRIPTION OF POUR COMPONENTS OF THE FIBRINOLYTIC SYSTEM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644611.

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The hormonal regulation of plasminogen activator (urokinase type (u-PA) and tissue-type (t-PA)) biosynthesis plays an important role in fibrinolysis and extracellular matrix turnover during invasive growth and cell migration. Recently, two genetically distinct inhibitors of both PA's (PA inhibitor 1 (PAI-1) and PA inhibitor 2 (PAI-2)) have been described which may contribute to the modulation of matrix stability. We have employed cloned cDNA probes to study the regulation of biosynthesis of these proteins in the human fibrosarcoma line HT1080. These cells constitutively express high levels of pro-u-PA. PAI-1, PAI-2 and t-PA are also present at relatively low levels. Treatment of the cells with the glucocorticoid dexamethasone (Dex; 10−7 M), almost completely suppresses u-PA gene transcription, as determined by measurement of in vitro elongation of initiated u-PA transcripts in isolated nuclei ("run-on" transcription assay). Concomitantly, Dex also induces PAI-1 and t-PA gene transcription, whereas PAI-2 gene transcription appeared to remain ' unaffected. These changes in transcription rates are also reflected at the level of mRNA: u-PA mRNA is decreased, whereas PAI-1 and t-PA mRNA are simultaneously induced. PAI-2 mRNA is apparently unchanged. These results demonstrate that glucocorticoid hormones reprogramne the expression of components of the fibrinolytic system, and are of possible relevance in the context of inflammatory disease and malignancy.
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Andreasen, P. A., A. Riccio, L. R. Lund, K. G. Welinder, F. Blasi, and K. Danø. "PLASMINOGEN ACTIVATOR INHIBITOR TYPE 1: STUDIES ON STRUCTURE AND REGULATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642810.

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Human plasminogen activator inhibitor type-1 is an Mr∼54,000 protein which specifically inhibits urokinase-type (u-PA) and tissue-type (t-PA) plasminogen activators. During inhibition, u-PA and t-PA convert PAI-1 to an inactive form with Mr∼50,000. We have determined the amino-terminal amino acid sequence of native and converted PAI-1, and isolated and partly sequenced PAI-1 cDNA. The data show that the conversion of PAI-1 consists of cleavage of an Arg-Met bond 33 residues from the carboxy-terminus, thus localizing the reactive center of the inhibitor to that position, and identifying PAI-1 as an "arg-serpin". PAI-1 activity is known to be influenced by a number of agents; we have studied the mechanisms of the stimulation of PAI-1 activity by transforming growth factor-β (TGF-β) and the synthetic glucocorticoid dexame-thasone in human WI-38 lung fibroblasts and HT-1080 fibrosarcoma cells. Bytheuse of PAI-1 cDNA, TGF-β was found to course a rapid increase in PAI-1 mRNA level in WI-38 cells, reaching a maximal 50-fold enhancement after 8 hours. Dexamethasone caused a 10-fold increase in PAI-1 mRNA in HT-1080 cells, which was detectable after 4 hours and became maximal after 16 hours. In both cases, the 3.4 as well as the 2.4 Kb-PAI-1-mRNA species were increased. Quantitative studies on the effect of these agents on PAI-1 protein levels in cell extracts and culture media by ELISA gave results consistent with the effects on PAI-1 mRNA. These studies suggest that TGF-β and glucocorticoids may exert important controls over plasminogen activation-mediated extracellular proteolysis through an enhancement of PAI-1 gene transcription.
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Crochiere, Marsha L., Trinayan Kashyap, Jean-Richard Saint-Martin, Sharon Shechter, Ori Kalid, Eran Shacham, William Senapedis, et al. "Abstract A188: SINE resistant fibrosarcoma cells reveal changes in profile of gene expression, but continue to be sensitive to combination treatment by proteasome inhibition." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-a188.

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