Log in

Relevant bibliographies by topics / OTX015 / Journal articles

To see the other types of publications on this topic, follow the link: OTX015.

Journal articles on the topic 'OTX015'

Author: Grafiati

Published: 4 June 2021

Last updated: 27 April 2022

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

Select a source type:

Consult the top 50 journal articles for your research on the topic 'OTX015.'

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.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

11

Boi, Michela, Paola Bonetti, Maurilio Ponzoni, et al. "The Brd-Inhibitor OTX015 Shows Pre-Clinical Activity in Anaplastic Large T-Cell Lymphoma (ALCL)." Blood 120, no. 21 (2012): 4872. http://dx.doi.org/10.1182/blood.v120.21.4872.4872.

Full text

Abstract:

Abstract Abstract 4872 Background: ALCL, is clinically/biologically heterogeneous disease, including ALK+ and ALK- systemic forms. Despite the progresses in understanding the molecular pathogenesis of ALCL, the therapy is still based on chemotherapy, thus the identification of new treatment modalities is needed. Bromodomain-containing proteins are components of transcription factors complexes and determinants of epigenetic memory. Inhibitors of BRD2/3/4, members of the Bromodomain and Extraterminal (BET) family, have recently shown antitumor activity in different hematological malignancies mod

APA, Harvard, Vancouver, ISO, and other styles

12

Servidei, Tiziana, Daniela Meco, Maurizio Martini, et al. "The BET Inhibitor OTX015 Exhibits In Vitro and In Vivo Antitumor Activity in Pediatric Ependymoma Stem Cell Models." International Journal of Molecular Sciences 22, no. 4 (2021): 1877. http://dx.doi.org/10.3390/ijms22041877.

Full text

Abstract:

Childhood ependymomas are heterogenous chemoresistant neoplasms arising from aberrant stem-like cells. Epigenome deregulation plays a pivotal role in ependymoma pathogenesis, suggesting that epigenetic modifiers hold therapeutic promise against this disease. Bromodomain and extraterminal domain (BET) proteins are epigenome readers of acetylated signals in histones and coactivators for oncogenic and stemness-related transcriptional networks, including MYC/MYCN (Proto-Oncogene, BHLH Transcritpion Factor)-regulated genes. We explored BET inhibition as an anticancer strategy in a panel of pediatri

APA, Harvard, Vancouver, ISO, and other styles

13

Balaji, Narayanan, Ramesh Mullangi, and A. Siva Kumar. "Development and Validation of a Chiral Liquid Chromatographic Method for Quantitative Determination of (+)-OTX015 in (−)-OTX015." Chromatographia 79, no. 19-20 (2016): 1317–23. http://dx.doi.org/10.1007/s10337-016-3138-5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Odore, Elodie, François Lokiec, Sophie Weill, et al. "Development and validation of an UPLC-MS/MS method for quantitative analysis of OTX015 in human plasma samples." Anal. Methods 6, no. 22 (2014): 9108–15. http://dx.doi.org/10.1039/c4ay02249a.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Su, Angela, Frank Ling, Camille Vaganay, et al. "The Folate Cycle Enzyme MTHFR Is a Critical Regulator of Cell Response to MYC-Targeting Therapies." Blood 134, Supplement_1 (2019): 877. http://dx.doi.org/10.1182/blood-2019-131255.

Full text

Abstract:

Metabolic rewiring of neoplastic cells engenders metabolic liabilities that can be exploited to design innovative therapeutic strategies, including those to increase the therapeutic index of existing anticancer therapies. We hypothesized that metabolic perturbation may substantially influence cell response to therapies targeting major oncogenes which are involved in active hijacking of neoplastic cell metabolism. In that regard, MYC represents a paradigmatic oncogene as this transcription factor is deregulated in more than 50% of human cancers and reprograms many aspect of cell metabolism. MYC

APA, Harvard, Vancouver, ISO, and other styles

16

Shi, Jixiang, Sha Song, Huiying Han, et al. "Potent Activity of the Bromodomain Inhibitor OTX015 in Multiple Myeloma." Molecular Pharmaceutics 15, no. 9 (2018): 4139–47. http://dx.doi.org/10.1021/acs.molpharmaceut.8b00554.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Wu, X., S. Yu, Z. Shi, M. Huynh, J. Chong, and S. T. Hwang. "693 BET inhibitor OTX015 reduces imiquimod-induced mouse psoriasiform dermatitis." Journal of Investigative Dermatology 139, no. 5 (2019): S119. http://dx.doi.org/10.1016/j.jid.2019.03.769.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Balaji, Narayanan, Murugan Chinnapattu, Abhishek Dixit, Promod Sahu, Suresh P S, and Ramesh Mullangi. "Validation of an enantioselective LC-MS/MS method to quantify enantiomers of (±)-OTX015 in mice plasma: Lack ofin vivoinversion of (−)-OTX015 to its antipode." Biomedical Chromatography 31, no. 4 (2016): e3853. http://dx.doi.org/10.1002/bmc.3853.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Thieblemont, Catherine, Anastasios Stathis, Giorgio Inghirami, et al. "A Phase 1 Study of the BET-Bromodomain Inhibitor OTX015 in Patients with Non-Leukemic Hematologic Malignancies." Blood 124, no. 21 (2014): 4417. http://dx.doi.org/10.1182/blood.v124.21.4417.4417.

Full text

Abstract:

Abstract Rationale: BET-bromodomain (BRD) proteins are DNA readers that bind acetylated histone (H) tails preferentially at hyperacetylated superenhancer promoter regions and trigger gene transcription. The expression of several oncogenes, including c-MYC, is epigenetically regulated by BRD. OTX015 is a BRD 2, 3 and 4 inhibitor that prevents BRD binding to acetylated H4 and downregulates gene expression of BRD-dependent genes. OTX015 has been shown to inhibit the growth of diffuse large B-cell lymphoma (DLBCL) cells in vitroand in animal models. Patients & Methods: Patients with non-leukem

APA, Harvard, Vancouver, ISO, and other styles

20

Saenz, Dyana T., Warren Fiskus, Kanak Raina, et al. "Superior Lethal Activity of Novel BET Protein Proteolysis Targeting Chimera (BETP-PROTACs) Versus Betp Bromodomain Inhibitor (BETi) Against Post-Myeloproliferative Neoplasm (MPN) Secondary (s) AML Cells." Blood 128, no. 22 (2016): 747. http://dx.doi.org/10.1182/blood.v128.22.747.747.

Full text

Abstract:

Abstract Hematopoietic stem/progenitor cells (HPCs) of BCR-ABL1-negative myeloproliferative neoplasms with myelofibrosis (MPN-MF) exhibit mutations in JAK2, c-MPL, or calreticulin (CALR) gene and display constitutive activation of JAK-STAT signaling. In MPN-MF, transformation to AML (sAML) occurs in up to 20% of patients. Ruxolitinib (R) is a type I, ATP-competitive, JAK1 & 2 inhibitor (JAKi), which is currently used in the therapy of MPN-MF. Treatment with R confers notable clinical benefit in MPN-MF, but exhibits only modest activity and does not significantly impact the clinical outcome

APA, Harvard, Vancouver, ISO, and other styles

21

Gu, Jie, Sha Song, Huiying Han, et al. "The BET Bromodomain Inhibitor OTX015 Synergizes with Targeted Agents in Multiple Myeloma." Molecular Pharmaceutics 15, no. 11 (2018): 5387–96. http://dx.doi.org/10.1021/acs.molpharmaceut.8b00880.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Dombret, Hervé, Claude Preudhomme, Céline Berthon, et al. "A Phase 1 Study of the BET-Bromodomain Inhibitor OTX015 in Patients with Advanced Acute Leukemia." Blood 124, no. 21 (2014): 117. http://dx.doi.org/10.1182/blood.v124.21.117.117.

Full text

Abstract:

Abstract Rationale: BET-bromodomain (BRD) proteins play a major role in the epigenetic regulation of gene transcription, notably of genes with superenhancer promoter regions including many oncogenes, such as MYC. OTX015 is a specific BRD 2, 3 and 4 inhibitor that blocks oncogene transcription, and triggers growth inhibition and apoptosis in acute leukemia cell lines and patient cells in vitro (Braun et al. ASH Annual Meeting 2013). Based on these findings, a Phase 1 study of OTX015 was designed for patients with advanced acute leukemia. Patients & Methods: Patients with various unselected

APA, Harvard, Vancouver, ISO, and other styles

23

Miliara, Sophia, Bogumil Kaczkowski, Takahiro Suzuki, et al. "Single-Cell Analysis of the Transcriptional Response in AML Patients Treated with BET-Inhibitors." Blood 132, Supplement 1 (2018): 5120. http://dx.doi.org/10.1182/blood-2018-99-117849.

Full text

Abstract:

Abstract Acute Myeloid Leukemia (AML) is the most common myeloid leukemia in adults. Although substantial progress has been made in recent years, the long-term prognosis for patients remains poor which is mainly due to the dated treatments that consist of cytotoxic drugs with low specificity. AML is a clonal disease with multiple co-existing clones in each patient. Often, patients that initially respond to treatment may develop resistance due to lingering leukemic stem cells (LSC), or sub-clones that survive the treatment and cause a relapse. Therefore, novel therapeutic strategies are needed

APA, Harvard, Vancouver, ISO, and other styles

24

Berthon, Céline, Emmanuel Raffoux, Xavier Thomas, et al. "Bromodomain inhibitor OTX015 in patients with acute leukaemia: a dose-escalation, phase 1 study." Lancet Haematology 3, no. 4 (2016): e186-e195. http://dx.doi.org/10.1016/s2352-3026(15)00247-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Ocana, Alberto, Veronica Corrales-Sanchez, Javier Perez Peña, et al. "Anti-proliferative activity of bromodomain inhibitors JQ1 and OTX015 in triple negative breast cancer." Journal of Clinical Oncology 33, no. 15_suppl (2015): e12078-e12078. http://dx.doi.org/10.1200/jco.2015.33.15_suppl.e12078.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Hu, Xiao, Lauren P. Schewitz-Bowers, Philippa J. P. Lait, et al. "The Bromodomain and Extra-Terminal Protein Inhibitor OTX015 Suppresses T Helper Cell Proliferation and Differentiation." Current Molecular Medicine 18, no. 9 (2019): 594–601. http://dx.doi.org/10.2174/1566524019666190126112238.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Coudé, Marie-Magdelaine, Thorsten Braun, Jeannig Berrou, et al. "BET inhibitor OTX015 targets BRD2 and BRD4 and decreases c-MYC in acute leukemia cells." Oncotarget 6, no. 19 (2015): 17698–712. http://dx.doi.org/10.18632/oncotarget.4131.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Sun, Baohua, Warren Fiskus, Liang Zhang, et al. "Novel BET Protein Proteolysis Targeting Chimeras (BETP-PROTACs) Exert Potent Single Agent and Synergistic Activity with Ibrutinib and Venetoclax Against Human Mantle Cell Lymphoma Cells." Blood 128, no. 22 (2016): 1058. http://dx.doi.org/10.1182/blood.v128.22.1058.1058.

Full text

Abstract:

Abstract Mantle Cell Lymphoma (MCL) exhibits pathogenetic mutations or deletion of RB1, ATM, p53, deletion of INK4a/ARF, as well as copy number gains of MYC, CDK4 and BCL2. Activated B cell receptor (BCR) signaling, and the ensuing downstream pro-growth and pro-survival NFkB activity, is also a notable feature of MCL. Collectively, the genetic alterations and the ensuing deregulated signaling and activity of transcription factors, including c-MYC and NFkB, creates the MCL-specific 'transcriptome' that promotes growth and survival of MCL cells. Ibrutinib, a covalent inhibitor of Bruton's tyrosi

APA, Harvard, Vancouver, ISO, and other styles

29

Fiskus, Warren, Christopher Peter Mill, Vrajesh Karkhanis, et al. "Pre-Clinical Efficacy of Co-Treatment with KDM1A (LSD1) Inhibitor and Ruxolitinib or BET Inhibitor Against Post-MPN-sAML Blast Progenitor Cells." Blood 134, Supplement_1 (2019): 1274. http://dx.doi.org/10.1182/blood-2019-130783.

Full text

Abstract:

LSD1 (KDM1A) is an FAD-dependent amine-oxidase that demethylates mono and dimethyl histone H3 lysine 4 (H3K4Me1 and H3K4Me2), which regulates active enhancers and transcription in AML stem/progenitor cells (LSCs). LSD1 is part of the repressor complexes involving HDACs, CoREST or GFI1, mediating transcriptional repression and differentiation block in LSCs that persist in the minimal residual disease (MRD) following attainment of clinical complete remission, leading to relapse and poor outcome in AML. In AML LSCs, genetic alterations and epigenetic dysregulation of enhancers affect levels of my

APA, Harvard, Vancouver, ISO, and other styles

30

Bonetti, P., M. Ponzoni, M. G. Tibiletti, et al. "528 The BRD-inhibitor OTX015 Shows Pre-clinical Activity in Diffuse Large B-cell Lymphoma (DLBCL)." European Journal of Cancer 48 (November 2012): 163. http://dx.doi.org/10.1016/s0959-8049(12)72325-0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Odore, Elodie, François Lokiec, Esteban Cvitkovic, et al. "Phase I Population Pharmacokinetic Assessment of the Oral Bromodomain Inhibitor OTX015 in Patients with Haematologic Malignancies." Clinical Pharmacokinetics 55, no. 3 (2015): 397–405. http://dx.doi.org/10.1007/s40262-015-0327-6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Dinardo, Courtney Denton, Christopher P. Mill, Warren Fiskus, et al. "Clinical observations of AML expressing mutant RUNX1 and pre-clinical studies of RUNX1-targeted novel therapy of AML." Journal of Clinical Oncology 35, no. 15_suppl (2017): 7030. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.7030.

Full text

Abstract:

7030 Background: Runt-related transcription factor 1 ( RUNX1) is critically involved in normal and malignant hematopoiesis. Somatic mutations in RUNX1 occur in ~10% of AML, especially in older patients with history of radiation or antecedent hematologic disorder. Presence of mRUNX1 is reported to confer relative resistance to therapy and poorer prognosis in AML, and there are no mRUNX1-targeted or specific therapies available. Methods: We retrospectively analyzed outcomes of 94 mRUNX1 and 444 wild-type RUNX1 AML patients treated at our institution from 9/2013 to 12/2016. We also determined the

APA, Harvard, Vancouver, ISO, and other styles

33

Gaudio, Eugenio, Chiara Tarantelli, Maurilio Ponzoni, et al. "Bromodomain inhibitor OTX015 (MK-8628) combined with targeted agents shows strong in vivo antitumor activity in lymphoma." Oncotarget 7, no. 36 (2016): 58142–47. http://dx.doi.org/10.18632/oncotarget.10983.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Ouafik, L., C. Berenguer, M. Cayol, et al. "469 OTX015, a novel BET-bromodomain (BET-BRD) inhibitor, is a promising anticancer agent for human glioblastoma." European Journal of Cancer 50 (November 2014): 153. http://dx.doi.org/10.1016/s0959-8049(14)70595-7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

Stathis, Anastasios, Emanuele Zucca, Mohamed Bekradda, et al. "Clinical Response of Carcinomas Harboring the BRD4–NUT Oncoprotein to the Targeted Bromodomain Inhibitor OTX015/MK-8628." Cancer Discovery 6, no. 5 (2016): 492–500. http://dx.doi.org/10.1158/2159-8290.cd-15-1335.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

Vázquez, Ramiro, Simonetta Andrea Licandro, Lucile Astorgues-Xerri, et al. "Promising in vivo efficacy of the BET bromodomain inhibitor OTX015/MK-8628 in malignant pleural mesothelioma xenografts." International Journal of Cancer 140, no. 1 (2016): 197–207. http://dx.doi.org/10.1002/ijc.30412.

Full text

APA, Harvard, Vancouver, ISO, and other styles

37

Ijaz, N., L. Astorgues-Xerri, E. Odore, et al. "565 Preclinical evaluation of OTX015, a novel BET-BRD inhibitor, on small cell lung cancer (SCLC) cell lines." European Journal of Cancer 50 (November 2014): 183. http://dx.doi.org/10.1016/s0959-8049(14)70691-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Birdwell, Christine, Warren C. Fiskus, Christopher Peter Mill та ін. "Pre-Clinical Efficacy of Targeting TBL1/R-β-Catenin-TCF7L2 Axis Against AML with 3q26 Lesions and EVI1 Overexpression". Blood 138, Supplement 1 (2021): 3349. http://dx.doi.org/10.1182/blood-2021-154285.

Full text

Abstract:

Abstract EVI1 gene maps to the MECOM locus at chromosome 3q26.2 and encodes for a zinc finger domain-containing transcriptional regulator. EVI1 supports hematopoietic stem cell self-renewal and blocks hematopoietic differentiation. EVI1 is overexpressed in up to 10% of AML, including those harboring chromosome translocation t(3;3)(q21;q26.2) or inv(3)(q21;q26.2), where the distal GATA2 hematopoietic enhancer is repositioned to induce EVI1 overexpression while repressing GATA2. EVI1 overexpression due to 3q26.2 lesions in MDS and AML is frequently associated with monosomy 7 and confers poor res

APA, Harvard, Vancouver, ISO, and other styles

39

Wang, Zezhou, Peter Dove, Aisha Shamas-Din, et al. "The Highly Potent Bromodomain (BRD) Inhibitor FV-281 Displays Preclinical Efficacy in Acute Myeloid Leukemia (AML)." Blood 126, no. 23 (2015): 1364. http://dx.doi.org/10.1182/blood.v126.23.1364.1364.

Full text

Abstract:

Abstract Recent studies have demonstrated the therapeutic potential of targeting BRD2, BRD3 and BRD4 in hematological malignancies including AML. Here, we report a novel orally bioavailable BRD inhibitor, FV-281, that displays preclinical efficacy in AML in vitro and in vivo. In a binding screen assay of 32 bromodomains (BromoScanTM), FV-281 selectively bound BRD2, BRD3 and BRD4 with Kd values of 2.7 to 7.3 nM and was 2-5 fold more potent than the leading bromodomain inhibitor, OTX015. In AML cell lines (OCI-AML2, Tex, HL-60 and MV4-11), FV-281 reduced cell growth and viability after 72 hour i

APA, Harvard, Vancouver, ISO, and other styles

40

Boi, Michela, Eugenio Gaudio, Paola Bonetti, et al. "The BET Bromodomain Inhibitor OTX015 Affects Pathogenetic Pathways in Preclinical B-cell Tumor Models and Synergizes with Targeted Drugs." Clinical Cancer Research 21, no. 7 (2015): 1628–38. http://dx.doi.org/10.1158/1078-0432.ccr-14-1561.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Amorim, Sandy, Anastasios Stathis, Mary Gleeson, et al. "Bromodomain inhibitor OTX015 in patients with lymphoma or multiple myeloma: a dose-escalation, open-label, pharmacokinetic, phase 1 study." Lancet Haematology 3, no. 4 (2016): e196-e204. http://dx.doi.org/10.1016/s2352-3026(16)00021-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Mensah, Afua, Luciano Cascione, Eugenio Gaudio, et al. "The BET Bromodomain Inhibitor (BETi) OTX015 (MK-8628) Upregulates miR-96-5p in Diffuse Large B-Cell Lymphomas (DLBCL)." Clinical Lymphoma Myeloma and Leukemia 16 (September 2016): S105. http://dx.doi.org/10.1016/j.clml.2016.07.151.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Djamai, Hanane, Jeannig Berrou, Mélanie Dupont, et al. "Biological Effects of BET Inhibition by OTX015 (MK-8628) and JQ1 in NPM1-Mutated (NPM1c) Acute Myeloid Leukemia (AML)." Biomedicines 9, no. 11 (2021): 1704. http://dx.doi.org/10.3390/biomedicines9111704.

Full text

Abstract:

BET inhibitors (BETi) including OTX015 (MK-8628) and JQ1 demonstrated antileukemic activity including NPM1c AML cells. Nevertheless, the biological consequences of BETi in NPM1c AML were not fully investigated. Even if of better prognosis AML patients with NPM1c may relapse and treatment remains difficult. Differentiation-based therapy by all trans retinoic acid (ATRA) combined with arsenic trioxide (ATO) demonstrated activity in NPM1c AML. We found that BETi, similar to ATO + ATRA, induced differentiation and apoptosis which was TP53 independent in the NPM1c cell line OCI-AML3 and primary cel

APA, Harvard, Vancouver, ISO, and other styles

44

Zhang, Xiaohui, Jing Lu, Yimin Qian, and Robert Z. Orlowski. "Proteolytic Targeting Chimeric Molecules (PROTACs) Specific for Bromodomain-Containing Protein (BRD) 4 Are Active Against Pre-Clinical Models of Multiple Myeloma." Blood 126, no. 23 (2015): 917. http://dx.doi.org/10.1182/blood.v126.23.917.917.

Full text

Abstract:

Abstract Background: BRD4, a bromodomain and extraterminal domain (BET) family member, has an important role in modulating the expression of essential oncogenes such as c-MYC, and is emerged as a promising therapeutic target in diverse cancer types. Pharmacologic BET inhibitors in development such as JQ1 and OTX015 display preclinical anti-myeloma activity, and induce preferential loss of BRD4 bound to super-enhancers leading to transcriptional repression of c-MYC. Another approach to target this pathway is through the use of bi-functional molecules, which incorporate a small molecule BRD4 bin

APA, Harvard, Vancouver, ISO, and other styles

45

Karkhanis, Vrajesh, Warren Fiskus, Christopher Peter Mill, et al. "Efficacy of Targeted Therapy in Novel Pre-Clinical in Vitro and In Vivo Models of Richter Transformation-Diffuse Large B-Cell Lymphoma (RT-DLBCL)." Blood 134, Supplement_1 (2019): 3961. http://dx.doi.org/10.1182/blood-2019-132041.

Full text

Abstract:

Richter Transformation (RT) is defined as the development of aggressive DLBCL (mostly ABC-type) in up to ~15% of patients with antecedent or concurrent diagnosis of CLL. Based on the comparison of immunoglobin gene rearrangements, approximately 80% of RT-DLBCL arise due to a direct clonal evolution of the underlying CLL clone, i.e., clonally related (CLR) RT-DLBCL, which exhibit poor median survival (MS) of one year. Approximately 20% of RT-DLBCLs are clonally unrelated (CUR) to the underlying CLL, arising most likely due to branched clonal evolution from a common pre-CLL progenitor. CUR RT-DL

APA, Harvard, Vancouver, ISO, and other styles

46

Fiskus, Warren, Christopher Peter Mill, Bernardo H. Lara, et al. "BET Protein Antagonist-Based Therapy of Novel Models of Richter Transformation-Diffuse Large B-Cell Lymphoma (RT-DLBCL)." Blood 136, Supplement 1 (2020): 17–18. http://dx.doi.org/10.1182/blood-2020-138637.

Full text

Abstract:

Richter Transformation (RT) is the development of aggressive DLBCL (mostly ABC sub-type) in up to ~15% of patients with antecedent CLL. Approximately 80% of RT-DLBCLs are clonally-related (CLR) to the underlying CLL, with a median survival (MS) of one year. Alternatively, ~20% of RT-DLBCLs are clonally-unrelated (CLUR) to the underlying CLL, exhibiting a better MS of 5 years. Chemo-immunotherapy, or monotherapy with the Bruton's tyrosine kinase (BTK) inhibitor ibrutinib, anti-apoptotic BCL2 inhibitor venetoclax or with anti-PD1 therapy fails to achieve prolonged disease-free survival, with a m

APA, Harvard, Vancouver, ISO, and other styles

47

Tarantelli, Chiara, Elena Bernasconi, Eugenio Gaudio, et al. "BET bromodomain inhibitor birabresib in mantle cell lymphoma: in vivo activity and identification of novel combinations to overcome adaptive resistance." ESMO Open 3, no. 6 (2018): e000387. http://dx.doi.org/10.1136/esmoopen-2018-000387.

Full text

Abstract:

BackgroundThe outcome of patients affected by mantle cell lymphoma (MCL) has improved in recent years, but there is still a need for novel treatment strategies for these patients. Human cancers, including MCL, present recurrent alterations in genes that encode transcription machinery proteins and of proteins involved in regulating chromatin structure, providing the rationale to pharmacologically target epigenetic proteins. The Bromodomain and Extra Terminal domain (BET) family proteins act as transcriptional regulators of key signalling pathways including those sustaining cell viability. Birab

APA, Harvard, Vancouver, ISO, and other styles

48

Odore, E., L. Astorgues-Xerri, M. Bekradda, et al. "587 Cellular pharmacokinetics and molecular pharmacodynamics studies of the BRD-BET inhibitor OTX015 in sensitive and resistant leukemic cell lines." European Journal of Cancer 50 (November 2014): 189. http://dx.doi.org/10.1016/s0959-8049(14)70713-0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Herait, P., H. Dombret, C. Thieblemont, et al. "BET-bromodomain (BRD) inhibitor OTX015: Final results of the dose-finding part of a phase I study in hematologic malignancies." Annals of Oncology 26 (March 2015): ii10. http://dx.doi.org/10.1093/annonc/mdv085.3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Astorgues-Xerri, Lucile, Ramiro Vázquez, Elodie Odore, et al. "Insights into the cellular pharmacological properties of the BET-inhibitor OTX015/MK-8628 (birabresib), alone and in combination, in leukemia models." Leukemia & Lymphoma 60, no. 12 (2019): 3067–70. http://dx.doi.org/10.1080/10428194.2019.1617860.

Full text

APA, Harvard, Vancouver, ISO, and other styles

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!