Relevant bibliographies by topics / GDF-15

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'GDF-15'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 March 2024

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'GDF-15.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "GDF-15"

1

Roos, Martin. "Innovation gegen GDF-15." Im Focus Onkologie 16, no. 1-2 (February 2013): 9. http://dx.doi.org/10.1007/s15015-013-0005-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Havránek, Štěpán, and Josef Marek. "Biomarker GDF-15 in cardiology." Vnitřní lékařství 67, no. 3 (May 26, 2021): e11-e14. http://dx.doi.org/10.36290/vnl.2021.045.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Huang, Hong, Zhongli Chen, Yan Li, Kunmei Gong, Le Xiao, Hao Fu, Jingjing Yang, Xianying Wang, and Qiang Meng. "GDF-15 Suppresses Atherosclerosis by Inhibiting oxLDL-Induced Lipid Accumulation and Inflammation in Macrophages." Evidence-Based Complementary and Alternative Medicine 2021 (September 7, 2021): 1–13. http://dx.doi.org/10.1155/2021/6497568.

Full text
Abstract:
The growth differentiation factor-15 (GDF-15) may be involved in atherosclerosis. However, the role of GDF-15 in atherosclerosis remains unclear. The main goal of this study was to verify the role and mechanism of GDF-15 in atherogenesis. We first compared the serum GDF-15 level between patients with coronary atherosclerosis and healthy people. And then one ApoE−/− mouse model of atherosclerosis was used to explore the effects of GDF-15 on oxidized low-density lipoprotein (oxLDL) accumulation, atherosclerosis-related gene expression, and lipid accumulation-related protein expression in mouse macrophages. As a result, the level of serum GDF-15 in patients with coronary atherosclerosis was significantly higher than that in healthy people. In the mouse model, GDF-15 expression was elevated in the core of plaque, and it was secreted mainly by the macrophages. In addition, GDF-15 decreased oxLDL-induced lipid accumulation and inflammation activation in macrophages. GDF-15 decreased the mRNA expressions of CD36, LOX1, and TLR4 that are associated with lipoprotein accumulation in macrophages. Further study showed that GDF-15 might suppress oxLDL-induced lipoprotein accumulation via inhibiting CD36 and LOX1 and decrease inflammation in macrophages by inhibiting TLR4. Thus, GDF-15 may suppress atherosclerosis and plaque formation by inhibiting lipoprotein accumulation and inflammation activation.
APA, Harvard, Vancouver, ISO, and other styles
4

Wischhusen, Joerg, Markus Haake, Neha Vashist, Sabrina Genßler, Kilian Wistuba-Hamprecht, Patrick Harter, Alexander Martens, et al. "Tumor-derived GDF-15 to suppress t-lymphocyte recruitment to the tumor microenvironment resulting in resistance to ANTI-PD-1 treatment." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): e14532-e14532. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e14532.

Full text
Abstract:
e14532 Background: Growth and differentiation factor 15 (GDF-15) is a divergent member of the TGF-β superfamily with low to absent expression in healthy tissue. GDF-15 has been linked to feto-maternal immune tolerance, to prevention of excessive immune cell infiltration during tissue damage, and to anorexia. Various major tumor types secrete high levels of GDF-15. In cancer patients, elevated GDF-15 serum levels correlate with poor prognosis and reduced overall survival (OS). Methods: Impact of a proprietary GDF-15 neutralizing antibody (CTL-002) regarding T cell trafficking was analyzed by whole blood adhesion assays, a HV18-MK melanoma-bearing humanized mouse model and a GDF-15-transgenic MC38 model. Additionally, patient GDF-15 serum levels were correlated with clinical response and overall survival in oropharyngeal squamous cell carcinoma (OPSCC) and melanoma brain metastases. Results: In whole blood cell adhesion assays GDF-15 impairs adhesion of T and NK cells to activated endothelial cells. Neutralization of GDF-15 by CTL-002 rescued T cell adhesion. In HV18-MK-bearing humanized mice CTL-002 induced a strong increase in TIL numbers. Subset analysis revealed an overproportional enrichment of T cells, in particular CD8+ T cells. As immune cell exclusion is detrimental for checkpoint inhibitor (CPI) therapy, a GDF-15-transgenic MC38 model was tested for anti-PD-1 therapy efficacy. In GDF-15 overexpressing MC38 tumors response to anti PD-1 therapy was reduced by 90% compared to wtMC38 tumors. Combining aPD-1 with CTL-002 resulted in 50% of the mice rejecting their GDF-15 overexpressing tumors. Clinically, inverse correlations of GDF-15 levels with CD8+ T cell infiltration were shown for HPV+ OPSCC and for melanoma brain metastases. GDF-15 serum levels were significantly higher in HPV- than in HPV+ OPSCC patient (p < 0.0001). Low GDF-15 levels corresponded to longer OS in both HPV- and HPV+ OPSCC. In two independent melanoma patient cohorts treated with nivolumab or pembrolizumab low baseline serum GDF-15 levels were predictive for clinical response to anti-PD1 treatment and superior OS. Bivariate analysis including LDH indicates that GDF-15 independently predicts poor survival in aPD-1 treated melanoma patients. Conclusions: Taken together our in vitro and in vivo data show that elevated GDF-15 levels block T-cell infiltration into tumor tissues. Neutralizing GDF-15 with CTL-002 restores the ability of T cells to extravasate blood vessels and enter tumor tissue both in vitro and in vivo. In melanoma, patients with higher GDF-15 levels have significantly shorter survival and are less likely to respond to anti-PD1 therapy. GDF-15 may thus serve as a new predictive biomarker for anti-PD1 response, but most importantly also represents a novel target for cancer immunotherapy to improve tumor immune cell infiltration and response to anti-PD1 therapy.
APA, Harvard, Vancouver, ISO, and other styles
5

Chen, Jingfei, Fei Luo, Zhenfei Fang, and Weishe Zhang. "GDF-15 levels and atherosclerosis." International Journal of Cardiology 257 (April 2018): 36. http://dx.doi.org/10.1016/j.ijcard.2017.10.037.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Wu, Guojin, Jinming Liang, Feng He, Meng Zhang, Zhengcheng Guo, and Jinying Ning. "Abstract 5301: GDF-15 neutralizing antibody restores cancer-induced cachexia." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5301. http://dx.doi.org/10.1158/1538-7445.am2022-5301.

Full text
Abstract:
Abstract Growth and differentiation factor 15 (GDF-15) is a member of the transforming growth factor β superfamily. Elevated GDF-15 level was often the result of pathological conditions, including autoimmune disease and cancer. Increased GDF-15 caused metabiotic disorders such as anorexia and cachexia, and GDF-15 became an attractive target for metabolic intervention. Here, we developed a humanized GDF-15 neutralizing antibody (H53E5-8V2) from hybridoma of mice immunized with GDF-15-mFc. H53E5-8V2 had high affinity to GDF-15 (Kd=0.05nM), and demonstrated a stronger binding to coated GDF-15-HIS than Ponsegnomab (Pfizer Inc.) with ELISA assay (EC50=0.33nM vs 0.73nM). H53E5-8V2 also had strong binding to cynoGDF15 (EC50=0.3nM). In ELISA blocking assay, H53E5-8V2 disrupted the interaction of GDF-15 and GFRAL with a lower concentration than Ponsegnomab (EC50=0.25nM vs. 0.5nM). In addition, H53E5-8V2 neutralized GDF-15 in the culture medium and blocked GDF-15 induced GFRAL signaling more efficiently than Ponsegnomab in reporter cell assay (EC50=0.13nM vs. 0.27nM). H53E5-8V2 was stable and had a serum half-life of 9 days in mice with a single antibody injection. And it prevented body weight decrease of the mouse with HT1080 xenograft tumor, MC38 overexpressing GDF-15, or subcutaneous injection of protein GDF-15 fused with mouse Fc at C terminal. These results suggested that H53E5-8V2 was a good candidate drug for the treatment of cachexia. Citation Format: Guojin Wu, Jinming Liang, Feng He, Meng Zhang, Zhengcheng Guo, Jinying Ning. GDF-15 neutralizing antibody restores cancer-induced cachexia [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5301.
APA, Harvard, Vancouver, ISO, and other styles
7

Xie, Baikang, Wenjing Tang, Shuang Wen, Fen Chen, Chao Yang, Min Wang, Yong Yang, and Wei Liang. "GDF-15 Inhibits ADP-Induced Human Platelet Aggregation through the GFRAL/RET Signaling Complex." Biomolecules 14, no. 1 (December 27, 2023): 38. http://dx.doi.org/10.3390/biom14010038.

Full text
Abstract:
Growth differentiation factor-15 (GDF-15) is proposed to be strongly associated with several cardiovascular diseases, such as heart failure and atherosclerosis. Moreover, some recent studies have reported an association between GDF-15 and platelet activation. In this study, we isolated peripheral blood platelets from healthy volunteers and evaluated the effect of GDF-15 on adenosine diphosphate (ADP)-induced platelet activation using the platelet aggregation assay. Subsequently, we detected the expression of GDF-15-related receptors on platelets, including the epidermal growth factor receptor (EGFR), human epidermal growth factor receptor 2 (HER2), human epidermal growth factor receptor 3 (HER3), transforming growth factor-beta receptor I (TGF-βRI), transforming growth factor-beta receptor II (TGF-βRII), glial-cell-line-derived neurotrophic factor family receptor α-like (GFRAL), and those rearranged during transfection (RET). Then, we screened for GDF-15 receptors using the GDF-15-related receptor microarray comprising these recombinant proteins. We also performed the immunoprecipitation assay to investigate the interaction between GDF-15 and the receptors on platelets. For the further exploration of signaling pathways, we investigated the effects of GDF-15 on the extracellular signal-regulated kinase (ERK), protein kinase B (AKT), and Janus kinase 2 (JAK2) pathways. We also investigated the effects of GDF-15 on the ERK and AKT pathways and platelet aggregation in the presence or absence of RET agonists or inhibition. Our study revealed that GDF-15 can dose-independently inhibit ADP-induced human platelet aggregation and that the binding partner of GDF-15 on platelets is GFRAL. We also found that GDF-15 inhibits ADP-induced AKT and ERK activation in platelets. Meanwhile, our results revealed that the inhibitory effects of GDF-15 can be mediated by the GFRAL/RET complex. These findings reveal the novel inhibitory mechanism of ADP-induced platelet activation by GDF-15.
APA, Harvard, Vancouver, ISO, and other styles
8

Breen, Danna, Donald Bennett, Srinath Jagarlapudi, Stephanie Joaquim, Chang Zou, Anita Patel, Zhidan Wu, Randy Seeley, Bei Betty Zhang, and Olivier Bezy. "Effect of growth differentiation factor 15 (GDF-15) inhibition on energy balance in cancer cachexia and in lipopolysaccharide (LPS)-induced sepsis mouse models." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e24153-e24153. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e24153.

Full text
Abstract:
e24153 Background: Growth differentiation factor 15 (GDF-15) is a cytokine that induces anorexia, weight loss and has been reported to be associated with cachexia and poor survival in illnesses characterized by inflammation such as cancer cachexia and heart failure. In preclinical cancer cachexia models, GDF-15 inhibition has been demonstrated to reverse cachexia and improve survival. Circulating GDF-15 is also elevated in patients with sepsis and is associated with increased complications and poor survival. However, the role of infection- and sepsis-induced GDF-15 in mouse models is controversial based on published reports. Methods: In this study, we examined the effect of GDF-15 inhibition on tumor and lipopolysaccharide (LPS)-induced anorexia, weight loss, and survival using a GDF-15 neutralizing antibody (mAB2) and GDF-15 knockout mice. Results: mAB2 efficacy was confirmed by reversing AAV-GDF-15-induced weight loss in wildtype mice. A cachectic (anorexia and weight loss) mouse tumor model was established with subcutaneous implantation of mouse renal cell carcinoma (RENCA) cells. The chemotherapy sorafenib was administered to slow tumor progression. Plasma GDF-15 was increased to ~2 ng/mL, similar to levels in cancer patients. Treatment with mAB2 rapidly reversed both anorexia and weight loss in the tumor-bearing mice. LPS injection (intraperitoneal, 5 mg/kg) increased circulating GDF-15 in wildtype mice reaching concentrations like that reported in septic patients within 90 minutes and remaining elevated after 48 hours (~1 ng/mL). LPS decreased food intake, body weight, and increased mortality (~20%). Different from the tumor model, GDF-15 neutralization with mAB2 did not prevent or exacerbate any of the effects of LPS. There were no observed detrimental effects of mAB2 treatment in either model. Similarly, in GDF-15 knockout mice the LPS effect on energy balance and survival was comparable to that observed in wildtype controls. Plasma GDF-15 was undetectable in the GDF-15 knockout mice. Conclusions: Taken together, these data suggest that GDF-15 is a critical regulator of energy balance and survival in selective pathophysiological states associated with weight loss.
APA, Harvard, Vancouver, ISO, and other styles
9

Lin, Wei, Wen-Wen Zhang, Ning Lyu, Hong Cao, Wen-Dong Xu, and Yu-Qiu Zhang. "Growth Differentiation Factor-15 Produces Analgesia by Inhibiting Tetrodotoxin-Resistant Nav1.8 Sodium Channel Activity in Rat Primary Sensory Neurons." Neuroscience Bulletin 37, no. 9 (June 2, 2021): 1289–302. http://dx.doi.org/10.1007/s12264-021-00709-5.

Full text
Abstract:
AbstractGrowth differentiation factor 15 (GDF-15) is a member of the transforming growth factor-β superfamily. It is widely distributed in the central and peripheral nervous systems. Whether and how GDF-15 modulates nociceptive signaling remains unclear. Behaviorally, we found that peripheral GDF-15 significantly elevated nociceptive response thresholds to mechanical and thermal stimuli in naïve and arthritic rats. Electrophysiologically, we demonstrated that GDF-15 decreased the excitability of small-diameter dorsal root ganglia (DRG) neurons. Furthermore, GDF-15 concentration-dependently suppressed tetrodotoxin-resistant sodium channel Nav1.8 currents, and shifted the steady-state inactivation curves of Nav1.8 in a hyperpolarizing direction. GDF-15 also reduced window currents and slowed down the recovery rate of Nav1.8 channels, suggesting that GDF-15 accelerated inactivation and slowed recovery of the channel. Immunohistochemistry results showed that activin receptor-like kinase-2 (ALK2) was widely expressed in DRG medium- and small-diameter neurons, and some of them were Nav1.8-positive. Blockade of ALK2 prevented the GDF-15-induced inhibition of Nav1.8 currents and nociceptive behaviors. Inhibition of PKA and ERK, but not PKC, blocked the inhibitory effect of GDF-15 on Nav1.8 currents. These results suggest a functional link between GDF-15 and Nav1.8 in DRG neurons via ALK2 receptors and PKA associated with MEK/ERK, which mediate the peripheral analgesia of GDF-15.
APA, Harvard, Vancouver, ISO, and other styles
10

Haake, Markus, Tina Schäfer, Beatrice Haack, Neha Vashist, Sabrina Genßler, Patrick Harter, Alexander Martens, et al. "568 Tumor-derived GDF-15 prevents therapy success of checkpoint inhibitors by blocking T-lymphocyte recruitment." Journal for ImmunoTherapy of Cancer 9, Suppl 2 (November 2021): A597. http://dx.doi.org/10.1136/jitc-2021-sitc2021.568.

Full text
Abstract:
BackgroundImmune checkpoint blockade (ICB) can achieve durable responses in a subgroup of patients with metastatic cancer, only. Poor immune effector cell infiltration into the tumor microenvironment is a major obstacle to successful therapy. Growth and differentiation factor 15 (GDF-15) is a divergent member of the TGF-β superfamily and has been linked to feto-maternal tolerance, anorexia but recently also to potent local immunosuppression under physiologic and pathophysiologic conditions. GDF-15 is overexpressed in a wide variety of tumors and may be key factor produced by tumors to prevent effective immune cell infiltration into the tumor and to potently block checkpoint inhibitor activity.MethodsEffects of recombinant GDF-15 and a proprietary GDF-15 neutralizing antibody (CTL-002) on immune cell trafficking and activation were analyzed by adhesion and interaction assays and in melanoma-bearing humanized mouse models. The impact of GDF-15 overexpression was tested in subcutaneously implanted, GDF-15-transgenic MC38 cells. Additionally, patient GDF-15 serum levels were correlated with immune infiltration and OS in cutaneous melanoma. Associations between GDF-15 serum levels, response to PD-1-based ICB and corresponding OS were assessed in two independent cohorts of melanoma patients.ResultsGDF-15 impairs adhesion of T and NK cells on activated endothelia. In HV18-MK bearing humanized mice, inhibition of GDF-15 strongly enhances infiltration of activated myeloid and lymphoid cells. In MC38 tumors, GDF-15 overexpression can abrogate tumor rejection upon anti-PD-1 therapy. 50% of the mice with GDF-15 overexpressing tumors were, however, rescued when anti-PD-1 was combined with anti-GDF-15 (CTL-002). Likewise, anti-GDF-15 improved responses to anti-CD40 + poly(I:C) in the same tumor model. Clinically, inverse correlations of GDF-15 levels with CD8+ T cell infiltration were shown for melanoma brain metastases. In two independent melanoma patient cohorts, low baseline serum GDF-15 levels predicted clinical response to anti-PD1 treatment and superior OS. Bivariate analysis including LDH indicates that GDF-15 is an independently predictor for poor survival in anti-PD-1 treated melanoma patients.ConclusionsTumor-derived GDF-15 blocks the infiltration of immune effector cells into tumor tissues. Neutralizing GDF-15 with CTL-002 restores the ability of immune cells to extravasate blood vessels and enter the tumor microenvironment in vivo. GDF-15 thus represents a promising target for cancer immunotherapy. Antibodies against GDF-15 may support treatments with anti-PD-1 and other immunotherapeutic agents. A clinical trial combining anti-GDF-15 (CTL002) with anti-PD-1 (NCT04725474, submitted Abstract ID 15073) is ongoing.Ethics ApprovalUse of patient samples for this study had been approved by the institutional ethics committee Tübingen (ethic vote 125/2015BO2). Use of surplus sera collected in the University of Zurich Hospital (USZ) Biobank during routine blood draws from consenting metastatic melanoma patients was performed according to IRB approval (KEK.Zh- 647/800) and followed the Declaration of Helsinki on Human Rights.ConsentAll patients had given written informed consent to have clinical data recorded by the Central Malignant Melanoma Registry (CMMR) database.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "GDF-15"

1

Ratnam, Nivedita Mohan. "NF-kB Regulates GDF-15 to Suppress Macrophage Surveillance During Early Tumor Development." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1505306161707059.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Kahli, Abdelkader. "Chirurgie cardiaque sous circulation extra-corporelle et ses biomarqueurs : rôle du Growth / Différentiation Factor 15 (GDF 15) : études cliniques." Thesis, Dijon, 2016. http://www.theses.fr/2016DIJOPE02/document.

Full text
Abstract:
La circulation extracorporelle compte parmi les progrès techniques majeurs associés à la chirurgie cardiaque. Elle constitue aussi l’une des causes de complications principales car responsable d’une réponse inflammatoire généralisée qui résulte de la conjugaison des effets du stress oxydant et des cytokines libérés, contribuerait à la dysfonction multi-organe aboutissant aux complications myocardiques et rénales survenant au cours des périodes per- et postopératoires. La première partie de notre travail avait pour objectif d’explorer l’évolution des taux circulants du GDF-15, cytokine associée au stress oxydant et à l’inflammation, dans ce contexte de chirurgie cardiaque. Notre étude prospective a démontré pour la première fois que cette procédure est accompagnée de l’augmentation du GDF-15 dont les taux plasmatiques sont associés aux lésions postopératoires cardiaques et rénales.L’évaluation du risque opératoire repose sur un ensemble de scores dont le calcul est basé essentiellement sur des caractéristiques cliniques. Ces scores présentent toutefois un certaines limitations. Chez les patients « médicaux » atteints de pathologies cardiovasculaires la stratification du risque est définie en associant des caractéristiques cliniques à l’évaluation des taux circulants de biomarqueurs. L’objectif de cette seconde partie a donc été de mettre en évidence le pouvoir prédictif du GDF-15 en tant que biomarqueur circulant dans la survenue de complications rénales au cours de la chirurgie cardiaque sous CEC. Nous avons mis en évidence que les patients présentant des taux préopératoires élevés de GDF-15 sont à risque de développer une insuffisance rénale aigue postopératoire
Ischemic cardiac diseases are the most frequent and deleterious pathologies leading to important cardiovascular-related mortality worldwide. One of the alternative therapies consists to treat these patients using cardiac surgery. Cardiopulmonary bypass was developed to greatly improve this surgical procedure. However, some adverse effects can occur during cardiac surgery associated with cardiopulmonary bypass due to the inflammatory response. This phenomenon is the result of various mechanisms including oxidative stress and inflammatory cytokines which lead to multi-organ failure and then to myocardial and renal injuries occurring during the peri- and post-operative periods.The first part of this work was designed to evaluate in the context of cardiac surgery the kinetics of plasma GDF-15 levels, an oxidative stress and inflammation related cytokine. Our prospective study demonstrated for the first time the kinetic increase in plasma GDF-15 levels which were associated to postoperative cardiac and renal injuries.Currently, operative risk evaluation is based on score calculation including clinical criteria. These risk scores present some limitations. Concerning other cardiac patients out of surgical fields, the risk assessment is defined using clinical parameters and biomarkers evaluation (cardiac troponin, BNP, Nt-proBNP). Thus, we aimed to determine whether pre-operative GDF-15 as plasma biomarker could help to identify patients at high risk of renal injuries. We found that patients with the highest pre-operative plasma GDF-15 levels are at risk for post-operative acute kidney injury
APA, Harvard, Vancouver, ISO, and other styles
3

Schiegnitz, Eik [Verfasser]. "GDF 15 als anti-apoptotischer und pro-hypertropher Faktor in ventrikulären Herzmuskelzellen der Ratte / Eik Schiegnitz." Gießen : Universitätsbibliothek, 2011. http://d-nb.info/1062972325/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Ackermann, Kathrin [Verfasser], and Ralf [Akademischer Betreuer] Kinscherf. "Atherosclerosis: The Role of Growth-Differentiation-Factor-15 (GDF-15) in human THP-1 Macrophages Autophagy and Lipid homeostasis / Kathrin Ackermann ; Betreuer: Ralf Kinscherf." Marburg : Philipps-Universität Marburg, 2020. http://d-nb.info/1218685832/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Wagner, Moritz [Verfasser], and Ralf [Akademischer Betreuer] Kinscherf. "Einfluss des Wachstums-Differenzierungs-Faktors-15 (GDF-15) auf die Gen- und Proteinexpression des Musculus gastrocnemius bei hypercholesterinämischen (knockout) Mäusen / Moritz Wagner ; Betreuer: Ralf Kinscherf." Marburg : Philipps-Universität Marburg, 2017. http://d-nb.info/1126115517/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Bouaouiche, Sarra. "Etude mécanistique des propriétés anti-tumorales du glycéryl trinitrate (gtn) : impact du monoxyde d'azote dans des voies de signalisation induites par des cytokines pro-inflammatoires et dans la régulation de marqueurs de résistance." Thesis, Bourgogne Franche-Comté, 2018. http://www.theses.fr/2018UBFCI010.

Full text
Abstract:
Une des difficultés majeures dans le traitement des cancers est l’acquisition de résistance par les cellules tumorales vis-à-vis de la mort induite par les différentes chimiothérapies. Au sein du laboratoire, nous nous intéressons aux propriétés anti-tumorales d’un donneur de monoxyde d’azote (NO), le Glycéryl TriNitrate (GTN), fréquemment utilisé dans le traitement de l’angine de poitrine. Au cours de ce travail, nous avons étudié les mécanismes moléculaires par lesquels le GTN sensibilise les cellules tumorales de plusieurs types de cancer (colique, mammaire, prostatique) à la mort impliquant des voies de signalisation régulées par des cytokines telles que le TNFα, l’IL-6 ou encore le GDF-15.Une meilleure compréhension des mécanismes sous-jacents à l’action anti-tumorale du GTN permettrait de potentialiser son utilisation comme nouvelle thérapie anti-cancéreuse.Modèle colique : le GTN, en présence de la cytokine pro-inflammatoire TNFα, sensibilise les cellules cancéreuses coliques et mammaires à l’apoptose. Du point de vue mécanistique, le GTN induit la S-nitrosylation de cIAP1, inhibant ainsi son activité ubiquitine E3 ligase. Ce qui abroge la voie de signalisation classique NF-кB de survie cellulaire activée par la voie TNFα/TNFR1 en faveur d’une voie de signalisation pro-apoptotique.Modèle mammaire : le GTN intervient au niveau de la migration cellulaire en altérant la voie de signalisation Jak2/STAT3 activée par la cytokine pro-inflammatoire IL-6, dans un modèle de cancer du sein triple négatif. En présence de dérivés du platine (carboplatine) générant de l’IL-6, le GTN freine la migration des cellules en induisant la S-nitrosylation, et probablement l’inactivation, de la kinase Jak-2, indispensable pour l’activation de la voie.Modèle prostatique : le GTN sensibilise à la mort les cellules cancéreuses prostatiques résistantes au docétaxel en modulant le taux de deux marqueurs de résistance à cette chimiothérapie : la clusterine (CLU) et le growth differentiation factor 15 (GDF-15). Au niveau moléculaire, le GTN diminue le taux de l'isoforme cytoprotectrice soluble de la CLU (sCLU) et augmente le taux de l'isoforme cytotoxique nucléaire (nCLU) dans les cellules prostatiques résistantes au docétaxel. Plus particulièrement, en présence de GTN, nous avons établi un lien entre le GDF-15 et la modulation du taux des isoformes de la CLU
One of the main difficulties in the treatment of cancers is the acquisition of resistance by the tumor cells vis-à-vis the death induced by the different chemotherapies. In the laboratory, we are interested in the anti-tumor properties of a nitric oxide (NO) donor, Glyceryl TriNitrate (GTN), frequently used in the treatment of angina pectoris. In this work, we investigated the molecular mechanisms by which GTN sensitizes tumor cells of several types of cancer (colonic, mammary, prostate) to death involving signaling pathways regulated by cytokines such as TNFα, IL-6 or GDF-15.A better understanding of the mechanisms underlying the GTN's anti-tumor action would make it possible to use it as a new anti-cancer therapy.Colon model: GTN, in the presence of the pro-inflammatory cytokine TNFα, sensitizes colon and mammary cancer cells to apoptosis. From a mechanistic point of view, GTN induces S-nitrosylation of cIAP1, thus inhibiting its ubiquitin E3 ligase activity. This abrogates the classical NF-κB signaling pathway of TNFα / TNFR1 activated cell survival in favor of a pro-apoptotic signaling pathway.Mammary model: GTN intervenes at the level of cell migration by altering the Jak2 / STAT3 signaling pathway activated by the pro-inflammatory cytokine IL-6, in a model of triple negative breast cancer. In the presence of platinum (carboplatin) derivatives generating IL-6, GTN inhibits cell migration by inducing S-nitrosylation, and probably inactivation, of Jak-2 kinase, essential for the activation of the way.Prostate model: GTN sensitizes prostatic prostate cancer cells to death by modulating the level of two markers of resistance to this chemotherapy: clusterin (CLU) and growth differentiation factor 15 (GDF-15). At the molecular level, GTN decreases the level of the soluble cytoprotective isoform of CLU (sCLU) and increases the level of nuclear cytotoxic isoform (nCLU) in prostatic cells resistant to docetaxel. More particularly, in the presence of GTN, we have established a link between GDF-15 and the modulation of the isoform rate of the CLU
APA, Harvard, Vancouver, ISO, and other styles
7

Junker, Markus [Verfasser], and Roland [Gutachter] Benz. "Development and characterization of monoclonal antibodies to GDF-15 for potential use in cancer therapy / Markus Junker. Gutachter: Roland Benz." Würzburg : Universität Würzburg, 2016. http://d-nb.info/1111888531/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Leyh, Tanja [Verfasser], and Volker [Gutachter] Kunzmann. "GDF-15-Spiegel bei Patienten mit HER2/neu positivem Mammakarzinom im frühen Stadium: eine klinische Pilotstudie / Tanja Leyh ; Gutachter: Volker Kunzmann." Würzburg : Universität Würzburg, 2021. http://d-nb.info/1238018440/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

XU, JIAN. "TRANSCRIPTIONAL REGULATION OF CARDIAC HYPERTROPHY AND HEART FAILURE." University of Cincinnati / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1148396901.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Walter, Sabrina [Verfasser], and Hilmar [Akademischer Betreuer] Bading. "GDF 15 deficiency induces a progressive Schwann cell loss in vivo and regulates their survival and migration in vitro / Sabrina Walter ; Betreuer: Hilmar Bading." Heidelberg : Universitätsbibliothek Heidelberg, 2014. http://d-nb.info/1177811162/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "GDF-15"

1

Giannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0036.

Full text
Abstract:
Biomarker testing in the evaluation of a patient with acute chest pain is best established for cardiac troponins that allow the diagnosis of myocardial infarction, risk estimation of short- and long-term risk of death and myocardial infarction, and guidance of pharmacological therapy, as well as the need and timing of invasive strategy. Newer, more sensitive troponin assays have become commercially available and have the capability to detect myocardial infarction earlier and more sensitively than standard assays, but they are hampered by a lack of clinical specificity, i.e. the ability to discriminate myocardial ischaemia from myocardial necrosis not related to ischaemia such as myocarditis, pulmonary embolism, or decompensated heart failure. Strategies to improve clinical specificity (including strict adherence to the universal myocardial infarction definition and the need for serial troponin measurements to detect an acute rise and/or fall of cardiac troponin) will improve the interpretation of the increasing number of positive results. Other biomarkers of inflammation, activated coagulation/fibrinolysis, and increased ventricular stress mirror different aspects of the underlying disease activity and may help to improve our understanding of the pathophysiological mechanisms of acute coronary syndromes. Among the flood of new biomarkers, there are several novel promising biomarkers, such as copeptin that allows an earlier rule-out of myocardial infarction in combination with cardiac troponin, whereas MR-proANP and MR-proADM appear to allow a refinement of cardiovascular risk. GDF-15 might help to identify candidates for an early invasive vs conservative strategy. A multi-marker approach to biomarkers becomes more and more attractive, as increasing evidence suggests that a combination of several biomarkers may help to predict individual risk and treatment benefits, particularly among troponin-negative subjects. Future goals include the acceleration of rule-in and rule-out of patients with suspected acute coronary syndrome, in order to shorten lengths of stay in the emergency department, and to optimize patient management and the use of health care resources. New algorithms using high-sensitivity cardiac troponin assays at low cut-offs alone, or in combination with additional biomarkers, allow to establish accelerated rule-out algorithms within 1 or 2 hours.
APA, Harvard, Vancouver, ISO, and other styles
2

Giannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0036_update_001.

Full text
Abstract:
Biomarker testing in the evaluation of a patient with acute chest pain is best established for cardiac troponins that allow the diagnosis of myocardial infarction, risk estimation of short- and long-term risk of death and myocardial infarction, and guidance of pharmacological therapy, as well as the need and timing of invasive strategy. Newer, more sensitive troponin assays have become commercially available and have the capability to detect myocardial infarction earlier and more sensitively than standard assays, but they are hampered by a lack of clinical specificity, i.e. the ability to discriminate myocardial ischaemia from myocardial necrosis not related to ischaemia such as myocarditis, pulmonary embolism, or decompensated heart failure. Strategies to improve clinical specificity (including strict adherence to the universal myocardial infarction definition and the need for serial troponin measurements to detect an acute rise and/or fall of cardiac troponin) will improve the interpretation of the increasing number of positive results. Other biomarkers of inflammation, activated coagulation/fibrinolysis, and increased ventricular stress mirror different aspects of the underlying disease activity and may help to improve our understanding of the pathophysiological mechanisms of acute coronary syndromes. Among the flood of new biomarkers, there are several novel promising biomarkers, such as copeptin that allows an earlier rule-out of myocardial infarction in combination with cardiac troponin, whereas MR-proANP and MR-proADM appear to allow a refinement of cardiovascular risk. GDF-15 might help to identify candidates for an early invasive vs conservative strategy. A multi-marker approach to biomarkers becomes more and more attractive, as increasing evidence suggests that a combination of several biomarkers may help to predict individual risk and treatment benefits, particularly among normal-troponin subjects. Future goals include the acceleration of rule-in and rule-out of patients with suspected acute coronary syndrome, in order to shorten lengths of stay in the emergency department, and to optimize patient management and the use of health care resources. New algorithms using high-sensitivity cardiac troponin assays at low cut-offs alone, or in combination with additional biomarkers, allow to establish accelerated rule-out algorithms within 1 or 2 hours.
APA, Harvard, Vancouver, ISO, and other styles
3

Giannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0036_update_002.

Full text
Abstract:
Biomarker testing in the evaluation of a patient with acute chest pain is best established for cardiac troponins that allow the diagnosis of myocardial infarction, risk estimation of short- and long-term risk of death and myocardial infarction, and guidance of pharmacological therapy, as well as the need and timing of invasive strategy. Newer, more sensitive troponin assays have become commercially available and have the capability to detect myocardial infarction earlier and more sensitively than standard assays, but they are hampered by a lack of clinical specificity, i.e. the ability to discriminate myocardial ischaemia from myocardial necrosis not related to ischaemia such as myocarditis, pulmonary embolism, or decompensated heart failure. Strategies to improve clinical specificity (including strict adherence to the universal myocardial infarction definition and the need for serial troponin measurements to detect an acute rise and/or fall of cardiac troponin) will improve the interpretation of the increasing number of positive results. Other biomarkers of inflammation, activated coagulation/fibrinolysis, and increased ventricular stress mirror different aspects of the underlying disease activity and may help to improve our understanding of the pathophysiological mechanisms of acute coronary syndromes. Among the flood of new biomarkers, there are several novel promising biomarkers, such as copeptin that allows an earlier rule-out of myocardial infarction in combination with cardiac troponin, whereas MR-proANP and MR-proADM appear to allow a refinement of cardiovascular risk. GDF-15 might help to identify candidates for an early invasive vs conservative strategy. A multi-marker approach to biomarkers becomes more and more attractive, as increasing evidence suggests that a combination of several biomarkers may help to predict individual risk and treatment benefits, particularly among normal-troponin subjects. Future goals include the acceleration of rule-in and rule-out of patients with suspected acute coronary syndrome, in order to shorten lengths of stay in the emergency department, and to optimize patient management and the use of health care resources. New algorithms using high-sensitivity cardiac troponin assays at low cut-offs alone, or in combination with additional biomarkers, allow to establish accelerated rule-out algorithms within 1 or 2 hours.
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "GDF-15"

1

Strelau, J., M. Böttner, P. Lingor, C. Suter-Crazzolara, D. Galter, J. Jaszai, A. Sullivan, A. Schober, K. Krieglstein, and K. Unsicker. "GDF-15/MIC-1 a novel member of the TGF-ß superfamily." In Advances in Research on Neurodegeneration, 273–76. Vienna: Springer Vienna, 2000. http://dx.doi.org/10.1007/978-3-7091-6301-6_18.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Strelau, J., A. Schober, A. Sullivan, L. Schilling, and K. Unsicker. "Growth/differentiation factor-15 (GDF-15), a novel member of the TGF-β superfamily, promotes survival of lesioned mesencephalic dopaminergic neurons in vitro and in vivo and is induced in neurons following cortical lesioning." In Advances in Research on Neurodegeneration, 197–203. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-0643-3_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Delrue, Charlotte, Reinhart Speeckaert, Joris R. Delanghe, and Marijn M. Speeckaert. "Growth differentiation factor 15 (GDF-15) in kidney diseases." In Advances in Clinical Chemistry. Elsevier, 2023. http://dx.doi.org/10.1016/bs.acc.2023.02.003.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Vila, Greisa, Michaela Riedl, Christian Anderwald, Michael Resl, Martin Clodi, Bernhard Ludvik, Gerhard Prager, Michael Krebs, and Anton Luger. "Increased GDF-15 Concentrations in Morbidly Obese Subjects Increase Further Following Gastric Bypass-Induced Weight Loss." In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego, P3–434—P3–434. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part3.p9.p3-434.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Smołucha, G., A. Piestrzyńska-Kajtoch, and B. Rejduch. "A novel mutation of BMP-15 and GDF-9 gene in the Romanov sheep breed in Poland." In Book of Abstracts of the 66th Annual Meeting of the European Association for Animal Production, 160. Brill | Wageningen Academic, 2015. http://dx.doi.org/10.3920/9789086868162_148.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Hegyesi, Hargita, James R., Nikolett Sandor, Boglarka Schilling-Toth, and Geza Safrany. "Validation of Growth Differentiation Factor (GDF-15) as a Radiation Response Gene and Radiosensitizing Target in Mammary Adenocarcinoma Model." In Breast Cancer - Recent Advances in Biology, Imaging and Therapeutics. InTech, 2011. http://dx.doi.org/10.5772/21019.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Vila, Greisa, Marie Helene Reiter, Michaela Riedl, Martin Clodi, and Anton Luger. "The Cardiovascular Biomarker GDF-15 Increases after LPS-Induced Endotoxemia in Healthy Men and Is Up-Regulated in PBMCs of Obese Patients." In BASIC/TRANSLATIONAL - Diabetes & Glucose Homeostasis: Genetic & Translational Approaches, P2–528—P2–528. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part3.p6.p2-528.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "GDF-15"

1

Amado Diago, Carlos Antonio, Paula Martín Audera, Daymara Boucle Tirador, Mayte García-Unzueta, Milagros Ruiz De Infante Pérez, Ana Berja, Armando Raúl Guerra, et al. "Association of GDF-15 with 6 minute walking test." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa3434.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Garcia Moyano, Marta, Borja Santos Zorrozua, Eva Tabernero Huguet, Francisco Javier Martinez Núñez, Vanessa Zorrilla Lorenzo, Beatriz González Quero, Beatriz Gómez Crespo, et al. "DIAGNOSTIC VALUE OF KL-6 AND GDF-15 IN LYMPHANGIOLEIOMYOMATOSIS." In ERS International Congress 2023 abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/13993003.congress-2023.pa3951.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Masters, B., J. L. Curtis, M. K. Han, F. J. Martinez, W. K. O'Neal, C. M. Freeman, G. J. Criner, et al. "Plasma GDF-15 Levels Improve Risk Assessments for Severe COPD Outcomes." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2860.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Nickel, N., T. Kempf, H. Golpon, KC Wollert, K. Olsson, C. deWall, T. Welte, and MM Hoeper. "GDF-15 in Follow up in Patients with Idiopathic Pulmonary Arterial Hypertension." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4869.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Lee, Jaeseob, Hansoo Lee, Jeongsuk Choi, Iha Park, Jeong-Hyung Lee, and Young-Myeong Kim. "Abstract 5147: Tumor angiogenesis-promoting activity of a hypoxia-inducible cytokine, growth differentiation factor-15 (GDF-15)." 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.am2011-5147.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Watanabe, Mototsugu, Yasutaka Masada, Shinsuke Hashida, Tomoaki Ohtsuka, Ken Suzawa, Yuho Maki, Hiromasa Yamamoto, et al. "Abstract 358: The role of GDF-15 on docetaxel resistance in lung cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-358.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Risbano, Michael G., Christine Meadows, Li Zhang, Rubin Tuder, Mark W. Geraci, and Todd M. Bull. "GDF-15 Is A Marker For Survival In Scleroderma Related Pulmonary Arterial Hypertension." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4861.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Foris, Vasile, Ceren Ayse Mutgan, Andrea Borenich, Gabor Kovacs, Philipp Douschan, Teresa Sassmannn, Katarina Zeder, Andrea Olschewski, Grazyna Kwapiszewska, and Horst Olschewski. "Dehydroepiandrosterone and GDF-15 for follow-up of patients with pulmonary arterial hypertension." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.oa144.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Haake, Markus, Neha Vashist, Sabrina Genssler, Kristin H. Eichler, Birgitt Fischer, Jessica Kammer, Paula S. Romer, et al. "Abstract 5597: Tumor-derived GDF-15 suppresses T-lymphocyte recruitment to the tumor microenvironment." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-5597.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Mariscal, Anaís, Leticia Alserawan, Iván Castellví, Esther Ortiz, Patricia Peñacoba, Teresa Franco-Leyva, José Luís Tandaipán, et al. "Usefulness of GDF-15 as a biomarker of respiratory worsening in COVID-19 patients." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa673.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "GDF-15"

1

Zhou, Zhongwei, Hongli Liu, Huixiang Ju, Hongmei Chen, Li Li, Hao Jin, and Mingzhong Sun. Circulating GDF-15 in relation to the progression and prognosis of chronic kidney disease: A systematic review and dose-response meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2022. http://dx.doi.org/10.37766/inplasy2022.10.0076.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'GDF-15' for particular source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography