Relevant bibliographies by topics / Wnt inhibitors

Academic literature on the topic 'Wnt inhibitors'

Author: Grafiati
Published: 10 December 2022
Last updated: 21 February 2023

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Journal articles on the topic "Wnt inhibitors"

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Pehlivan, Melek, Ceyda Caliskan, Zeynep Yuce, and Hakkı Ogun Sercan. "Forced expression of Wnt antagonists sFRP1 and WIF1 sensitizes chronic myeloid leukemia cells to tyrosine kinase inhibitors." Tumor Biology 39, no. 5 (May 2017): 101042831770165. http://dx.doi.org/10.1177/1010428317701654.

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Chronic myeloid leukemia is a clonal myeloproliferative disorder that arises from the neoplastic transformation of the hematopoietic stem cell, in which the Wnt/β-catenin signaling pathway has been demonstrated to play an important role in disease progression. However, the role of Wnt signaling antagonists in therapy resistance and disease progression has not been fully investigated. We aimed to study the effects of Wnt/β-catenin pathway antagonists—secreted frizzled-related protein 1 and Wnt inhibitory factor 1—on resistance toward tyrosine kinase inhibitors in chronic myeloid leukemia. Response to tyrosine kinase inhibitors was analyzed in secreted frizzled-related protein 1 and Wnt inhibitory factor 1 stably transfected K562 cells. Experiments were repeated using a tetracycline-inducible expression system, confirming previous results. In addition, response to tyrosine kinase inhibitor treatment was also analyzed using the secreted frizzled-related protein 1 expressing, BCR-ABL positive MEG01 cell line, in the presence and absence of a secreted frizzled-related protein 1 inhibitor. Our data suggests that total cellular β-catenin levels decrease in the presence of secreted frizzled-related protein 1 and Wnt inhibitory factor 1, and a significant increase in cell death after tyrosine kinase inhibitor treatment is observed. On the contrary, when secreted frizzled-related protein 1 is suppressed, total β-catenin levels increase in the cell and the cells become resistant to tyrosine kinase inhibitors. We suggest that Wnt antagonists carry the potential to be exploited in designing new agents and strategies for the advanced and resistant forms of chronic myeloid leukemia.
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Watanabe, K., and X. Dai. "Winning WNT: Race to Wnt signaling inhibitors." Proceedings of the National Academy of Sciences 108, no. 15 (March 30, 2011): 5929–30. http://dx.doi.org/10.1073/pnas.1103102108.

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Rogaczewski, Patryk, Michał Janiak, Kamil Borysewicz, Tadeusz Głos, Navid Ahmadi, and Łukasz Szylberg. "Clinical significancy of WNT pathway inhibition in various cancers." Journal of Education, Health and Sport 12, no. 11 (November 3, 2022): 183–91. http://dx.doi.org/10.12775/jehs.2022.12.11.024.

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The tumor microenvironment (TME) plays an important role in the cell cycle. There is a correlation between the Wnt/B–catenin signaling pathway and TME. This article reviews methods of inhibiting Wnt Pathway, a useful process in the treatment of various cancers. Compounds of Wnt/β–Catenin Signaling Pathway, such as TCF–1, have an impact on the differentiation and migration of CD8+ T cells. CCL4 expression is regulated by the beta–catenin protein to recruit CD103+ dendritic cells, which enables CD8+ T cell activation. Inhibition of the Wnt/β–catenin pathway has an impact on ovarian cancer patients’ prognosis, reducing the development of ovarian cancer. Research shows that inhibition of the pathway with the use of the LGK974 inhibitor may boost immunity, especially when applied with a Paclitaxel mix. After treatment, expression of the inhibitory receptors CTLA–4, TIM3, PD–1 on CD8+ T cells decreased. The combination of LGK974 and Paclitaxel can cause the death of tumor cells and significantly inhibit their proliferation. The application of dose–dense Paclitaxel avoids toxicity related to the maximum dose needed to protect the patient's immune system by increasing CD8+ TILs. There are concerns regarding toxicity of the LGK 974, especially for cells dependent on the Wnt/β–catenin pathway to maintain homeostasis. Many Wnt/β–catenin pathway inhibitors are tested against colorectal cancer (CRC) with successful results. These include NSAIDs, porcupine inhibitors, tankyrase inhibitors, Wnt5A inhibitors, and disheveled protein inhibitors.The Wnt/β–catenin pathway, when expressed in Triple Negative Breast Cancer (TNBC), leads to the transition of epithelial to mesenchymal cells. In early clinical development, there are multiple inhibitors (ex. KYA1797K) targeting the Wnt/β–catenin pathway in TNBC cells, which could become a viable anticancer strategy.
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Griffiths, Elizabeth A., Craig M. Hooker, Michael A. McDevitt, Judith E. Karp, James G. Herman, and Hetty E. Carraway. "Acute Myeloid Leukemia Is Characterized by Wnt Pathway Inhibitor Promoter Methylation." Blood 112, no. 11 (November 16, 2008): 2253. http://dx.doi.org/10.1182/blood.v112.11.2253.2253.

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Abstract The Wnt pathway contributes to a stem-cell like phenotype in a variety of cancer subtypes. Nuclear localization of non-phosphorylated, active β-catenin is a surrogate marker for Wnt pathway activation and has been associated with adverse outcome in patients with acute myeloid leukemia (AML). Wnt pathway inhibitors including APC, DKK1, DKK3, LKB1/STK11, RASSF1A, RUNX3, SFRP1, SFRP2, SFRP4, SFRP5, SOX17, and WIF1 contain extensive promoter region CpG islands. Wnt pathway inhibitors are silenced by promoter methylation in many malignancies including lung cancer, colon cancer and acute lymphoid leukemias. To determine if methylation of these Wnt pathway inhibitors is present in AML, we evaluated leukemia cell lines (i.e., K562, HNT34, KG1, KG1A, U937, and HL60) for evidence of promoter methylation. Additionally, 188 AML patient (median age 61 years) samples from the Johns Hopkins Hospital leukemia tumor bank were assessed for the presence of Wnt pathway inhibitor methylation. All samples were bisulfite treated and evaluated for promoter methylation using methylation specific PCR. Diagnostic samples from a subgroup of patients with normal cytogenetics (n=73) who received high dose induction therapy were evaluated for potential associations between methylation of individual Wnt pathway inhibitor genes or total number of methylated genes and event free or overall survival. RESULTS: Extensive promoter methylation of the Wnt pathway inhibitor genes was observed in leukemia cell lines. Of the primary leukemia samples, 85% had at least one methylated gene. Promoter methylation of Wnt inhibitors was common in these samples with the following frequencies: DKK1 (16%;30/188), DKK3 (8%;15/188), RUNX3 (27%;50/188), SFRP1 (34%;63/188), SFRP2 (66%;124/188), SFRP4 (9%;16/188), SFRP5 (54%;102/188), SOX17 (29%;54/188), and WIF1 (32%;61/188). This is among the first comprehensive evaluations of Wnt pathway inhibitor methylation in primary samples from AML patients. The frequency of methylation seen here is comparable to that observed in established tumor suppressor genes in patients with AML, including p15INK4B, SOCS1 and CDH1. In marked contrast with epithelial tumors, methylation of APC (2%;2/108) and RASSF1A (0%;0/188) was rare. LKB1/STK11 methylation was also uncommon (2%;2/108). Previous reports have associated Wnt pathway activation with poor prognosis. In our treated patients with normal cytogenetics, no correlation was observed between methylation of Wnt pathway inhibitors and event free or overall survival. In conclusion, in patients with AML (a) there is a high frequency of Wnt pathway inhibitor methylation; (b) Wnt pathway inhibitor methylation is distinct from that observed in epithelial malignancies; and (c) methylation of Wnt pathway genes does not correlate with adverse clinical outcome.
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Filipovich, Alexandra, Iris Gehrke, Simon J. Poll-Wolbeck, and Karl-Anton Kreuzer. "Physiological inhibitors of Wnt signaling." European Journal of Haematology 86, no. 6 (May 17, 2011): 453–65. http://dx.doi.org/10.1111/j.1600-0609.2011.01592.x.

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Román-Gómez, José, Lucia Cordeu, Xabier Agirre, Antonio Jiménez-Velasco, Edurne San José-Eneriz, Leire Garate, María José Calasanz, Anabel Heiniger, Antonio Torres, and Felipe Prosper. "Epigenetic regulation of Wnt-signaling pathway in acute lymphoblastic leukemia." Blood 109, no. 8 (December 5, 2006): 3462–69. http://dx.doi.org/10.1182/blood-2006-09-047043.

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Abstract Activation of the Wnt/β-catenin signaling pathway is a hallmark of a number of solid tumors. We analyzed the regulation of the Wnt/β-catenin pathway in acute lymphoblastic leukemia (ALL) and its role in the pathogenesis of the disease. We found that expression of the Wnt inhibitors sFRP1, sFRP2, sFRP4, sFRP5, WIF1, Dkk3, and Hdpr1 was down-regulated due to abnormal promoter methylation in ALL cell lines and samples from patients with ALL. Methylation of Wnt inhibitors was associated with activation of the Wnt-signaling pathway as demonstrated by the up-regulation of the Wnt target genes WNT16, FZ3, TCF1, LEF1, and cyclin D1 in cell lines and samples and the nuclear localization of β-catenin in cell lines. Treatment of ALL cells with the Wnt inhibitor quercetin or with the demethylating agent 5-aza-2′-deoxycytidine induced an inactivation of the Wnt pathway and induced apoptosis of ALL cells. Finally, in a group of 261 patients with newly diagnosed ALL, abnormal methylation of Wnt inhibitors was associated with decreased 10-year disease-free survival (25% versus 66% respectively, P < .001) and overall survival (28% versus 61% respectively, P = .001). Our results indicate a role of abnormal Wnt signaling in ALL and establish a group of patients with a significantly worse prognosis (methylated group).
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Elyamany, Ghaleb, Hassan Rizwan, Ariz Akhter, Mansour S. Aljabry, Sultan Alotaibi, Mohammad A. Hameed Albalawi, Meer-Taher Shabani-Rad, Tariq Mahmood Roshan, and Adnan Mansoor. "“Losing the Brakes”—Suppressed Inhibitors Triggering Uncontrolled Wnt/ß-Catenin Signaling May Provide a Potential Therapeutic Target in Elderly Acute Myeloid Leukemia." Current Issues in Molecular Biology 45, no. 1 (January 9, 2023): 604–13. http://dx.doi.org/10.3390/cimb45010040.

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Dysregulated Wnt/β-catenin signal transduction is implicated in initiation, propagation, and poor prognosis in AML. Epigenetic inactivation is central to Wnt/β-catenin hyperactivity, and Wnt/β-catenin inhibitors are being investigated as targeted therapy. Dysregulated Wnt/β-catenin signaling has also been linked to accelerated aging. Since AML is a disease of old age (>60 yrs), we hypothesized age-related differential activity of Wnt/β-catenin signaling in AML patients. We probed Wnt/β-catenin expression in a series of AML in the elderly (>60 yrs) and compared it to a cohort of pediatric AML (<18 yrs). RNA from diagnostic bone marrow biopsies (n = 101) were evaluated for key Wnt/β-catenin molecule expression utilizing the NanoString platform. Differential expression of significance was defined as >2.5-fold difference (p < 0.01). A total of 36 pediatric AML (<18 yrs) and 36 elderly AML (>60 yrs) were identified in this cohort. Normal bone marrows (n = 10) were employed as controls. Wnt/β-catenin target genes (MYC, MYB, and RUNX1) showed upregulation, while Wnt/β-catenin inhibitors (CXXR, DKK1-4, SFRP1-4, SOST, and WIFI) were suppressed in elderly AML compared to pediatric AML and controls. Our data denote that suppressed inhibitor expression (through mutation or hypermethylation) is an additional contributing factor in Wnt/β-catenin hyperactivity in elderly AML, thus supporting Wnt/β-catenin inhibitors as potential targeted therapy.
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Li, Bo, Jinxia Liang, Feng Lu, Guandi Zeng, Jindao Zhang, Yinxing Ma, Peng Liu, Qin Wang, Qian Zhou, and Liang Chen. "Discovery of Novel Inhibitor for WNT/β-Catenin Pathway by Tankyrase 1/2 Structure-Based Virtual Screening." Molecules 25, no. 7 (April 6, 2020): 1680. http://dx.doi.org/10.3390/molecules25071680.

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Aberrant activation of the WNT/β-catenin signaling pathway is implicated in various types of cancers. Inhibitors targeting the Wnt signaling pathway are intensively studied in the current cancer research field, the outcomes of which remain to be determined. In this study, we have attempted to discover novel potent WNT/β-catenin pathway inhibitors through tankyrase 1/2 structure-based virtual screening. After screening more than 13.4 million compounds through molecular docking, we experimentally verified one compound, LZZ-02, as the most potent inhibitor out of 11 structurally representative top hits. LiCl-induced HEK293 cells containing TOPFlash reporter showed that LZZ-02 inhibited the transcriptional activity of β-catenin with an IC50 of 10 ± 1.2 μM. Mechanistically, LZZ-02 degrades the expression of β-catenin by stabilizing axin 2, thereby diminishing downstream proteins levels, including c-Myc and cyclin D1. LZZ-02 also inhibits the growth of colonic carcinoma cell harboring constitutively active β-catenin. More importantly, LZZ-02 effectively shrinks tumor xenograft derived from colonic cell lines. Our study successfully identified a novel tankyrase 1/2 inhibitor and shed light on a novel strategy for developing inhibitors targeting the WNT/β-catenin signaling axis.
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Ye, Zhen-Nan, Feng Yuan, Jie-Qing Liu, Xing-Rong Peng, Tao An, Xue Li, Ling-Mei Kong, Ming-Hua Qiu, and Yan Li. "Physalis peruviana-Derived 4β-Hydroxywithanolide E, a Novel Antagonist of Wnt Signaling, Inhibits Colorectal Cancer In Vitro and In Vivo." Molecules 24, no. 6 (March 22, 2019): 1146. http://dx.doi.org/10.3390/molecules24061146.

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Deregulation of the Wnt signaling pathway leads to colorectal cancer progression. Natural dietary compounds serve as promising candidates for development as chemopreventive agents by suppressing the Wnt/β-catenin signaling pathway. Physalis peruviana-derived 4βHWE showed a significant inhibitory activity with a calculated IC50 of 0.09 μΜ in a screening of novel inhibitors of Wnt signaling with the dual-luciferase reporter assay. This study investigated the anti-tumor effect of 4βHWE and the potential Wnt signaling inhibitory mechanism. Both the western blot analysis and immunofluorescence assay showed that 4βHWE promoted the phosphorylation and degradation of β-catenin and the subsequent inhibition of its nuclear translocation to attenuate the endogenous Wnt target gene expression in colorectal cancer (CRC) cells. The cell viability assay indicated that 4βHWE preferentially inhibited the proliferation of CRC compared with CCD-841-CoN, a normal human colonic epithelial cell line. 4βHWE-mediated G0/G1 cell cycle arrest and apoptosis induction contributed to the suppression of the proliferation of CRC in the cell cycle and Annexin V-FITC/Propidium Iodide apoptosis analysis. Moreover, in vivo, 4βHWE dramatically inhibited tumor growth in HCT116 xenografts by attenuating the Wnt/β-catenin signaling pathway. In conclusion, our study suggested that 4βHWE could be of potential use in anti-tumor agent development as a novel Wnt signaling inhibitor.
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Mii, Yusuke, and Masanori Taira. "Secreted Wnt “inhibitors” are not just inhibitors: Regulation of extracellular Wnt by secreted Frizzled-related proteins." Development, Growth & Differentiation 53, no. 8 (October 2011): 911–23. http://dx.doi.org/10.1111/j.1440-169x.2011.01299.x.

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Dissertations / Theses on the topic "Wnt inhibitors"

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Ho, Sze-hang, and 何思恆. "Differential expression of Wnt inhibitors Dickkopf-1 (Dkk-1) and Wnt inhibitory factor-1 (Wif1) in the regulation of urorectal development." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/207999.

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In mammals, the external genitalia, urinary tract and anorectal tract are developed from a common embryonic primordium, the urorectum. Cloaca is the hollow space inside the urorectum that connects the hindgut and the urogenital sinus. During the urorectal development, the external genitalia is formed from the outgrowth of genital tubercle (GT) protruding from the urorectum, while the future urinary tract and anorectal tract are formed by the partition of cloaca during cloacal septation. GT outgrowth and cloacal septation are important developmental events for the formation of genitourinary and anorectal system. In human, dysregulation of these developmental events results in congenital anorectal malformations (ARM). Wnt signaling is one of the key signaling pathways that regulates urorectal development. The activity of Wnt signaling is initiated by the binding of Wnt ligands to cell surface receptors, which can be antagonized by secretory Wnt inhibitors. Dickkopf1 (Dkk1) and Wnt inhibitory factor 1 (Wif1) are secretory Wnt inhibitors implicated in urorectal development. However, the functions of other secretory Wnt inhibitors during urorectal developments remain to be elucidated. In this study, expression analyses showed that Dkk1, Dickkopf2 (Dkk2), Dickkopf4 (Dkk4), Secreted Frizzled-related Protein 1 (Sfrp1) and Wif1 were expressed in the developing urorectum. The dynamic, overlapping and restricted expression patterns of these Wnt inhibitors were closely associated with the GT outgrowth and the cloacal septation events, implying that these Wnt inhibitors functioned in a coordinated manner in defining the field of Wnt signaling activities in the developing urorectum. Wif1 knockout mice (〖Wif1〗^(-/-)) was used as the model to investigate the functions of and the interplay between secretory Wnt inhibitors in urorectal development. GT outgrowth and cloacal septation defects were observed in 〖Wif1〗^(-/-) embryos. Most of the 〖Wif1〗^(-/-) embryos displayed varying degrees of GT outgrowth defects, while septation defects were only occasionally observed. This suggested that GT outgrowth and cloacal septation were regulated by Wif1 via different regulatory mechanisms. In the urorectum of 〖Wif1〗^(-/-) embryos, Dkk1 was significantly upregulated in the peri-cloacal mesenchyme. Further expression analysis suggested that Dkk1 was sufficient to rescue cloacal septation defects but not GT outgrowth defects in 〖Wif1〗^(-/-)embryos. In the 〖Wif1〗^(-/-) embryos with severe GT outgrowth defects, the Fgf8-expressing distal urethral epithelium, the signaling center in the urorectum, was absent, suggesting that the GT outgrowth defects could be contributed by the loss of dUE-expressing signals such as Fgf8. This study demonstrated the importance of secretory Wnt inhibitors in the GT outgrowth and cloacal septation and suggested that secretory Wnt inhibitors played partially overlapping roles in urorectal development. A rescue mechanism for cloacal septation performed by Dkk1 upon Wif1 deletion was proposed. Such auto-regulatory mechanism within the Wnt signaling pathway indicated that Wnt inhibitors play essential regulatory roles in the urorectal development and a balanced Wnt signaling activity modulated by Wnt inhibitors is crucial to the development of urorectum.
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Jandu, Arvinder Singh. "Characterization of Novel Canonical WNT Signaling Inhibitors in Prostate and Colorectal Cancers." Thesis, The University of Arizona, 2013. http://hdl.handle.net/10150/297656.

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Objectives: The objectives of this study were to (1) characterize the levels of WNT signaling in DLD-1 colorectal cancer cells with mutant APC and DU145 prostate cancer cells with wild type APC, (2) to conduct an investigation of novel tankyrase inhibitors in both colorectal and pancreatic cancer cells. WNT signaling has been shown to play an integral role in the proliferation and metastasis of both cancer types; therefore, it is of interest to evaluate inhibitors of the signaling pathway to assess their potential applications in targeted cancer therapeutics. Methods: To characterize WNT signaling activity in colorectal cancer cells (1), DLD-1 cells transduced with a TCF/LEF luciferase reporter and selected with puromycin were grown out in both a two dimensional culture and as tumorspheres to comparatively examine signaling between the different morphologies, as well as at different plating densities. To probe the mechanism of the tankyrase inhibitors (2), DLD-1 and DU145 pancreatic cancer cells were grown to confluency, treated with 1 uM of each inhibitor, and harvested for lysate preparation after 24 hours. Western blots of β-catenin, AXIN1, and AXIN2 were performed and quantified for comparative analysis. Additional assays were performed using DLD-1 cells to assess effects of the inhibitors on proliferation and migration. Results: In DLD-1 cells, it was observed that all tumorsphere cultures exhibited significantly decreased levels of WNT signaling. In DU145 cells, inhibitor D was demonstrated (western blot) to knock down β- catenin levels, as well as stabilize both AXIN1 and AXIN2 levels. Inhibitor A3 was able to decrease β- catenin levels, as well as stabilize AXIN2 levels. Surprisingly, inhibitor A1 was found (via densitometry) to increase both beta-catenin levels and AXIN2 levels. A2 and IWR were found to only decrease β- catenin protein amounts. In DLD-1 cells, all inhibitors exhibited some decrease in beta-catenin levels; however, only A1, A3, A5, and A6 were found to significantly decrease proliferation (MTT assay), and only A1, A4, and A7 were found to significantly stunt migration (scratch assay). Conclusions: In DU145 cells, tankyrase inhibitors D and A3 display the most promise by being able to modulate both catenin and AXIN protein levels. In DLD-1 cells, growth and proliferation assays demonstrate that some inhibitors result in differential phenotypic effects, suggesting that different gene targets downstream of β-catenin are being effected. Further blots for such targets will prove useful to clarify these results. In addition, similar phenotypic characterizations in DU145 cells are necessary to connect the tankyrase mechanisms to observable effects.
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García, Reyes Balbina [Verfasser]. "Validation of new Casein Kinase 1 (CK1) small molecule inhibitor compounds and characterization of Inhibitors of Wnt Production (IWPs) as inhibitors of CK1δ / Balbina García Reyes." Ulm : Universität Ulm, 2018. http://d-nb.info/1151938424/34.

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Ali, Youmna Tantawy Abdou Ahmed. "Molecular regulation on the activity and expression of human organic anion transporting polypeptides (OATPs) and organic anion transporters (OATs)." Thesis, The University of Sydney, 2022. https://hdl.handle.net/2123/28906.

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Organic anion transporters polypeptides and organic anion transporter are 2 main subfamilies of SLC transporters that are located all over the body. They are influx membrane transporters that govern the movement of endogenous and exogenous compounds across the cell membrane. Endogenous compounds such as thyroid hormones, prostaglandins, and bile acids as well as exogenous compounds like antibiotics, anti-hypertensive, statins, and anti-cancer drugs can be transported by SLCs. Altered expression of OATPs and OATs leads to several diseases and impacts drug’s pharmacokinetic and pharmacodynamic properties, which may lead to variable drug responses. In Chapter 1 we studied SLC transporters, mainly OATs’ structure, localization, function, and molecular regulation. Genetic variation of SLCs and/or molecular regulation “by manipulating different signaling pathways” significantly altered the function and expression of transporters leading to inadequate drug efficacy, drug toxicity, and /or drug-drug interaction. Nowadays, due to the recent approach towards herbal medicine for the treatment of several diseases we studied the involvement of human organic anion transporting polypeptides (OATPs) in drug-herb/food interactions (Chapter 2). We found that several herbal medicines and natural compounds that exist in food can impact the function of several SLC transporters. As the transporters are responsible for the uptake of several drugs this could cause drug-herb/food interactions. Increasing the awareness of these interactions could help us to improve clinical outcomes and avoid unexpected toxicities of drug therapies in patients. Next, we studied the molecular mechanism by which drugs (Wnt inhibitors in Chapter 3), or natural compounds (PL in Chapter 4) affect the function and activity of transporters. The function and expression of OATs and OATPs are regulated by multiple signaling kinases, including protein kinase C and protein kinase A. The canonical Wnt/β-catenin signaling pathway regulates cell proliferation, differentiation, and morphology. In Chapter 3 we found that Wnt inhibitors modulated the expression and function of important OAT and OATP transporters. PRI-724 (newly developed Wnt inhibitor in clinical trials) decreased the substrate uptake by OAT4 and OATP2B1 with less pronounced decreases in OAT1, OAT3, and OAT1A2. Two other models of Wnt inhibitors - FH535 and 21H7 - were also tested in comparative studies, where they also strongly decreased the activities and membrane expression of multiple OATs/OATPs. Thus, implicating the Wnt signaling pathway in the regulation of the function and activity of OATPs and OATs. Piperlongumine (PL) is a natural compound traditionally used for the treatment of respiratory tract infectious diseases. Recently, PL is used in novel therapies for the treatment of different kinds of cancers. It was found that PL regulates several signaling pathways (e.g., AMP-activated protein kinase) that influence the function and activity of OATPs and OATs. Therefore, in Chapter 4 we studied the regulatory effect of PL on human organic anion transporting polypeptides (OATPs) and organic anion transporters (OATs). PL selectively increased the function of OATP2B1 and OAT4. The regulatory effect of PL is mediated through upregulating the cell surface expression of OATP2B1 and OAT4 and increasing the Vmax of both transporter proteins. Altered SLC transporter’s function may impact the pharmacokinetics and pharmacodynamics of drugs, drug treatment outcomes, unexpected toxicities, and/or drug-drug interactions. Overall, SLC transporters play a significant role in human health and disease. Studying SLCs and their molecular regulation will help us to improve the safety and efficacy of drugs as well as understanding several human diseases in which SLC transporters are involved.
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Quevedo, Camilo E. "Design and synthesis of Quinazolinone-based libraries for inhibitation of Kinase activity and hit-to-lead optimisation of Wnt pathway inhibitors." Thesis, Institute of Cancer Research (University Of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510367.

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Kragelund, Dominik [Verfasser]. "Untersuchungen der Serum-Konzentrationen des proinflammatorischen Glykoproteins wnt-5a und seines antiinflammatorischen Inhibitors sFRP-5 bei an Sepsis erkrankten Patienten im Verlauf / Dominik Kragelund." Kiel : Universitätsbibliothek Kiel, 2016. http://d-nb.info/111754060X/34.

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Park, Kyoungmin. "The characterization of PEDF's broad activity in the ocular disease." Oklahoma City : [s.n.], 2010.

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Ng, Chun-laam, and 吳圳嵐. "Wnt inhibitory factor 1 (Wif-1) coordinates Shh and Wnt signaling activities in urorectal development." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48329629.

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In vertebrates, the urogenital sinus and the hindgut are connected at a hollow region called cloaca. A midline mesenchymal structure known as urorectal septum (urs) descends from the ventral body wall to separate the urogenital sinus from the hindgut before the formation of an anal opening. Subsequent cloaca membrane regression at the ventral midline of the genital tubercle (GT) is crucial for the formation of an anal opening. These two events are important during cloaca septation in urorectal development. Mice with defective Shh or Wnt signaling displayed similar urorectal defects such as GT agenesis, un-partitioned cloaca (persistent cloaca) and proximal urethral opening that are attributable to increased cell apoptosis. Furthermore, Shh and Wnt signal transduction coordinate with each other and regulate cell survival of the developing urorectum. However, the molecular mechanisms by which these two signaling pathways coordinate in urorectal development remain unclear. We previously identified Wnt inhibitory factor1 (Wif1) from Affymetrix array analysis for genes/pathways that is implicated in urorectal development. Wif1 is a secreted protein that binds directly to Wnt ligands preventing Wnts from binding to receptors. This leads to -catenin degradation and thereby inhibits their activities. It is known that Wif1 binds to Wnt3a and Wnt5a with high affinity and deletion of Wnt3a, Wnt5a and -catenin in mice caused GT agenesis, persistent cloaca and proximal hypospadias. Using ETU-induced anorectal malformations model, I found out that Wif1 is ectopically expressed in the un-tubularized and un-septated urorectum. Wif1 is mainly expressed at the fusing endoderm that associates with programmed cell death during cloaca septation. Exogenous addition of Wif1 protein in urorectum culture also caused cloaca membrane disintegration, and proximal urethral opening that may be due to aberrant apoptosis. Shh and Wif1 are differentially expressed at the cloaca endoderm. In normal mice, Shh is highly expressed at the cloaca endoderm except those Wif1-expressing endodermal cells. Blockage of Shh pathway by cyclopamine in urorectum culture induced ectopic expression of Wif1, concomitant with genital tubercle hypoplasia and un-septated cloaca. More importantly, deletion of Shh in mice hastened Wif1 expression at the cloaca membrane endoderm and elicited increased cell death in the Wif1 expressing endoderm. Wif1-/- embryos display urorectal defects including delayed genital outgrowth and proximal hypospadias. Therefore, disruption of spatiotemporal expression of Wif1 could lead to defective Wnt signaling and contributes to abnormal urorectal development in Shh-/- mutant. Current study revealed that Wif1 is involved in urorectal development and is implicated in urorectal defects. It may function as a pro-apoptotic factor to regulate endodermal cell death which is essential for the septation process. Its specific expression is restricted at the midline cloaca endoderm by Shh signaling to inhibit local Wnt--catenin activities during cloaca septation. I proposed novel hypothetical models to explain (1) the significance of the tempo-spatial expression of Wif1; (2) the significance of cell death; and (3) the molecular mechanism that Shh signaling regulates Wnt signaling activities through Wif1 in urorectal development.
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Sena, Elena. "The Transcription Factor Barhl2 Inhibits Wnt Canonical Signaling during Xenopus Embryogenesis." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS090/document.

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Le développement embryonnaire est un processus hautement contrôlé où différentes voies de signalisation se coordonnent pour la construction d'un organisme. L'une des principales voies de signalisation impliquées dans ce processus est la voie canonique Wnt. La longue quête pour comprendre la cascade de signalisation Wnt/β-catenine a révélé que la réponse transcriptionelle induite par le signal Wnt/β-catenine est dépendante du contexte, ou compétence, cellulaire. Peu de choses sont connues sur les évènements moléculaires qui influencent cette compétence cellulaire. Dans les embryons de X. laevis Wnt/β-catenine est le signal inducteur pour l'Organisateur de Spemann. On ne sait pas ce qui limite l'activité Wnt dans ce territoire et par voie de conséquence la taille de l'Organisateur. Les résultats présentés dans ce manuscrit de thèse montrent que le facteur de transcription Barhl2 affecte le développement de l'organisateur de Spemann. Nous démontrons que Barhl2 inhibe l'activité Wnt via son interaction avec le corépresseur Groucho et le facteur de transcription Tcf, et mobilise l'activité de Hdac1 qui agit sur la structure chromatinienne. En utilisant des expériences in vitro et in vivo sur des cellules en culture et des embryons de Xénope nous démontrons que la régulation de Barhl2 sur les activités Groucho-Tcf est maintenue pendant l'embryogenèse et joue un rôle dans le confinement des progéniteurs neuraux dans le cerveau. Ensemble, nos résultats fournissent un mécanisme nouveau et important agissant sur le contrôle de l'activité transcriptionelle Wnt et la compétence des cellules à répondre à ce signal
Embryonic development is a highly controlled process where different signaling pathways participate into the elaboration of an organism. One of the main signaling pathways is the Wnt canonical pathway. The long-lasting search to understand Wnt/β-catenin transduction cascade revealed that the net transcriptional read out of Wnt/β-catenin signaling is highly dependent on the cellular context. In X. laevis embryos Wnt/β-catenin signaling is the informative signal for the Spemann Organizer induction. However little is known on what limits Wnt activity in this territory and consequently the size of the Spemann Organizer. The results presented in this manuscript provide evidence that the evolutionarily conserved transcription factor Barhl2 limits the development of the Spemann organizer. In this territory Barhl2 inhibits Wnt activity via its interaction with the co-repressor Groucho and the transcription factor Tcf. It participates to the recruitment of the chromatin remodeling enzyme, Hdac1 that represses the expression of Spemann organizer genes. Using a Xenopus tropicalis Tcf reporter line we demonstrate that Barhl2 inhibitory effect on Groucho-Tcf activities is maintained during embryogenesis and plays a role in the confinement of neural progenitors in the brain. Together, our results provide a new and important mechanism for the control of Wnt transcriptional activity
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Alsaedi, Manal. "The role of WNT inhibitory factor I in adipose tissue development." Thesis, Tennessee State University, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10158616.

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Fat tissue is involved in many aspects of biology such as appetite regulation, vascular diseases, diabetes, hypertension, and obesity. It plays an important role in these processes through its endocrine factors and other secretory products. Thus, there is a need to understand better the mechanisms and molecules that control the formation of adipocytes and the expansion of adipose tissue. WNT signaling is one of several important factors that plays a crucial role in development, and may also be important for adipogenesis. The activity of WNT signaling is modulated by a plethora of extracellular modulators that mostly antagonize WNT signaling. The extracellular WNT antagonists consist of four conserved families: Wnt-inhibitory factor 1 (WIF1), secreted frizzled related protein (SFRP), Cerberus, and Dickkopf (Dkk). It has been found that WIF1 is upregulated in abdominal fat tissue in chickens during early development. Thus, we hypothesize that WIF1 plays a role in adipose tissue development by inhibiting WNT signaling, and thereby stimulating adipogenic gene expression. The objective of this research is to examine the in vitro regulation of adipogenesis by WIF1. Mouse WIF1 expression vector (pCMV6-ENTRY-WIF1) was prepared, and used to transfect the mouse pre-adipocyte cell line 3T3-L1.The mRNA levels for WIF1, PPARγ and C/EBPα were then examined with real time RT-qPCR. Results indicate that the transgene was expressed in the transfected cells within 30 hours after transfection, and the mRNA level of WNT target genes and CEBPα were affected. However, the mRNA level of PPARγ was not affected. In conclusion, exogenous WIF1 was expressed in 3T3-L1 cells, at least at the mRNA level. The exogenous WIF1 expression caused an elevation of CEBPα mRNA. Future studies should examine other genes, and more investigation should take place to better understand the mechanisms of adipogenesis.

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Books on the topic "Wnt inhibitors"

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Nelson, Tammy. Getting the Sex You Want: Shed Your Inhibitions and Reach New Heights of Passion Together. Quayside, 2008.

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Getting the Sex You Want: Shed Your Inhibitions and Reach New Heights of Passion Together. Quayside, 2013.

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Book chapters on the topic "Wnt inhibitors"

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Bovolenta, Paola, Anne-Kathrin Gorny, Pilar Esteve, and Herbert Steinbeisser. "Secreted Wnt Inhibitors or Modulators." In Wnt Signaling in Development and Disease, 177–93. Hoboken, NJ, USA: John Wiley & Sons, Inc, 2014. http://dx.doi.org/10.1002/9781118444122.ch13.

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Edwards, Claire M., and Gregory R. Mundy. "Proteasome Inhibitors and the Wnt Signaling Pathway in Myeloma Bone Disease." In Myeloma Bone Disease, 211–29. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-554-5_12.

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Shan, Jufang, and Jie J. Zheng. "Virtual Ligand Screening Combined with NMR to Identify Dvl PDZ Domain Inhibitors Targeting the Wnt Signaling." In Rational Drug Design, 17–28. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-008-3_2.

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Tortolina, Lorenzo, Nicoletta Castagnino, Cristina De Ambrosi, Annalisa Barla, Alessandro Verri, Gabriele Zoppoli, Luca Bagnasco, et al. "Dynamic Simulations of Pathways Downstream of TGFβ, Wnt and EGF-Family Growth Factors, in Colorectal Cancer, including Mutations and Treatments with Onco-Protein Inhibitors." In New Challenges for Cancer Systems Biomedicine, 127–42. Milano: Springer Milan, 2012. http://dx.doi.org/10.1007/978-88-470-2571-4_7.

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Nemoto, Eiji, Yohei Koshikawa, Sousuke Kanaya, Masahiro Tsuchiya, Masato Tamura, Martha J. Somerman, and Hidetoshi Shimauchi. "Wnt signaling inhibits cementoblast differentiation." In Interface Oral Health Science 2009, 113–15. Tokyo: Springer Japan, 2010. http://dx.doi.org/10.1007/978-4-431-99644-6_16.

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Wolf, Vladimir, Yoshimi Endo, and Jeffrey S. Rubin. "Purification and Wnt-Inhibitory Activities of Secreted Frizzled-Related Proteins." In Methods in Molecular Biology, 31–44. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-249-6_3.

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Izumi, Kanji, Motoaki Yoshida, Takeshi Koja, Eisuke Munekata, Takao Nakanishi, and Takeo Fukuda. "Taurine Inhibits Wet-Dog Shakes and Hippocampal Seizures Induced by Opioid Peptides in Rats." In Advances in Experimental Medicine and Biology, 227–35. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4899-0405-8_24.

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Holsworth, Daniel D., and Stefan Krauss. "Recent Advances in Wnt/β-Catenin Pathway Small-Molecule Inhibitors." In Annual Reports in Medicinal Chemistry Volume 47, 393–409. Elsevier, 2012. http://dx.doi.org/10.1016/b978-0-12-396492-2.00026-6.

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Pulica, Rachael, Karine Cohen Solal, and Ahmed Lasfar. "Role of RUNX2 in Melanoma: A New Player in Tumor Progression and Resistance to Therapy." In Melanoma. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97105.

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RUNX2, a transcription factor, initially known for its indispensable role in skeletal development. RUNX2 is essential for osteoblast differentiation and the maintain of the osteocyte balance. RUNX2 acts directly on osteoblasts via Fgf pathway or on mesenchymal progenitors through Hedgehog, Wnt, Pthlh and DLX5. Currently, many reports point its critical role in the progression and metastasis of several cancer types. RUNX2 is involved in EMT process, invasion and metastasis through the modulation of important oncogenic pathways, including Wnt, FAK/PTK and AKT. In melanoma, RUNX2 is a key player in mediating intrinsic RTK-associated pro-oncogenic properties. We have showed a dramatic up regulation of RUNX2 expression with concomitant up-regulation of EGFR, IGF-1R and AXL, in melanoma cells rendered resistant to BRAF mutant inhibitors. Approximately half of melanomas carry BRAF mutations which enhance tumor invasion and metastasis. In this chapter, we describe the potential mechanisms, leading to the upregulation of RUNX2 in melanoma with BRAF mutations. We also highlight the critical role of PI3K/AKT in the expression and activation of RUNX2, and its consequences on the regulation of many critical factors, controlling cancer invasion and metastasis.
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Sivaprakasam, Prathibha, Sureshkumar Anandasadagopan, Tamilselvi Alagumuthu, and Ashok Kumar Pandurangan. "Current Update on Natural Agents Against Triple Negative Breast Cancer." In Advanced Pharmacological Uses of Medicinal Plants and Natural Products, 91–113. IGI Global, 2020. http://dx.doi.org/10.4018/978-1-7998-2094-9.ch005.

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Breast cancer (BC) is sub-categorized into several well-recognized subtypes including estrogen receptor (ER), progesterone receptor (PR), and HER2 triple-negative breast cancer (TNBC). It is a heterogeneous disease entity constituting about 15% of breast cancer cases worldwide. TNBC is associated with poor prognosis and lack of sustained response to conventional chemotherapeutic agents. Although no approved targeted therapy is available for TNBCs, molecular-profiling efforts have revealed promising molecular targets such as the Wnt/β-catenin, STAT3, VEGF, EGFR, polyadenosine ribose polymerase inhibitors (PARPi) and DNA repair pathway, androgen pathway, and NOTCH pathway. Moreover, more research needs to be performed in the area of TNBC aiming at dissecting potential pathways and identifying potential molecular signatures to develop new targeted biologic modifiers. Natural agents are the abundant chemical compounds available from diverse plants. The authors aimed to summarize the current evidence and discuss the natural agents that target TNBC using different pathways.
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Conference papers on the topic "Wnt inhibitors"

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Pan, Shifeng, Jun Liu, Dai Cheng, Dong Han, Guobao Zhang, Mindy Hsieh, Nicholas Ng, et al. "Abstract IA35: Discovery of porcupine inhibitors targeting Wnt signaling in cancer." In Abstracts: Fourth AACR International Conference on Frontiers in Basic Cancer Research; October 23-26, 2015; Philadelphia, PA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.fbcr15-ia35.

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Tilley, Ann E., Rui Wang, Rachel K. Zwick, Yael Strulovici-Barel, and Ronald G. Crystal. "Inhibitors Of The Wnt Pathway In Human Airway Epithelial Basal Cells." 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.a6758.

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Cho, Joon-Ho, Manjari Dimri, and Goberdhan P. Dimri. "Abstract 1794: Cross-regulation of polycomb group protein BMI1 and WNT inhibitors." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1794.

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Zhan, T., G. Ambrosi, AM Wandmacher, B. Rauscher, J. Betge, N. Rindtorff, RS Häussler, et al. "MEK inhibitors activate Wnt signalling and induce stem cell plasticity in colorectal cancer." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695401.

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Low, Joo-Leng, Weina Du, Tenzin Gocha, Oguz Gokce, Xiaoqian Zhang, Daniel G. Yim, Adaikalavan Ramasamy, Hao Fan, and Ramanuj DasGupta. "Abstract 509: Discovery of novel small molecule inhibitors of Wnt signaling throughin silicomolecular docking." 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.am2020-509.

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Ross, Jenny, Timothy Hoey, Ann Kapoun, John Lewicki, Austin Gurney, and Christopher L. Murriel. "Abstract 1733: Wnt antagonists synergize with immune checkpoint inhibitors to enhance anti-tumor responses." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1733.

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Madan, Babita, Zhiyuan Ke, Shermaine Q. y. Lim, Jenefer Alam, Soo Yei Ho, Duraiswamy A. Jeyaraj, Kakaly Ghosh, et al. "Abstract C248: Novel PORCN inhibitors are safe and effective in the treatment of WNT-dependent cancers." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-c248.

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Dowling, James E. "Abstract B47: Potent and selective CK2 kinase inhibitors with effects on Wnt pathway signaling in vivo." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-b47.

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Lin, Hsiao-Hui, Wen-Chi Feng, LI-Chun Lu, Ta-Wen Hsu, Ann-Lii Cheng, and Chih-Hung Hsu. "Abstract 2625: Increased sensitivity to Wnt/beta-catenin inhibitors in hepatocellular carcinoma cells harboring activating mutation of beta-catenin." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2625.

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Uno, Yuko, Hideki Moriyama, Shigeki Kashimoto, Yusuke Kawase, Miki Shitashige, Masaaki Sawa, and Tesshi Yamada. "Abstract B265: Targeting Wnt signaling: Discovery and characterization of novel thiazole-based Traf2- and NCK-interacting kinase (TNIK) inhibitors." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-b265.

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Reports on the topic "Wnt inhibitors"

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Robling, Alexander G. Secreted Wnt Signaling Inhibitors in Disuse-Induced Bone Loss. Fort Belvoir, VA: Defense Technical Information Center, July 2014. http://dx.doi.org/10.21236/ada613318.

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Zi, Xiaolin, Noriko Yokoyama, and Blair Christopher. Cotargeting VEGF and Neuropilins With Bevacizumab and Secreted Wnt Inhibitors in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada592130.

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