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Relevant bibliographies by topics / TUMOR DERIVED FACTORS

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Academic literature on the topic 'TUMOR DERIVED FACTORS'

Author: Grafiati

Published: 11 September 2023

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Journal articles on the topic "TUMOR DERIVED FACTORS"

1

Russo, Vincenzo, and Maria Pia Protti. "Tumor-derived factors affecting immune cells." Cytokine & Growth Factor Reviews 36 (August 2017): 79–87. http://dx.doi.org/10.1016/j.cytogfr.2017.06.005.

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Cao, Yihai, and Weide Zhong. "Tumor-derived lymphangiogenic factors and lymphatic metastasis." Biomedicine & Pharmacotherapy 61, no. 9 (October 2007): 534–39. http://dx.doi.org/10.1016/j.biopha.2007.08.009.

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Zong, Jinbao, Anton A. Keskinov, Galina V. Shurin, and Michael R. Shurin. "Tumor-derived factors modulating dendritic cell function." Cancer Immunology, Immunotherapy 65, no. 7 (March 16, 2016): 821–33. http://dx.doi.org/10.1007/s00262-016-1820-y.

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Hernandez-Guerrero, Tatiana, Bernard Doger, Jesus Garcia-Foncillas, Michael Jude Wick, and Victor Moreno. "Predictive factors for successful growth of patient derived xenografts (PDX)." Journal of Clinical Oncology 40, no. 16_suppl (June 1, 2022): e15069-e15069. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.e15069.

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e15069 Background: PDXs have become a core component of translational cancer research. Developing these models can become challenging since little is known about which factors influence engraftment rates. We sought to determine which clinical, pathological, or molecular factors may predict better engraftment rates in PDXs. Methods: Between March 2017 and January 2021, biopsies obtained from patients with primary or metastatic cancer were implanted into athymic nude mice. Statistical analyses were performed to identify factors that could correlate with final engraftment defined as achievement of at least three passes and sampling of PDXs tumors. We focused on clinical (patient factors) pathological (patients’ tumor samples) and molecular characteristics (patients’ tumor samples) analyzed either by immunohistochemistry (IHC) or next generation sequencing (NGS). Results: 585 tumor samples were collected and implanted. 21 failed to engraft due lack of malignant cells. Of 564 tumor-positive samples, 187 (33.2%) PDXs achieved successful growth at time of analysis (Feb, 21). The following clinical characteristics were correlated with engraftment: systemic antibiotics within 2 weeks of sampling: (38.1% (72/117) antibiotics- group vs 30.7% (115/260) no-antibiotics) (p = 0.048); systemic steroids within 2 weeks (41.5% (34/48) the steroids-receiving group vs 31.7% (153/329) no-steroids) (p: 0.05). For women, menopausal status was predictive: 34.9% (95/177) in postmenopausal achieved growth, Vs 20,4% (10/39) for premenopausal (p = 0.031). Baseline LDH levels: 74.9% (140/187) LDH levels above the upper limit of normality (ULN) against 25.1% (47/187) with normal LDH (p = 0.034). Tumor grade: Grade 1: 25.4% (47/187); grade 2: 34.8% (65/187) and grade 3: 40.1% (75/187) tumors achieved successful growth (p = 0.043). Similarly, higher ki67 levels were also correlated with better engraftment rates: (low (Ki67 < 15%): 8.9% (9/45) achieved growth, Vs high (Ki67 > 15%): 31% (35/113) (p:0.002). Presence of lymphovascular invasion in tumor sample was also predictive: 42.2% (97/230) with lymphovascular Vs 26.9% (90/334) of samples with no invasion (p = 0.0001). Likewise, 41.8% (59/141) of neural invasion-positive samples achieved growth against 30.3% (128/428) (p = 0.008). Mismatch repair deficient tumors showed better engraftment rates: 62.1% (18/29) achieved growth vs 40.8% (75/184) of proficient tumors (p = 0.026). 84 PDX were breast models, among which 57.9% (11/19) ER negative models grew, Vs 15.4% (10/65) of ER positive models (p = 0.0001). Conclusions: tumors with higher grade and Ki67, lymphovascular and/or perineural invasion, with dMMR and ER expression negative have higher chance of PDX development. Some clinical characteristics can also interfere with PDXs development such as use of steroids or antibiotics prior sampling.

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Pan, Ping-Ying, George X. Wang, Bingjiao Yin, Junko Ozao, Teresa Ku, Celia M. Divino, and Shu-Hsia Chen. "Reversion of immune tolerance in advanced malignancy: modulation of myeloid-derived suppressor cell development by blockade of stem-cell factor function." Blood 111, no. 1 (January 1, 2008): 219–28. http://dx.doi.org/10.1182/blood-2007-04-086835.

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Tumor growth induced a significant increase of myeloid-derived suppressor cells (MDSCs) in the tumor-bearing host. In our previous study, we showed that MDSCs induced tumor-specific T-cell tolerance and the development of T regulatory cells (Tregs). Tumor-derived factors have been implicated in the accumulation of MDSCs. We hypothesize that reduction of MDSC accumulation in tumor-bearing hosts, through the blockade of tumor factors, can prevent T-cell anergy and Treg development and thereby improve immune therapy for the treatment of advanced tumors. Several tumor-derived factors were identified by gene array analysis. Among the candidate factors, stem- cell factor (SCF) is expressed by various human and murine carcinomas and was selected for further study. Mice bearing tumor cells with SCF siRNA knockdown exhibited significantly reduced MDSC expansion and restored proliferative responses of tumor-infiltrating T cells. More importantly, blockade of SCF receptor (ckit)–SCF interaction by anti-ckit prevented tumor-specific T-cell anergy, Treg development, and tumor angiogenesis. Furthermore, the prevention of MDSC accumulation in conjunction with immune activation therapy showed synergistic therapeutic effect when treating mice bearing large tumors. This information supports the notion that modulation of MDSC development may be required to achieve effective immune-enhancing therapy for the treatment of advanced tumors.

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Preuss, Stephanie F., Denise Grieshober, and Hellmut G. Augustin. "Systemic Reprogramming of Endothelial Cell Signaling in Metastasis and Cachexia." Physiology 38, no. 4 (July 1, 2023): 000. http://dx.doi.org/10.1152/physiol.00001.2023.

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Proliferating cancer cells secrete a multitude of factors impacting metabolism, interorgan communication, and tumor progression. The distribution of tumor-derived factors to distant organs occurs via the circulation, which provides an extensive reactive surface lined by endothelial cells. Primary tumor-derived proteins impact cancer progression by modulating endothelial cell activation at the (pre-)metastatic niche, which affects tumor cell dissemination as well as the outgrowth of seeded metastatic cells into overt tumors. In addition, new insight indicates that endothelial cell signaling contributes to metabolic symptoms of cancer, including cancer-associated cachexia, opening a new field of vascular metabolism research. This review addresses how tumor-derived factors systemically affect endothelial cell signaling and activation and impact distant organs as well as tumor progression.

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Chen, Chuanzhi, Wu Lin, Yingying Huang, Xiangliu Chen, Haohao Wang, and Lisong Teng. "The Essential Factors of Establishing Patient-derived Tumor Model." Journal of Cancer 12, no. 1 (2021): 28–37. http://dx.doi.org/10.7150/jca.51749.

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Haimovitz-Friedman, A., DJ Falcone, A. Eldor, V. Schirrmacher, I. Vlodavsky, and Z. Fuks. "Activation of platelet heparitinase by tumor cell-derived factors." Blood 78, no. 3 (August 1, 1991): 789–96. http://dx.doi.org/10.1182/blood.v78.3.789.789.

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Abstract The nature of the cooperation between platelets and tumor cells during the process of blood-borne metastasis is essentially unknown. In previous in vitro studies we showed that platelets participated in the formation of gaps in the endothelial cell lining, and that concomitantly heparan sulfate glycosaminoglycans were degraded by the platelet heparitinase, released on activation of platelets. In the current study we show that the ability to degrade proteoheparan sulfate derived from endothelial extracellular matrix is gradually eliminated when the number of human platelets is decreased from 5 x 10(7) to 10(6) cells/mL. When aliquots of conditioned media or lysates of either Eb or heat-inactivated ESb mouse lymphoma cells (both of which showed no heparanase activity) were added to freeze-thawed lysates of 10(6) platelets, a reappearance of platelet heparitinase activity was observed. A similar activation was not elicited by lysates of several normal mammalian cells. These data suggest that in its native form, a fraction of the platelet heparitinase is stored in an inactive form that can be activated by a factor secreted by lymphoma, but not by normal cells. Partial characterization of the heparitinase-activating factor showed that it is a heat-stable polyanionic molecule, devoid of proteolytic activity and resistant to both proteolytic and chondroitinase digestions. Activation of platelet heparitinase was also observed on coincubation with chondroitinases ABC and AC, suggesting that the inactive form of platelet heparitinase could result from a complex formation with a chondroitinase-sensitive proteoglycan. The lymphoma-derived heparitinase activating factor itself is, however, not a chondroitinase, because activity of chondroitinase could not be detected in Eb and ESb cells. A possible mechanism by which tumor cells recruit and regulate the activity of platelet heparitinase, and its relevance to the progression of blood borne metastasis, is discussed.

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Haimovitz-Friedman, A., DJ Falcone, A. Eldor, V. Schirrmacher, I. Vlodavsky, and Z. Fuks. "Activation of platelet heparitinase by tumor cell-derived factors." Blood 78, no. 3 (August 1, 1991): 789–96. http://dx.doi.org/10.1182/blood.v78.3.789.bloodjournal783789.

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The nature of the cooperation between platelets and tumor cells during the process of blood-borne metastasis is essentially unknown. In previous in vitro studies we showed that platelets participated in the formation of gaps in the endothelial cell lining, and that concomitantly heparan sulfate glycosaminoglycans were degraded by the platelet heparitinase, released on activation of platelets. In the current study we show that the ability to degrade proteoheparan sulfate derived from endothelial extracellular matrix is gradually eliminated when the number of human platelets is decreased from 5 x 10(7) to 10(6) cells/mL. When aliquots of conditioned media or lysates of either Eb or heat-inactivated ESb mouse lymphoma cells (both of which showed no heparanase activity) were added to freeze-thawed lysates of 10(6) platelets, a reappearance of platelet heparitinase activity was observed. A similar activation was not elicited by lysates of several normal mammalian cells. These data suggest that in its native form, a fraction of the platelet heparitinase is stored in an inactive form that can be activated by a factor secreted by lymphoma, but not by normal cells. Partial characterization of the heparitinase-activating factor showed that it is a heat-stable polyanionic molecule, devoid of proteolytic activity and resistant to both proteolytic and chondroitinase digestions. Activation of platelet heparitinase was also observed on coincubation with chondroitinases ABC and AC, suggesting that the inactive form of platelet heparitinase could result from a complex formation with a chondroitinase-sensitive proteoglycan. The lymphoma-derived heparitinase activating factor itself is, however, not a chondroitinase, because activity of chondroitinase could not be detected in Eb and ESb cells. A possible mechanism by which tumor cells recruit and regulate the activity of platelet heparitinase, and its relevance to the progression of blood borne metastasis, is discussed.

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Hamburger, Anne W., Christine P. White, Karin Lurie, and Richard Kaplan. "Monocyte-Derived Growth Factors for Human Tumor Clonogenic Cells." Journal of Leukocyte Biology 40, no. 4 (October 1986): 381–92. http://dx.doi.org/10.1002/jlb.40.4.381.

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Dissertations / Theses on the topic "TUMOR DERIVED FACTORS"

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Kam, Siu-kei Christy. "The role of TGF-[beta] signaling in the initiation of TNF-[beta] expression in human PBMC derived macrophages." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B38746049.

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Kam, Siu-kei Christy, and 甘笑琪. "The role of TGF-{221} signaling in the initiation of TNF-α expression in human PBMC derived macrophages." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B38746049.

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MOSCHETTI, Marta. "Tumor-derived exosomes as factors that promote metastatic niche formation: evaluation of the effects induced by colon cancer derived exosomes on functional activities and structural features of Hepatocytes." Doctoral thesis, Università degli Studi di Palermo, 2023. https://hdl.handle.net/10447/580510.

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Molgat, André. "The Effect of Macrophage-secreted Factors on Preadipocyte Survival." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23628.

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Adipose tissue (AT) expansion and remodeling that maintains healthy function relies on stromal preadipocytes capable of differentiating into new adipocytes (adipogenesis). During chronic positive energy balance, a relative deficit in adipogenesis, from either a decrease in preadipocyte number or their capacity to differentiate, leads to excessive adipocyte hypertrophy and AT dysfunction. AT contains macrophages whose number and activation state is dynamically regulated with changes in AT mass. This study aims to investigate the effect of macrophage-secreted factors on preadipocyte survival. To assess the effect of macrophage-secreted factors on preadipocytes, murine 3T3-L1 preadipocytes or human primary preadipocytes were incubated with macrophage-conditioned medium (MacCM), prepared from either murine (J774A.1, RAW264.7, bone marrow-derived) or human (THP-1, monocyte-derived) macrophage models, respectively. MacCM inhibited preadipocyte apoptosis and activated pro-survival signaling in both preadipocyte models. Inhibition of PDGFR, Akt, or ERK1/2 reduced the pro-survival effect of MacCM in 3T3-L1 preadipocytes. Inhibition of reactive oxygen species (ROS) generation, or enhancement of ROS clearance, reduced MacCM-dependent 3T3-L1 preadipocyte survival. Whereas anti-inflammatory activated macrophages retained the ability to prevent preadipocyte apoptosis, pro-inflammatory activated macrophages did not. TNF-α immunoneutralization restored the survival activity of pro-inflammatory MacCM on 3T3-L1 preadipocytes. These studies reveal a novel pro-survival effect of MacCM on preadipocytes, and identify signaling molecules (PDGF, Akt, ERK1/2, and ROS) that underlie this action. Macrophage activation was found to regulate the pro-survival activity of MacCM. These in vitro cell culture studies are consistent with a model in which the extent of preadipocyte apoptosis in vivo may determine preadipocyte number and the ability of AT to expand while maintaining healthy function during chronic positive energy balance.

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Elstow, S. F. "The angiogenesis factors of the eye and their relationship to tumour derived angiogenesis factors." Thesis, University of Manchester, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.355902.

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Delfini, Marcello. "Jun regulates monocyte-derived macrophage accumulation and tumour progression." Thesis, Aix-Marseille, 2019. http://www.theses.fr/2019AIXM0076.

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Les macrophages sont des cellules immunitaires innées présentes dans chaque organe. Ils sont des cibles thérapeutiques dans de nombreuses maladies, dont le cancer. En dépit de travaux récents sur l'origine des macrophages, les mécanismes régulant leur différenciation sont mal définis. L'expression de Jun, membre de la famille AP-1, augmente pendant la différenciation des macrophages, mais son rôle dans ce processus n'est pas connu.Au cours de mon doctorat, nous avons caractérisé le rôle de Jun dans le développement et l'homéostasie des macrophages, dans un modèle de souris avec délétion conditionnelle de Jun dans la lignée myéloïde (JunΔCsf1r). Nous montrons que Jun contrôle la différenciation, induite par CSF1, des monocytes en macrophages. In vivo, Jun régule l'accumulation de macrophages dérivés de monocytes dans les poumons et intestins. Les macrophages associés aux tumeurs (TAMs) jouent un rôle crucial dans la progression des cancers. L’absence de Jun freine la croissance d’un mélanome et la différenciation, induite par CSF1, des TAMs dérivés de monocytes qui participent à l’angiogénèse tumorale. Cependant, lors d'une inflammation aiguë, Jun n’affecte pas le recrutement de macrophages inflammatoires.En conclusion, nos résultats identifient Jun comme un régulateur central de la différenciation des macrophages. Dans un modèle de mélanome, les macrophages Jun-dépendants exercent des fonctions pro-tumorales. Le fait que Jun soit un régulateur sélectif du développement des macrophages dépendants de CSF-1 permettra de définir de nouvelles approches ciblant sélectivement la différenciation des macrophages, sans altérer les réponses immunitaires dépendantes des monocytes
Macrophages are immune cells present in every organ. Given their variety of functions, macrophages are therapeutic targets in many diseases including cancer. Despite the research efforts to characterise their origins, the molecular mechanisms regulating macrophage differentiation are still poorly defined. Expression of the AP-1 factor, Jun, increases during differentiation, but its role in macrophage development is not known.During my PhD, we characterised how Jun affects macrophage development and homeostasis. We developed a conditional mouse model in which Jun is deficient in the myeloid lineage (JunΔCsf1r). We showed that Jun controls CSF1-mediated monocyte to macrophage differentiation, proliferation and survival. In vivo, Jun loss limits macrophage accumulation in lungs and intestine. Tumour-associated macrophages (TAMs) play critical roles in cancer progression. We observed that Jun deficiency dampens melanoma growth and the differentiation of CSF1-dependent monocyte-derived TAMs. We further showed that Jun-dependent TAMs mediate vessel normalisation in melanoma. During inflammation, Jun was dispensable for the recruitment of monocyte-derived inflammatory macrophages.Altogether, our results identify Jun as a master regulator of macrophage differentiation, without altering monocyte effector functions. In a melanoma model, we showed that Jun-dependent TAMs play tumour-promoting roles. Therefore, Jun is a selective regulator of CSF-1-dependent macrophage development, which is redundant during inflammation; this observation should help to define novel approaches to selectively target macrophage differentiation, without altering monocyte-dependent immune responses

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Lam, Chi-tat, and 林知達. "Identification of brain-derived neurotrophic factor (BDNF) as a novel angiogenic factor in tumor angiogenesis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41290355.

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Lam, Chi-tat. "Identification of brain-derived neurotrophic factor (BDNF) as a novel angiogenic factor in tumor angiogenesis." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41290355.

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Sanders, Paul Michael. "Mechanism of action of a tumour derived lipid mobilising factor." Thesis, Aston University, 2003. http://publications.aston.ac.uk/11005/.

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Cancer cachexia comprises unintentional and debilitating weight loss associated with certain tumour types. Fat loss in cachexia is mediated by a 43kDa Lipid Mobilising Factor (LMF) sharing homology with endogenous Zinc-a2-Glycoprotein (ZAG). LMF and ZAG induced significant lipolysis in isolated epidydimal adipose tissue. This is attenuated by co-incubation with 10mM of antagonist SR59230A and partially attenuated by 25mM PD098059 (indicating b3-AR and MAPK involvement respectively). LMF/ZAG induced in vitro lipid depletion in differentiated 3T3-L1 adipocytes that seen to comprise a significant increase in lipolysis (p<0.01), with only a modest decrease in lipid synthesis (p=0.09). ZAG significantly increased in vitro protein synthesis (p<0.01) in C2C12 myotubes (without an effect on protein degradation). This increase was activated at transcription and attenuated by co-incubation with 10mM SR59230A. Proteolytic digestion of ZAG and LMF followed by sephadex G50 chromatography yielded active fragments of 6-15kDa, indication the entire molecule was not required for bioactivity. Cachexigenic MAC16 cells demonstrated significant in vitro ZAG expression over non-cachexigenic MAC13 (p<0.001). WAT and BAT excised from MAC16 mice of varying weight loss demonstrated increased ZAG expression compared to controls. Dosing of NMRI mice with s/c ZAG failed to reproduce this up-regulation, thus another cachectic factor is responsible. 0.58nM LMF conferred significant protection against hydrogen peroxide, paraquat and bleomycin-induced oxidative stress in the non-cachexigenic MAC13 cell line. This protection was attenuated by 10mM SR59230A indicating a b3-AR mediated effect. In addition, 0.58nM LMF significantly up regulated UCP2 expression (p<0.001), (a mitochondrial protein implicated in the detoxification of ROS) implying this to be the mechanism by which survival was achieved. In vitro, LMF caused significant up-regulation of UCP1 in BAT and UCP2 and 3 in C2C12 myotubes. This increase in uncoupling protein expression further potentiates the negative energy balance and wasting observed in cachexia.

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Halin, Sofia. "Targeting the prostate tumor microenvironment and vasculature : the role of castration, tumor-associated macrophages and pigment epithelium-derived factor." Doctoral thesis, Umeå universitet, Patologi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-30300.

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BACKGROUND: Prostate cancer is the most common cancer among Swedish men. For patients with metastatic prostate cancer the standard therapy is castration, a treatment that initially provides symptomatic relief but unfortunately is not curative. New therapeutic targets for advanced prostate cancer are therefore needed. Prostate cancers are composed of tumor epithelial cells as well as many non-epithelial cells such as cancer associated fibroblasts, blood vessels and inflammatory cells. Many components of the tumor microenvironment such as tumor associated macrophages and angiogenesis have been shown to stimulate tumor progression. This thesis aims to explore mechanisms by which the local environment influences prostate tumor growth and how such mechanisms could be targeted for treatment. MATERIALS AND METHODS: We have used animal models of prostate cancer, in vitro cell culture systems and clinical materials from untreated prostate cancer patients with long follow up. Experiments were evaluated with stereological techniques, immunohistochemistry, western blotting, quantitative real-time PCR, PCR arrays and laser micro dissection. RESULTS: We found that the presence of a tumor induces adaptive changes in the surrounding non-malignant prostate tissue, and that androgen receptor negative prostate tumor cells respond to castration treatment with temporarily reduced growth when surrounded by normal castration-responsive prostate tissue. Further, we show that macrophages are important for prostate tumor growth and angiogenesis in the tumor and in the surrounding non-malignant tissue. In addition, the angiogenesis inhibitor Pigment epithelium-derived factor (PEDF) was found to be down-regulated in metastatic rat and human prostate tumors. Over-expression of PEDF inhibited experimental prostate tumor growth, angiogenesis and metastatic growth and stimulated macrophage tumor infiltration and lymphangiogenesis. PEDF was found to be down-regulated by the prostate microenvironment and tumor necrosis factor (TNF) α. CONCLUSIONS: Our studies indicate that not only the nearby tumor microenvironment but also the surrounding non-malignant prostate tissue are important for prostate tumor growth. Both the tumor and the surrounding non-malignant prostate were characterized by increased angiogenesis and inflammatory cell infiltration. Targeting the surrounding prostate tissue with castration, targeting tumor associated macrophages, or targeting the vasculature directly using inhibitors like PEDF were all shown to repress prostate tumor growth and could prove beneficial for patients with advanced prostate cancer.

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Book chapters on the topic "TUMOR DERIVED FACTORS"

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Pinzon-Charry, Alberto, and J. Alejandro López. "Tumor-Derived Factors Responsible for Dendritic Cell Dysfunction." In Dendritic Cells in Cancer, 103–17. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-88611-4_7.

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Chang, Joan, and Andrew C. Dudley. "The Function and Diagnostic Potential of Adipocyte-Derived Factors in the Tumor Microenvironment." In Biomarkers of the Tumor Microenvironment, 129–66. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-39147-2_6.

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Gabrilovich, Dmitry I. "A Role for STAT3 in Dendritic Cell Regulation by Tumor-Derived Factors." In Dendritic Cells in Cancer, 143–55. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-88611-4_10.

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Chan, Jerry K. Y., and Paula Lam. "Soluble Factors from Human Fetal Bone Marrow-Derived Mesenchymal Stem Cells: Preparation of Conditioned Medium and Its Effect on Tumor Cells." In Mesenchymal Stem Cells, 467–75. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3584-0_28.

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Martinho, Olga, and Rui Manuel Reis. "Malignant Gliomas: Role of Platelet-Derived Growth Factor Receptor A (PDGFRA)." In Tumors of the Central Nervous System, Volume 1, 109–18. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-94-007-0344-5_12.

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Rossi, Gertrud, Selma Alijagic, Dagmar Schoeler, Markus Schmitt, Hermann Graf, Beate M. Czarnetzki, and David Wallach. "Tumor Necrosis Factor Receptors of the Monocyte Derived Langerhans Cell Phenotype “MoLC”." In Advances in Experimental Medicine and Biology, 129–33. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1971-3_28.

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Bogdan, C., Y. Vodovotz, and C. F. Nathan. "Regulation of macrophage functions by macrophage deactivating factor, a tumor cell-derived cytokine." In Mononuclear Phagocytes, 381–88. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-015-8070-0_51.

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Wallach, D., K. Cantell, S. Hirvonen, L. Toker, D. Aderka, and H. Holtmann. "Presence of Tumor Necrosis Factor and Lymphotoxin in Clinical Interferon Preparations Derived from Leukocytes." In The Biology of the Interferon System 1986, 251–56. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3543-3_35.

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Bertini, R., W. Luini, B. Bottazzi, A. R. Mackay, D. Boraschi, J. Van Damme, and A. Mantovani. "Identification of a Novel Tumor-Derived Monocyte Chemotactic Factor: Relationship with Tissue Inhibitor of Metalloproteinase." In Advances in Experimental Medicine and Biology, 222. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2952-1_75.

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Ambrus, J. L., C. M. Ambrus, C. A. Toumbis, P. Forgach, C. P. Karakousis, and P. Niswander. "Tumor Induced Angiogenesis: Effect of Platelet Derived Growth Factor (PDGF), Pentoxifylline, Sodium Diethyldithiocarbamate, Epsilon Amino Caproic Acid and Tranexamic Acid." In Angiogenesis in Health and Disease, 185–94. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3358-0_17.

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Conference papers on the topic "TUMOR DERIVED FACTORS"

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Walshe, Tony E., Justin Bourdelais, Arleide Lee, Rakibou Ouro-Djobo, Vivek Vishnudas, Rangaprasad Sarangarajan, and Niven Narain. "Abstract A22: Identification of novel tumor derived factors that inhibit angiogenesis." In Abstracts: AACR Special Conference: Tumor Angiogenesis and Vascular Normalization: Bench to Bedside to Biomarkers; March 5-8, 2015; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-8514.tumang15-a22.

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Candolfi, Marianela, Kader Yagiz, Hikmat Assi, Akm G. Muhammad, Chunyan Liu, David Foulad, Gabrielle Alzadeh, et al. "Abstract 3645: Glioma-derived factors induce the expansion of myeloid derived suppressor cells which mediate immune suppression and tumor progression." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3645.

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Xia, Ying, Jenny E. Chu, Benjamin Chin-Yee, David Goodale, Alysha K. Croker, and Alison L. Allan. "Abstract B10: Soluble lung-derived factors mediate breast cancer cell migration and growth via CD44 receptor-ligand interactions." In Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-b10.

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Sullivan, Laura A., Juliet G. Carbon, Jason Toombs, Yang Xie, John D. Minna, and Rolf A. Brekken. "Abstract 367: Identification of tumor cell-derived factors associated with resistance to anti-VEGF therapy in non-small cell lung cancer." 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.am10-367.

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Konzok, Sebastian, Susann Dehmel, Christian Werno, Peter Braubach, Gregor Warnecke, Patrick Zardo, Danny Jonigk, et al. "Modulation of tumor-microenvironmental factors and cancer growth in co-cultures of fresh human lung tissue and patient-derived cancer cells." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa2851.

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Bowen-Pope, D. F., C. Gajdusek, J. Harlan, P. Nawroth, R. Ross, K. S. Sakariassen, and D. Stern. "REGULATION OF GROWTH FACTOR PRODUCTION BY ENDOTHELIAL CELLS IN RESPONSE TO COAGULATION AND INFLAMATORY FACTORS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642947.

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Abstract:

Platelet-derived growth factor (PDGF) is a polypeptide growth factor first discovered in, and purified from, human blood platelets. As assayed by its ability to stimulate proliferation of cultured vascular smooth muscle cells, PDGF is the major mitogen in human whole blood serum. PDGF has also been reported to be chemotactic for fibroblasts, vascular smooth muscle cells, and leukocytes, and to be able to stimulate contraction of arterial smooth muscle. This, spectrum of activities suggests that PDGF could play a significant role in several vascular processes, including wound repair and the formation of atherosclerotic lesions (reviewed in Ross et al., 1986 Cell 46:155). Several cell types in addition to the platelet have now been shown to be capable of secreting PDGF-like molecules. In culture, vascular endothelial cells from many sources secrete significant levels of PDGF (DiCorleto and Bowen-Pope, 1983 PNAS 80:1919). Rates of secretion can be increased four fold and more bythe activated procoagulants thrombin (Harlan et al 1986 J. Cell Biol. 103:1129) and factor Xa (Gajdusek et al 1986 J. Cell Biol. 103:419). Thrombin stimulates secretion by the earliest times measurable (about 1.5hr) and this early response is not diminished by inhibitors of protein and RNA synthesis. Nevertheless, unlike secretion from the platelet, stimulated secretion does not represent release of sequestered active PDGF since no reservoir of active PDGF can be detected within the cells prior to stimulation. It is likely therefore that stimulation of secrtion involves the activation or unmasking of an inactive form of PDGF. The proteolytic activities of thrombin and Xa are necessary for activation of secretion but the mechanism does not seem to to involve direct proteolytic activation by thrombin of a precursor since thrombin treatment does not generate active PDGF in freeze-thawed preparations of endothelial cells. We have recently found that tumor necrosis factor alpha (TNF) and gamma interferon (IFN) can stimulate increased rates of secretion of PDGF by cultured human saphenous vein and umbilical vein endothelial cells. Stimulation by a combination of the two is more than additive. In contrast to the rapid kinetics of stimulation by thrombin and Xa, TNF and IFN do not measurably increase secretion for at lease four hrs. This delayed kinetics is paralleled by increases in mRNA encoding the two subunit chains of PDGF ("A" and "B") and it seems likely that in this case stimulation of secretion results from increased rates of mRNA and protein synthesis. Since evidence is accumulating that TNF and IFN are both present in human atherosclerotic lesions, it is possible that they help stimulate production of endothelial cell-derived mitogens, including PDGF and thus contribute to the development of the lesion.

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Lam, CT, ZF Yang, ST Fan, and RTP Poon. "Abstract 1305: The proangiogenic role of brain-derived neurotrophic factor in tumor development." 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.am10-1305.

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Sizemore, Gina, Anisha Mathur, Katie Thies, Chelsea Bolyard, Steven Sizemore, Raleigh Kladney, Anthony Trimboli, Balveen Kaur, Gustavo Leone, and Michael Ostrowski. "Abstract C28: Platelet-derived growth factor receptor-β (PDGFRβ) in the breast metastatic tumor microenvironment." In Abstracts: AACR Special Conference: The Function of Tumor Microenvironment in Cancer Progression; January 7-10, 2016; San Diego, CA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tme16-c28.

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Loeuillard, Emilien, Juan Wang, Jingchun Yang, Haidong Dong, Gregory Gores, and Sumera Ilyas. "Abstract P072: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) foster myeloid-derived suppressor cell-mediated tumor immune evasion in cholangiocarcinoma." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 5-6, 2021. American Association for Cancer Research, 2022. http://dx.doi.org/10.1158/2326-6074.tumimm21-p072.

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Steffan, Joshua J., Sweaty Koul, Thomas R. Johnson, Hari K. Koul, and Randall B. Meacham. "Abstract 3431: Prostate-derived ETS factor expression decreases prostate tumor cell aggressivenessin vitroand metastasisin vivo." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3431.

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Reports on the topic "TUMOR DERIVED FACTORS"

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Hui, Xu. Enhancement of Tumor Immunotherapy by Blockade of a Prostate Tumor Derived Immunosuppressive Factor. Fort Belvoir, VA: Defense Technical Information Center, August 2006. http://dx.doi.org/10.21236/ada462748.

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