Relevant bibliographies by topics / E0771

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Academic literature on the topic 'E0771'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 April 2022

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Journal articles on the topic "E0771"

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Micallef, Peter, Yanling Wu, Marco Bauzá-Thorbrügge, Belén Chanclón, Milica Vujičić, Eduard Peris, C. Joakim Ek, and Ingrid Wernstedt Asterholm. "Adipose Tissue—Breast Cancer Crosstalk Leads to Increased Tumor Lipogenesis Associated with Enhanced Tumor Growth." International Journal of Molecular Sciences 22, no. 21 (November 2, 2021): 11881. http://dx.doi.org/10.3390/ijms222111881.

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We sought to identify therapeutic targets for breast cancer by investigating the metabolic symbiosis between breast cancer and adipose tissue. To this end, we compared orthotopic E0771 breast cancer tumors that were in direct contact with adipose tissue with ectopic E0771 tumors in mice. Orthotopic tumors grew faster and displayed increased de novo lipogenesis compared to ectopic tumors. Adipocytes release large amounts of lactate, and we found that both lactate pretreatment and adipose tissue co-culture augmented de novo lipogenesis in E0771 cells. Continuous treatment with the selective FASN inhibitor Fasnall dose-dependently decreased the E0771 viability in vitro. However, daily Fasnall injections were effective only in 50% of the tumors, while the other 50% displayed accelerated growth. These opposing effects of Fasnall in vivo was recapitulated in vitro; intermittent Fasnall treatment increased the E0771 viability at lower concentrations and suppressed the viability at higher concentrations. In conclusion, our data suggest that adipose tissue enhances tumor growth by stimulating lipogenesis. However, targeting lipogenesis alone can be deleterious. To circumvent the tumor’s ability to adapt to treatment, we therefore believe that it is necessary to apply an aggressive treatment, preferably targeting several metabolic pathways simultaneously, together with conventional therapy.
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McHowat, Jane, Gail Gullickson, Richard G. Hoover, Janhavi Sharma, John Turk, and Jacki Kornbluth. "Platelet-activating factor and metastasis: calcium-independent phospholipase A2β deficiency protects against breast cancer metastasis to the lung." American Journal of Physiology-Cell Physiology 300, no. 4 (April 2011): C825—C832. http://dx.doi.org/10.1152/ajpcell.00502.2010.

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We determined the contribution of calcium-independent phospholipase A2β (iPLA2β) to lung metastasis development following breast cancer injection into wild-type (WT) and iPLA2β-knockout (iPLA2β-KO) mice. WT and iPLA2β-KO mice were injected in the mammary pad with 200,000 E0771 breast cancer cells. There was no difference in primary tumor size between WT and iPLA2β-KO mice at 27 days postinjection. However, we observed an 11-fold greater number of breast cancer cells in the lungs of WT mice compared with iPLA2β-KO animals ( P < 0.05). Isolated WT lung endothelial cells demonstrated a significant increase in platelet-activating factor (PAF) production when stimulated with thrombin [1 IU/ml, 10 min, 4,330 ± 555 vs. 15,227 ± 1,043 disintegrations per minute (dpm), P < 0.01] or TNF-α (10 ng/ml, 2 h, 16,532 ± 538 dpm, P < 0.01). Adherence of E0771 cells to WT endothelial cells was increased by thrombin (4.8 ± 0.3% vs. 70.9 ± 6.3, P < 0.01) or TNF-α (60.5 ± 4.3, P < 0.01). These responses were blocked by pretreatment with the iPLA2β-selective inhibitor ( S)-bromoenol lactone and absent in lung endothelial cells from iPLA2β-KO mice. These data indicate that endothelial cell iPLA2β is responsible for PAF production and adherence of E0771 cells and may play a role in cancer cell migration to distal locations.
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Nguyen, Hong-My, Othon Almanza, and Dipongkor Saha. "Abstract P3-11-01: Oncolytic herpes simplex virus immunovirotherapy eradicates breast cancer and prevents tumor relapse." Cancer Research 82, no. 4_Supplement (February 15, 2022): P3–11–01—P3–11–01. http://dx.doi.org/10.1158/1538-7445.sabcs21-p3-11-01.

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Abstract Syngeneic mouse tumor models are critical to investigating new immunotherapeutic modalities and providing a rationale for clinical translation. Oncolytic herpes simplex virus (oHSV) is an emerging treatment strategy for breast cancer. Genetically modified oHSV selectively replicates in cancer cells (sparring healthy cells), induces immunogenic cancer cell death, and stimulates innate/adaptive anti-tumor immune responses. The therapeutic success of oHSV depends on a dynamic interaction between oHSV, the tumor, and the host. Here, we evaluated the anti-tumor effects of G47Δ-IL12, a genetically engineered oHSV expressing interleukin-12 (IL-12), in two orthotopic immunocompetent mouse models of breast cancer, E0771 (some classified this model as luminal B subtype and some as triple-negative) and EMT6 (triple-negative subtype), which are syngeneic to C57BL/6 and BALB/c mice, respectively. Intratumoral G47Δ-IL12 treatment led to complete eradication of orthotopic E0771 and EMT6 mammary tumors and prevention of lung metastases, resulting in 100% long-term survivors, which remained tumor-free during the observation period (&gt;100 days following the last G47Δ-IL12 treatment). In a contralateral orthotopic mammary tumor model, G47Δ-IL12 treatment of primary tumors led to the eradication of both treated and untreated distal tumors, confirming the abscopal and anti-metastatic effect of G47Δ-IL12 virotherapy. All cured mice from G47Δ-IL12-treated groups rejected lethal tumor re-challenge in the contralateral naïve mammary fat pad, indicating successful generation of a protective memory response. In both E0771 and EMT6 models, cell-specific IFN-γ responses and the presence of effector memory T cells (CD4+CD44highCD62Llow phenotype) in spleens of long-term survivors, possibly contributing to tumor relapse prevention. G47Δ-IL12-mediated anti-tumor efficacy was associated with significant increases in CD4+ and CD8+ tumor-infiltrating lymphocytes (TILs) (vs. mock group) in both E0771 and EMT6 tumor lesions. G47Δ-IL12 monotherapy also led to a significantly increased CD8+/FoxP3+ ratio (an important parameter for immunotherapy success) in both tumor models. Interestingly, immune cell depletion studies demonstrated that efficacy requires both CD4+ and CD8+ T cells in the E0771 model while only CD8+ T cells were required in the EMT6 model. Conclusions: G47Δ-IL12 monotherapy was effective in eradicating both orthotopic and metastatic tumors and generating long-term protective memory responses in two syngeneic breast cancer models. Treatment efficacy of G47Δ-IL12 was associated with significant immunologic alterations of the TME. G47Δ-IL12 utilized distinct immunologic mechanisms of action to eradicate tumors: CD8+ T cell-dependent action in the EMT6 model, whereas CD4+ and CD8+ T cell-dependent efficacy in the E0771 model. Altogether, our data suggest that G47Δ-IL12 is an efficient inflammatory modulator and beneficially exploits the immune system to eradicate breast tumors. These studies provide the necessary supporting evidence for the clinical translation of this agent into breast cancer patients. Citation Format: Hong-My Nguyen, Othon Almanza, Dipongkor Saha. Oncolytic herpes simplex virus immunovirotherapy eradicates breast cancer and prevents tumor relapse [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P3-11-01.
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Gong, Jian, Michael Gray, Jeff Hutchins, and Bruce Freimark. "Anti-Tumor Responses By Ibrutinib and Anti-PD-1 Blockade Is Enhanced By Phosphatidylserine-Targeting Antibody Therapy." Blood 128, no. 22 (December 2, 2016): 5379. http://dx.doi.org/10.1182/blood.v128.22.5379.5379.

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Abstract Introduction: Phosphatidylserine (PS) is a phospholipid normally residing in the inner leaflet of the plasma membrane that becomes exposed on vascular endothelial cells and tumor cells in the tumor microenvironment, particularly in response to chemotherapy and irradiation. Binding of antibodies targeting PS on the tumor endothelial cells and tumors induces the recruitment of immune cells and engages the immune system to destroy tumor and associated vasculature and by blocking the immunosuppressive action of PS. Recent studies have demonstrated that PS-targeting antibodies enhance the anti-tumor activity of immune checkpoint antibody blockade to CTLA-4 and PD-1 in mouse breast and melanoma tumor models (Freimark et al. Cancer Immunol. Res. 2016; Gray et al. Breast Cancer Res 2016). Ibrutinib is an approved anticancer drug targeting B-cell malignancies that is a selective, covalent inhibitor of the enzyme Bruton's tyrosine kinase(BTK) in B-cell tumors. Data from recent mouse tumor studies demonstrate that ibrutinib in combination with anti-PD-1 antibody blockade inhibits growth of solid tumors (lacking BTK expression) suggesting that ibrutinib may inhibit kinases of the immune system such as interleukin-2 inducible T-cell kinase (ITK), to enhance specific anti-tumor responses (Sagiv-Barfli et al. PNAS 20 2015). Methods: The present study was conducted to evaluate the anti-tumor effects of combination therapy including PS-targeting antibody mouse chimeric 1N11 (mch1N11), ibrutinib (32765) and anti-PD-1 antibody using C57BL/6 mice bearing triple negative E0771 breast tumors. Tumors were staged to an initial volume of ~100mm3and randomized to treatment groups (N=10) with mch1N11 or isotype at 10 mg/kg qw, anti-PD-1 at 2.5 mg/kg qw or ibrunitib 6 mg/kg or vehicle qd x 8. Tumor volumes were measured twice per week to determine tumor growth inhibition (TGI) relative to control treated animals until a maximum volume of 1500-2000mm3. The in vitro sensitivity of E0771 tumor cells to ibrutinib was compared to drug sensitive Jeko-1 lymphoma cells in a 72 hour growth and viability assay. Results: The E0771 cell line is resistant in vitroto 10 mM ibrutinib compared to the drug-sensitive Jeko-1 cell line (Figure 1). Mice bearing E0771 tumors treated with mch1N11, ibrutinib and anti-PD-1 alone had 22.2%, 23.5% and 32.6% TGI respectively. Combination of two agents increased the TGI for mch1N11 and ibrutinib to 30.5%, ibrutinib and anti-PD-1 to 34.5%, mch1N11 and anti-PD-1 to 36.1%. A triple combination therapy had statistically greater TGI compared to control treated mice (59.9%, p = 0.0084) and was greater than single and double combination therapies. Conclusion:Treatment of solid tumors with a combination of inhibitors that target PS, ITK and the PD-1/PD-L1 axis in the tumor microenvironment provides a novel treatment for solid tumors, including triple negative breast cancer. Figure 1 Figure 1. Figure 2 Figure 2. Disclosures Gong: Peregrine Pharmaceuticals, Inc.: Employment. Gray:Peregrine Pharmaceuticals, Inc.: Employment. Hutchins:Peregrine Pharmaceuticals, Inc.: Employment. Freimark:Peregrine Pharmaceuticals, Inc.: Employment.
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Sato, Katsutoshi, Stacey J. Baker, E. P. Reddy, and Hanna Y. Irie. "Abstract PD3-08: Novel cancer stem cell inhibitor 108600 modulates tumor immunomicroenvironment of triple negative breast cancer (TNBC)." Cancer Research 82, no. 4_Supplement (February 15, 2022): PD3–08—PD3–08. http://dx.doi.org/10.1158/1538-7445.sabcs21-pd3-08.

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Abstract 108600, a novel CK2/DYRK1/TNIK inhibitor, targets and inhibits cancer stem cells (CSC) in triple negative breast cancer (TNBC), inhibiting tumor growth and metastases in patient-derived xenograft models. CSC’s have been shown to promote immune evasion of several types of cancer. Specifically, over-expression of CK2 has been shown to promote intratumoral recruitment of myeloid derived suppressor cells. We investigated the effects of 108600 treatment on the immune microenvironment of triple negative breast cancer since targeting CSC’s could promote favorable anti-tumor immune responses and mechanistically contribute to tumor growth inhibition. Methods:C57BL/6 mice bearing murine triple negative E0771 tumors were generated by orthotopic injection and treated either with vehicle control or 108600 for 5 days. Tumor growth was assessed by daily caliper measurement All tumors were recovered at endpoint, and processed for RNA sequencing, flow cytometry or Western blot analysis. Results:108600 treatment significantly inhibited growth of E0771 tumors in vivo, demonstrating for the first time efficacy of 108600 against TNBC in immunocompetent models. 108600 treatment decreased intratumoral phosphorylation and expression of 108600 targets AKT1 (Ser 129) and Cyclin D1, which are substrates of CK2α and Dyrk1, respectively. To further explore nature of transcriptional and signaling pathways affected by 108600 treatment in vivo, RNA sequencing was performed. DGE and subsequent annotation analysis showed that various immune (GO:0006955, GO) and inflammatory (GO:0006954, GO) signaling pathways associated with Stat1 (mmu04062, KEGG) and IFNγ (mmu04060, KEGG) were down-regulated in 108600-treated E0771 tumors. GSEA (Gene set enrichment analysis) indicated that the regulatory T cell (Treg) population (GSE42021, GSE40685) was suppressed by 108600 treatment. To validate these findings, tumor infiltrating leukocytes (TIL) were isolated from vehicle or 108600-treated tumors and analyzed by flow cytometry. CD4, CD25, and FOXP3 expression was used to gate the Treg population. The Treg population was significantly suppressed by 108600 treatment, confirming the RNA sequencing results. 108600 also likely regulates expression of immunomodulatory molecules in TNBC tumor cells since 108600 treatment increased PD-L1 surface expression on E0771 cells in vitro. Conclusions:Our study supports 108600, an inhibitor that targets breast cancer stem cells, as a modulator of the immune microenvironment of TNBC. 108600 suppresses the Treg population among the TIL population and increases tumoral expression of PD-L1. Tregs have been associated with disease progression and metastases of TNBC. Further studies are ongoing to clarify the functional consequences of these changes in the setting of tumor growth inhibition. Synergies between 108600 and checkpoint inhibition are also under investigation and could lead to novel combination therapies for TNBC. Citation Format: Katsutoshi Sato, Stacey J. Baker, E. P. Reddy, Hanna Y. Irie. Novel cancer stem cell inhibitor 108600 modulates tumor immunomicroenvironment of triple negative breast cancer (TNBC) [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr PD3-08.
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Chen, Xu, and Yong Wang. "GW29-e0771 β-cryptoxanthin prevents H2O2 induced myocardial cell damage by targeting RXRα." Journal of the American College of Cardiology 72, no. 16 (October 2018): C24—C25. http://dx.doi.org/10.1016/j.jacc.2018.08.093.

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Nief, Corrine A., Júlia Sroda Agudogo, Alana Gonzales, Rebecca A. Previs, Smita K. Nair, and Nimmi Ramanujam. "Resetting the tumor microenvironment to favor anti-tumor immunity after local ablation." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): 2561. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.2561.

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2561 Background: Percutaneous tumor ablation is a non-surgical method of tumor destruction that leaves necrotic tumor debris in situ. Tumor associated antigens released after ablation have the potential to initiate a systemic anti-tumor immune response, however the hostile tumor microenvironment hinders antigen presentation and T cell activity. We hypothesized that resetting the tumor microenvironment with oral sodium bicarbonate to decrease tumor acidity and low-dose cyclophosphamide to deplete pro-tumor immune cells would improve the ability of ablation to initiate anti-tumor immunity. Methods: Tumor growth, overall survival, and metastatic burden was assessed in orthotopic tumor models of triple-negative breast cancer (67NR, 4T1, and E0771). Tumor ablation was performed on palpable tumors using percutaneous ethanol injection (PEI) with 6% ethylcellulose to improve retention in the tumor. Surgical excision was used as a negative control to test the role of in situ tumor debris. Before ablation mice were placed on 200 mM of sodium bicarbonate (SB) in their drinking water and received a single intraperitoneal injection of 200 mg/kg of cyclophosphamide (CP). Mice surviving to 60 days after tumor implant without a primary tumor or signs of metastases were considered "cured" and re-challenged with 50e5 tumor cells in the contralateral mammary pad. T cell dependance was assessed with in vivo CD8 depletions. Results: The combination of PEI+SB+CP produced a potent anti-tumor response, curing a majority of mice (5/7 of E0771, 8/12 of 67NR, 7/12 of 4T1). No mice were cured using PEI alone, SB alone, CP alone, or any combination of two therapies (0/51 of E0771, 0/73 of 67NR, 0/75 of 4T1,). Re-challenge tumor growth was hindered in mice cured with PEI+SB+CP. Mice receiving PEI+SB+CP had significantly less metastases and lived longer than mice receiving surgical excision alone or surgical excision with SB+CP. Additionally the anti-metastatic response of PEI+SB+CP was undone when CD8+ T cells were depleted. Conclusions: Here the anti-tumor response of local ablation produced by PEI was enhanced by priming the tumor with low-dose CP and oral SB in metastatic breast cancer. These results suggest that tumor ablation with CP and SB can create a T cell dependent, personalized immune response to a tumor using only low-cost, easily accessible supplies, and the host’s own tumor.
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Wang, Wei, Priyanka S. Rana, Akram Alkrekshi, Katarzyna Bialkowska, Vesna Markovic, William P. Schiemann, Edward F. Plow, Elzbieta Pluskota, and Khalid Sossey-Alaoui. "Targeted Deletion of Kindlin-2 in Mouse Mammary Glands Inhibits Tumor Growth, Invasion, and Metastasis Downstream of a TGF-β/EGF Oncogenic Signaling Pathway." Cancers 14, no. 3 (January 27, 2022): 639. http://dx.doi.org/10.3390/cancers14030639.

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Breast cancer (BC) is one of the leading causes of cancer-related deaths due in part to its invasive and metastatic properties. Kindlin-2 (FERMT2) is associated with the pathogenesis of several cancers. Although the role of Kindlin-2 in regulating the invasion-metastasis cascade in BC is widely documented, its function in BC initiation and progression remains to be fully elucidated. Accordingly, we generated a floxed mouse strain by targeting the Fermt2 (K2lox/lox) locus, followed by tissue-specific deletion of Kindlin-2 in the myoepithelial compartment of the mammary glands by crossing the K2lox/lox mice with K14-Cre mice. Loss of Kindlin-2 in mammary epithelial cells (MECs) showed no deleterious effects on mammary gland development, fertility, and lactation in mice bearing Kindlin-2-deletion. However, in a syngeneic mouse model of BC, mammary gland, specific knockout of Kindlin-2 inhibited the growth and metastasis of murine E0771 BC cells inoculated into the mammary fat pads. However, injecting the E0771 cells into the lateral tail vein of Kindlin-2-deleted mice had no effect on tumor colonization in the lungs, thereby establishing a critical role of MEC Kindlin-2 in supporting BC tumor growth and metastasis. Mechanistically, we found the MEC Kindlin-2-mediated inhibition of tumor growth and metastasis is accomplished through its regulation of the TGF-β/ERK MAP kinase signaling axis. Thus, Kindlin-2 within the mammary gland microenvironment facilitates the progression and metastasis of BC.
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Bohlen, Joseph F., Tyler McClanahan, Sarah Dodd, Linda Vona-Davis, and Emidio E. Pistilli. "E0771 Adenocarcinoma Breast Cancer Tumors Induce Muscle Fatigue and Wasting in C57BL/6 Mice." Medicine & Science in Sports & Exercise 48 (May 2016): 359. http://dx.doi.org/10.1249/01.mss.0000486088.15052.db.

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Knickle, Allison, Andrea Rasmussen, and David W. Hoskin. "Myricetin induces apoptosis mediated by oxidative stress in 4T1 and E0771 mammary cancer cells." Molecular & Cellular Toxicology 16, no. 3 (June 8, 2020): 283–89. http://dx.doi.org/10.1007/s13273-020-00089-3.

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Dissertations / Theses on the topic "E0771"

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Roussy, Geneviève. "Rôle des récepteurs NTS1 et NTS2 de la neurotensine dans un nouveau modèle de douleur cancéreuse osseuse." Thèse, Université de Sherbrooke, 2012. http://hdl.handle.net/11143/6646.

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Un cancer du sein invasif forme préférentiellement des métastases osseuses menant à des épisodes de douleur sévère. Pour soulager cette douleur chronique, le traitement de choix actuel demeure la morphine malgré ses effets secondaires induits par la prise de fortes doses. Le développement de modèles animaux de douleur osseuse cancéreuse a permis d'améliorer notre compréhension de cette physiopathologie, favorisant ainsi la découverte de traitements alternatifs. Le premier objectif de ma Thèse a donc consisté à développer un modèle animal de douleur cancéreuse mimant les douleurs induites par les métastases osseuses. Ce nouveau modèle est basé sur l'injection de cellules syngéniques du cancer du sein métastatique (E0771) au niveau du fémur de souris C57BL/6. Nous avons tout d'abord mis en évidence le caractère invasif et hormono-dépendant des E0771 in vitro et in vivo en observant l'expression de MMP9 et d'ER[alpha]. Par la suite, nous avons suivi l'impact de la croissance tumorale sur le remodelage osseux, l'évolution de la douleur et la plasticité neuronale. Dès le 11ème jour post-implantation, l'analyse par Faxitron, microtomographie et IRM révèle la présence d'une destruction de la matrice osseuse. Ce remodelage osseux progresse jusqu'au jour 18 et conduit à l'apparition de douleur chez les souris porteuses d'une tumeur osseuse. Cette douleur s'est manifestée sous forme d'allodynie mécanique, de douleur ambulatoire induite par le mouvement forcé et d'inconfort ambulatoire entre les jours 11 et 18. L'apparition de cette douleur corrèle avec une augmentation de l'activité neuronale au niveau spinal. La seconde partie de ma Thèse a consisté à examiner le potentiel analgésique d'agonistes neurotensinergiques injectés par voie intrathécale sur la douleur osseuse cancéreuse. Dans un premier temps, nous avons étudié les effets d'agonistes des récepteurs NTS1 et NTS2 sur la douleur persistante lors du test à la formaline. Nous avons ainsi pu démontrer que l'injection de 10 [micro]g/kg de PD149163 (agoniste sélectif NTS1) ou de 30 [micro]g/kg de JMV-431 (agoniste sélectif NTS2) induisait une réponse analgésique puissante. Ces mêmes analogues ont alors été testés sur des souris sauvages ou invalidées pour NTS1 ou NTS2, développant un cancer osseux métastatique. Les résultats obtenus indiquent que NTS1 et NTS2 ne semblent pas être impliqués dans la dégradation osseuse observée suite à l'injection des E0771. En revanche, l'activation de ces récepteurs réduit la douleur induite par la tumeur osseuse. Le PD149163 diminue l'allodynie mécanique, cependant ses effets secondaires locomoteurs limitent son efficacité analgésique. Pour sa part, le JMV-431 réduit l'allodynie mécanique et la douleur induite par le mouvement forcé. Les résultats obtenus avec les souris invalidées pour NTS1 ou NTS2 corrèlent avec les résultats observés avec les agonistes ou ont démontré l'implication possible de systèmes compensatoires. En conclusion, notre modèle reflète davantage la réalité clinique par l'utilisation de cellules syngéniques du cancer du sein et le récepteur NTS2 se révèle être une cible potentielle pour soulager la douleur cancéreuse osseuse.
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Šlaufová, Marta. "Vzájemné interakce mezi nádorovým mikroprostředím a kalikreinovými proteázami v myším modelu karcinomu mléčné žlázy." Master's thesis, 2021. http://www.nusl.cz/ntk/nusl-446587.

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Breast cancer is the most common cancer type with a high annual death rate. Finding meaningful tissue-related or body-fluid-accessible biomarkers is necessary to characterize cancer subtype, predict tumor behavior, choose the most effective therapy, predict severe treatment-related toxicities, and also the opportunity to personalize treatments for each patient. There is increasing evidence that various kallikrein-related peptidases (Klk) gene family members can modulate the immune response and are differentially regulated in breast cancer, and therefore are proposed to be potential prognostic biomarkers. This work established and validated an experimental setup to study the roles of selected kallikrein-related peptidases (KLK5, KLK7, KLK14) in breast cancer in vivo using gene-deficient mouse models previously generated in our laboratory. We used the CRISPR/Cas9 (clustered regularly interspaced short palindromic repeats) editing system to generate several E0771 cell line-based reporter and gene-deficient cell lines. These allowed enhanced monitoring of cancer progression in vivo and studying KLKs roles in tumor immune microenvironment of C57Bl/6N mice. Finally, we present the analysis of the initial in vivo experiments using these tools combined with established Klk-deficient mouse models. Our...
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Conference papers on the topic "E0771"

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Fadden, Patrick, Thi Bui, Kelli Davis, David Hurtado, Emily Sugg, Abigail Svancarek, Ian Belle, and Chassidy Hall. "Abstract 1558: Radiation therapy and immune checkpoint inhibitor combinations in the E0771 medullary breast adenocarcinoma." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1558.

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Gulyaeva, E., and Yulia G. Semikina. "Project Activity as a Means of Multicultural Values Development in the Internet-Mediated Learning Environment." In IFTE 2020 - VI International Forum on Teacher Education. Pensoft Publishers, 2020. http://dx.doi.org/10.3897/ap.2.e0771.

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Senchenkov, Nikolai. "Problems of Professional Identity of Modern Teachers: Comparative Analysis of Research Data of Russian and Latvian Teachers." In IFTE 2019 - V International Forum on Teacher Education. Pensoft Publishers, 2019. http://dx.doi.org/10.3897/ap.1.e0571.

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Zanina, L., A. Miroshnichenko, and O. Radchenko. "Continuing Pedagogical Education in the Conditions of Digitalization: The Risks of Alternative Society." In IFTE 2019 - V International Forum on Teacher Education. Pensoft Publishers, 2019. http://dx.doi.org/10.3897/ap.1.e0772.

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Zeleeva, Vera. "Pedagogical Effects of Qualitative Research Methods (Focus Group and Phenomenological Interviews) in Pedagogical Training for Graduate and Postgraduate Students." In IFTE 2019 - V International Forum on Teacher Education. Pensoft Publishers, 2019. http://dx.doi.org/10.3897/ap.1.e0778.

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Babiyants, Karine A., and Olga V. Manuylova. "Reflexive Game in the Work with Students from Post-conflict Regions." In IFTE 2020 - VI International Forum on Teacher Education. Pensoft Publishers, 2020. http://dx.doi.org/10.3897/ap.2.e0171.

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Grigoryan, Telman G., and Tatyana N. Lomteva. "Mobile Technologies as a Digital Didactic Environment for Teaching French in Secondary Schools: a Regional Aspect." In IFTE 2020 - VI International Forum on Teacher Education. Pensoft Publishers, 2020. http://dx.doi.org/10.3897/ap.2.e0751.

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Grushetskaya, Irina N., Olga S. Shcherbinina, and Aleksandr P. Trubnikov. "Features of Socio-Pedagogical Work with Gifted Children in Organizations of Supplementary Education." In IFTE 2020 - VI International Forum on Teacher Education. Pensoft Publishers, 2020. http://dx.doi.org/10.3897/ap.2.e0761.

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Guslyakova, Nina I., and Alla V. Guslyakova. "Emotional Intelligence as a Driving Force in the Study of Foreign Languages in Higher Education." In IFTE 2020 - VI International Forum on Teacher Education. Pensoft Publishers, 2020. http://dx.doi.org/10.3897/ap.2.e0781.

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Efimova, Lyubov, Agrafena Ivanova, and Nadezhda A.Mikhailova. "Features of the implementation of inclusive education for children and young people with disabilities in the Scandinavian countries." In IFTE 2021 - VII International Forum on Teacher Education. Pensoft Publishers, 2022. http://dx.doi.org/10.3897/ap.5.e0371.

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