Relevant bibliographies by topics / Bcatenin pathway

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'Bcatenin pathway'

Author: Grafiati
Published: 1 April 2023
Last updated: 31 July 2025

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Journal articles on the topic "Bcatenin pathway"

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Huang, Weiqi, Elizabeth Horvath, and Elizabeth A. Eklund. "Bcr/Abl Increases Bcatenin Protein and Activity in An ICSBP-Dependent Manner in Myeloid Cells." Blood 114, no. 22 (2009): 2958. http://dx.doi.org/10.1182/blood.v114.22.2958.2958.

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Abstract Abstract 2958 Poster Board II-934 The interferon consensus sequence binding protein (ICSBP) is an interferon regulatory transcription factor (also referred to as IRF8). Similar to other IRF proteins, ICSBP regulates transcription of genes involved in the inflammatory response. However, ICSBP also functions as a myeloid leukemia tumor suppressor. Specifically, decreased ICSBP expression in myeloid progenitor cells results in cytokine hypersensitivity and resistance to apoptosis in response to Fas-activation or IL3 withdrawal. Consistent with function as a tumor suppressor, decreased IC
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Chalamalasetty, Ravindra B., William C. Dunty,, Kristin K. Biris, et al. "The Wnt/bcatenin target, Mesogenin1 (Msgn1), directly regulates the Notch pathway during mammalian somitogensis." Developmental Biology 356, no. 1 (2011): 259. http://dx.doi.org/10.1016/j.ydbio.2011.05.493.

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Fuchs, Quentin, Stephanie Legras, Benoit Lhermitte, et al. "DIPG-30. HIF2 OVEREXPRESSION DICTATES AGGRESSIVENESS ADDITIONALLY TO TP53 MUTATIONS IN H3.3K27M PEDIATRIC HIGH-GRADE GLIOMAS THROUGH RAS-MAPK AND WNT/BCATENIN PATHWAYS." Neuro-Oncology 25, Supplement_1 (2023): i19—i20. http://dx.doi.org/10.1093/neuonc/noad073.077.

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Abstract Diffuse midline (DMG) and brainstem (DIPG) high-grade gliomas (HGG) bearing H3.3K27M driver mutation are aggressive and uncurable brain tumors. We evidenced by the past HIF-2a and its transcriptional gene, EPAS1, as a marker of resistance when targeting mTor/HIF-1a pathway. To understand HIF-2α potential role in chronically active hypoxic environment in DIPG/DMG, we investigate its status in a cohort of pediatric HGGs comprising notably H3.3K27M mutant tumors and in their paired in vitro derived models. Using concomitantly the low-input chromatin immunoprecipitation sequencing method
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Obrador-Hevia, A., F. Chin, S. Gonzalez, et al. "Wnt signaling somatic alterations in apc-associated fap adenomas." Journal of Clinical Oncology 27, no. 15_suppl (2009): e22046-e22046. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e22046.

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e22046 Background: APC mutations are believed to constitutively activate the wnt pathway in colorectal tumors. Our goal was to comprehensively characterize Wnt signaling components in a set of APC-associated FAP tumors both at the DNA and RNA levels. Methods: Sixty adenomas from FAP cases harboring pathogenic APC mutations were included (10 adenomas and 1 normal mucosa per case). Somatic APC and KRAS alterations, β-catenin immunostaining and qRT-PCR of APC, MYC, AXIN2 and SFRP1 were analyzed. aCGH was also assessed in 26 FAP adenomas and 24 additional paired normal-adenoma-carcinoma samples. R
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Chung, Jihyun, Vrajesh Karkhanis, Said Sif та Robert A. Baiocchi. "Protein Arginine Methyltransferase 5 Supports MYC, Survivin and Cyclin D1 Activity in Aggressive Lymphomas By Regulating the WNT/β-Catenin Pathway". Blood 124, № 21 (2014): 58. http://dx.doi.org/10.1182/blood.v124.21.58.58.

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Abstract Introduction: Aggressive histologic subtypes of lymphoma such as mantle cell (MCL) and activated B cell (ABC) are considered incurable and affected patients often have a short median survival despite multimodal therapy. It is well established that altered expression of oncogenes and epigenetic dysregulation of tumor suppressor and regulatory genes promote cellular transformation of normal B cells into malignant lymphoma. Hypermethylation of histone proteins (H3R8 and H4R3) by the protein arginine methyltransferase 5 (PRMT5) enzyme has been documented in multiple cancer types and has b
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Teofili, Luciana, Maurizio Martini, Eugenia Rosa Nuzzolo, et al. "Defective WNT Signaling and Genetic Profile Of Endothelial Cells In Patients With Low Risk Myelodysplastic Syndromes Suggest a Contribution Of Vascular Niches To Myelodysplasia." Blood 122, no. 21 (2013): 860. http://dx.doi.org/10.1182/blood.v122.21.860.860.

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Abstract Endothelial cells are relevant to normal hematopoiesis. Vascular niches within the bone marrow allow hematopoietic stem cell proliferation and differentiation. In vivo, the contemporary administration of endothelial progenitor cells in BALB/c mice fosters the homing of transplanted hematopoietic cells (Salter et al. Blood 2009; 113:2104). In vitro, the differentiation of CD34+ progenitors is facilitated by the presence of an underlying confluent layer of endothelial colony forming cells (ECFCs Ingram et al. Blood. 2004;104: 2752), even though this effect is highly dependent from the p
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Sharifi, Sajjad, Shima Mehrabadi, Farzad Rahmani та ін. "PNU-74654 Enhanced the Antiproliferative Activity of Gemcitabine by Targeting Wnt/β-Catenin Pathway in Pancreatic Cancer". Clinical Cancer Drugs 11 (21 жовтня 2024). http://dx.doi.org/10.2174/012212697x293676240916114229.

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Background: The Wnt/beta-catenin pathway is one of the pathways that is deregulated in pancreatic cancer and is reported to be associated with a poor prognosis. This indicates the need for the identification of novel agents to improve the efficacy of current therapy or have an improved efficacy. Therefore, in the present study, we explored the anticancer activity of PNU- 74654 alone or in combination with gemcitabine in 2 and 3-dimensional cell culture models of pancreatic cancer. Methods: The MTT assay was carried out to determine the viability of PC cancerous cells (PCCs), while the cytotoxi
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Dissertations / Theses on the topic "Bcatenin pathway"

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COSTA, ALICE. "Dissecting the role of G9a/GLP histone methyltransferases in Platinum-resistant ovarian cancer." Doctoral thesis, Università degli Studi di Trieste, 2021. http://hdl.handle.net/11368/2988156.

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Epithelial Ovarian Cancer (EOC) is the most aggressive gynecological malignancy, mainly due to the advanced stage at diagnosis and the development of drug-resistant recurrences. Epigenetic modifications, such as histone methylation/acetylation, are emerging as key regulators of tumor growth and response to therapies. To verify if they are also involved in the onset of drug re-sistance in EOC, we performed a high-throughput Epigenetic Modifiers (EMs)-based screening using four different models of EOC isogenic Platinum-Resistant (PT-Res) cells. The screening identified G9a/GLP histone methyltran
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