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Relevant bibliographies by topics / OTX015

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Journal articles

Academic literature on the topic 'OTX015'

Author: Grafiati

Published: 4 June 2021

Last updated: 27 April 2022

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Journal articles on the topic "OTX015"

1

Bonetti, Paola, Michela Boi, Maurilio Ponzoni, et al. "The Brd-Inhibitor OTX015 Is Active in Pre-Clinical Models of Mature B-Cell Lymphoid Tumors." Blood 120, no. 21 (2012): 1657. http://dx.doi.org/10.1182/blood.v120.21.1657.1657.

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Abstract Abstract 1657 Background: Bromodomain-containing proteins play an important role in gene expression regulation, via chromatin structure remodelling. Antitumor activity has been reported in acute and chronic hematological malignancies using inhibitors of BRD2/3/4, members of the Bromodomain and Extraterminal (BET) family. Here, we report anti-proliferative activity of OTX015, a novel selective orally bioavailable BRD2/3/4 inhibitor, in a large panel of cell lines derived from mature B-cell lymphoid tumors. Material and Methods: Established human cell lines derived from 13 diffuse large

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2

Coudé, Marie-Magdelaine, Thorsten Braun, Jeannig Berrou, et al. "Bromodomain Inhibition By OTX015 Regulates c-MYC and HEXIM1 in a Panel of Human Acute Leukemia Cell Lines." Blood 124, no. 21 (2014): 5957. http://dx.doi.org/10.1182/blood.v124.21.5957.5957.

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Abstract Background: The bromodomain-containing protein 4 (BRD4) activates the transcription elongation factor b (P-TEFb) which regulates RNA polymerase II. Conversely, hexamethylene bisacetamide (HMBA) inducible protein 1 (HEXIM1) inactivates P-TEFb. BRD4/HEXIM1 interplay influences cell cycle progression and tumorigenesis. It has been widely demonstrated that BRD4 knockdown or inhibition by JQ1 is associated with c-MYC downregulation and antileukemic activity. We recently reported that the small molecule BRD2/3/4 inhibitor OTX015 (Oncoethix, Lausanne, Switzerland), currently in clinical deve

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3

Roulin, Louise, Ashfaq Ali, Aline Masse, et al. "Activity of OTX015 (MK-8628), a BET-Bromodomain Inhibitor, in Acute Myeloid Leukemia (AML) Progenitor Cells." Blood 126, no. 23 (2015): 2588. http://dx.doi.org/10.1182/blood.v126.23.2588.2588.

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Abstract CONTEXT: Eradication of leukemic progenitor cells, defined by functional assays such as long-term culture (leukemic long-term culture initiating cells [L-LTC-IC]) is the goal of therapy in AML. Bromodomain and ExtraTerminal (BET) proteins are epigenetic readers that regulate the expression of genes with super-enhancers, including CMYC. BET inhibitors (BETi) such as JQ1 induce proliferation arrest and apoptosis in murine models of AML, in human AML cell lines and primary blasts. Their activity in human leukemic progenitors has not yet been reported. OTX015 (MK-8626) is an orally availa

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4

Bernasconi, Elena, Chiara Tarantelli, Eugenio Gaudio, et al. "The BET-Bromodomain Inhibitor OTX015 Is Active As a Single Agent and in Combination with Other Targeted Drugs in Preclinical Models of Mantle Cell Lymphoma." Blood 124, no. 21 (2014): 3113. http://dx.doi.org/10.1182/blood.v124.21.3113.3113.

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Abstract Background. Mantle cell lymphoma (MCL), which is characterized by the deregulation of cyclin D1 (CCND1), is one of the most common lymphoma subtypes, accounting for 5-10% of all cases. MCL prognosis is often very poor. Several novel non-chemotherapeutic agents have shown promising activity in MCL, but novel agents and in particular new drug combinations are needed to improve patients' outcome. Aberrant changes in histone modifications, DNA methylation and expression levels of non-coding RNA contribute to MCL pathogenesis and represent potential therapeutic targets. Bromodomain and ext

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5

Riveiro, Maria Eugenia, Lucile Astorgues-Xerri, Charlotte Canet-jourdan, et al. "Preclinical Evaluation of the BET-Bromodomain (BET-BRD) Inhibitor OTX015 in Leukemia Cell Lines Harboring the JAK2 V617F Mutation." Blood 124, no. 21 (2014): 873. http://dx.doi.org/10.1182/blood.v124.21.873.873.

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Abstract Background: Exposure of cancer cells to BET-BRD protein inhibitors has been associated with a significant downregulation of C-MYC expression, leading to suppression of the transcriptional program linked to proliferation and survival. C-MYC mRNA expression, mediated by STAT5 activation, is induced by the JAK2 (V617F) mutation (JAK2mu) in transfected BA/F3 cells (Funakoshi-Tago, et al. 2013). We selected JAK2mu leukemia-derived cell lines for preclinical evaluation of OTX015 (Oncoethix, Switzerland), a selective orally-bioavailable inhibitor of BET-BRD proteins with promising early resu

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6

Gaudio, Eugenio, Ivo Kwee, Andrea Rinaldi, et al. "Genetic Factors Predicting The Response To BET Bromodomain Inhibitors In Lymphoma Lead To New Synergistic Combinations." Blood 122, no. 21 (2013): 3070. http://dx.doi.org/10.1182/blood.v122.21.3070.3070.

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Abstract Epigenome deregulation in cancer cells affects transcription of oncogenes and tumor suppressor genes. BET Bromodomain proteins recognize chromatin modifications and act as epigenetic readers contributing to gene transcription. BET Bromodomain inhibitors showed promising pre-clinical activity in hematological and solid tumors and are currently in phase I studies. The mechanism of action and relevant affected genes are not fully characterized and there are no established response predictors. We have shown activity of BET Bromodomain OTX015 in lymphoma cell lines (ASH 2012; ICML 2013). T

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7

Megiorni, Francesca, Simona Camero, Paola Pontecorvi, et al. "OTX015 Epi-Drug Exerts Antitumor Effects in Ovarian Cancer Cells by Blocking GNL3-Mediated Radioresistance Mechanisms: Cellular, Molecular and Computational Evidence." Cancers 13, no. 7 (2021): 1519. http://dx.doi.org/10.3390/cancers13071519.

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Ovarian cancer (OC) is the most aggressive gynecological tumor worldwide and, notwithstanding the increment in conventional treatments, many resistance mechanisms arise, this leading to cure failure and patient death. So, the use of novel adjuvant drugs able to counteract these pathways is urgently needed to improve patient overall survival. A growing interest is focused on epigenetic drugs for cancer therapy, such as Bromodomain and Extra-Terminal motif inhibitors (BETi). Here, we investigate the antitumor effects of OTX015, a novel BETi, as a single agent or in combination with ionizing radi

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8

Cascione, Luciano, Eugenio Gaudio, Elena Bernasconi, et al. "BET Bromodomain Inhibitor OTX015 Affects the Expression of Micrornas Involved in the Pathogenesis of Diffuse Large B-Cell Lymphoma." Blood 124, no. 21 (2014): 4495. http://dx.doi.org/10.1182/blood.v124.21.4495.4495.

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Abstract Background. Diffuse large B-cell lymphoma (DLBCL) is the most common lymphoma, accounting for 30%-40% of all cases. Despite a major improvement in the cure rate, a large number of DLBCL patients lack therapeutic options. Aberrant changes in histone modifications, DNA methylation and expression levels of non-coding RNA, including microRNA (miRNA), contribute to DLBCL pathogenesis and represent potential therapeutic targets. OTX015 targets bromodomain and extra-terminal (BET) proteins, which are epigenetic readers contributing to gene transcription. It has shown preclinical activity in

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9

Gaudio, Eugenio, Luciano Cascione, Maurilio Ponzoni, et al. "The BET Inhibitor OTX015 (MK-8628) Shows in Vivo Antitumor Activity in Combination with Additional Targeted Agents in Diffuse Large B-Cell Lymphoma (DLBCL)." Blood 126, no. 23 (2015): 5119. http://dx.doi.org/10.1182/blood.v126.23.5119.5119.

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Abstract OTX015 (MK-8628) has shown anti-lymphoma activity in both the preclinical and clinical settings (Boi et al, CCR 2015; Stathis et al, EORT-NCI-AACR 2014). Here we report in vivo data on OTX015 in combination with four targeted compounds in DLBCL. Methods. NOD-Scid (NOD.CB17-Prkdcscid/NCrHsd) mice were subcutaneously engrafted with the activated B-cell like DLBCL cell line SUDHL2 (15 x106 cells) and then divided into 10 groups (6 mice each). Treatment with OTX015 was started 3 days after the graft, and treatments with other drugs were initiated when mice developed palpable tumors (100 m

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10

Braun, Thorsten, marie Magdelaine Coude, Jeannig Berrou, et al. "Preclinical Study Of The Bromodomain Inhibitor OTX015 In Acute Myeloid (AML) and Lymphoid (ALL) Leukemias." Blood 122, no. 21 (2013): 4218. http://dx.doi.org/10.1182/blood.v122.21.4218.4218.

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Abstract Background Bromodomain and extra-terminal (BET) proteins, including the ubiquitous BRD2/3/4 proteins, are epigenetic readers implicated in c-MYC transcription, cellular proliferation, cell-cycle progression, RNA elongation and DNA damage response. Using shRNA screening and BRD inhibitors, BRD4 has been established as a promising therapeutic target in acute leukemia (Zuber, Nature 2011). In the present study, we investigated the in vitro anti-leukemic effects of the small-molecule BRD2/3/4 inhibitor OTX015 (Oncoethix, Lausanne, Switzerland). Methods Expression of BRD2/3/4 and c-MYC was

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