Thematische Bibliographien / Lymphomas leukemia Histone deacetylase

Inhaltsverzeichnis

  1. Zeitschriftenartikel
  2. Dissertationen
  3. Bücher
  4. Buchteile
  5. Konferenzberichte
  6. Berichte der Organisationen

Auswahl der wissenschaftlichen Literatur zum Thema „Lymphomas leukemia Histone deacetylase“

Autor: Grafiati
Veröffentlicht am 4. Juni 2021
Zuletzt aktualisiert am 16. Februar 2022

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Zeitschriftenartikel zum Thema "Lymphomas leukemia Histone deacetylase"

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Richter-Larrea, Jose A., Eloy F. Robles, Vicente Fresquet, et al. "Reversion of epigenetically mediated BIM silencing overcomes chemoresistance in Burkitt lymphoma." Blood 116, no. 14 (2010): 2531–42. http://dx.doi.org/10.1182/blood-2010-02-268003.

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AbstractIn Burkitt lymphoma/leukemia (BL), achievement of complete remission with first-line chemotherapy remains a challenging issue, as most patients who respond remain disease-free, whereas those refractory have few options of being rescued with salvage therapies. The mechanisms underlying BL chemoresistance and how it can be circumvented remain undetermined. We previously reported the frequent inactivation of the proapoptotic BIM gene in B-cell lymphomas. Here we show that BIM epigenetic silencing by concurrent promoter hypermethylation and deacetylation occurs frequently in primary BL sam
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Lane, Andrew A., and Bruce A. Chabner. "Histone Deacetylase Inhibitors in Cancer Therapy." Journal of Clinical Oncology 27, no. 32 (2009): 5459–68. http://dx.doi.org/10.1200/jco.2009.22.1291.

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PurposeEpigenetic processes are implicated in cancer causation and progression. The acetylation status of histones regulates access of transcription factors to DNA and influences levels of gene expression. Histone deacetylase (HDAC) activity diminishes acetylation of histones, causing compaction of the DNA/histone complex. This compaction blocks gene transcription and inhibits differentiation, providing a rationale for developing HDAC inhibitors.MethodsIn this review, we explore the biology of the HDAC enzymes, summarize the pharmacologic properties of HDAC inhibitors, and examine results of s
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Chen, Jing, Meili Zhang, Wei Ju, and Thomas A. Waldmann. "Effective treatment of a murine model of adult T-cell leukemia using depsipeptide and its combination with unmodified daclizumab directed toward CD25." Blood 113, no. 6 (2009): 1287–93. http://dx.doi.org/10.1182/blood-2008-04-149658.

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Abstract Adult T-cell leukemia (ATL) is caused by human T-cell lymphotropic virus I (HTLV-1) and is an aggressive malignancy of CD4, CD25-expressing leukemia, and lymphoma cells. There is no accepted curative therapy for ATL. Depsipeptide, a histone deacetylase inhibitor, has demonstrated major antitumor effects in leukemias and lymphomas. In this study, we investigated the therapeutic efficacy of depsipeptide alone and in combination with daclizumab (humanized anti-Tac) in a murine model of human ATL. The Met-1 ATL model was established by intraperitoneal injection of ex vivo leukemic cells i
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Rodd, Annabelle L., Katherine Ververis, and Tom C. Karagiannis. "Current and Emerging Therapeutics for Cutaneous T-Cell Lymphoma: Histone Deacetylase Inhibitors." Lymphoma 2012 (August 16, 2012): 1–10. http://dx.doi.org/10.1155/2012/290685.

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Cutaneous T-cell lymphoma is a term that encompasses a spectrum of non-Hodgkin’s T-cell lymphomas with primary manifestations in the skin. It describes a heterogeneous group of neoplasms that are characterised by an accumulation of malignant T cells of the CD4 phenotype that have the propensity to home and accumulate in the skin, lymph nodes, and peripheral blood. The two most common variants of cutaneous T-cell lymphoma include mycosis fungoides and the leukemic variant, the Sézary syndrome. While numerous treatments are available for cutaneous T-cell lymphoma and have shown to have success i
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Kitadate, Akihiro, Sho Ikeda, Fumito Abe, et al. "Histone Deacetylase Inhibitors Downregulate CCR4 Expression and Decrease Mogamulizumab Efficacy in CCR4-Positive Mature T-Cell Lymphomas." Blood 130, Suppl_1 (2017): 720. http://dx.doi.org/10.1182/blood.v130.suppl_1.720.720.

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Abstract Background: Histone deacetylase inhibitors (HDACis) are promising agents for various T-cell lymphomas, including cutaneous T-cell lymphoma (CTCL), peripheral T-cell lymphoma (PTCL), and adult T-cell lymphoma/leukemia (ATLL). CCR4 is an important therapeutic target molecule because mogamulizumab, an anti-CCR4 antibody, has shown promising efficacy against CTCL, PTCL, and ATLL. However, their combined effects and interactions have not been examined thus far. We previously showed that CCR6, a chemokine receptor, is overexpressed in cutaneous T-cell lymphomas (Ito et al., 2014 Blood). Mor
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Richter, Jose A., Antonio Rullan, Elena Beltran, et al. "Epigenetic Silencing of BIM Mediates Chemotherapy Resistance of Patients with Burkitt Lymphoma That Can Be Overcome by Therapeutic Reactivation of BIM in Mouse and Human Lymphoma Models." Blood 112, no. 11 (2008): 607. http://dx.doi.org/10.1182/blood.v112.11.607.607.

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Abstract The most critical challenge in Burkitt lymphoma is to achieve complete remission (CR) with initial high-dose chemotherapy, as most of these patients will be eventually cured. However, those not achieving CR usually die early after diagnosis. Thus, to identify the refractory cases and how to overcome initial therapeutic resistance remain unsolved issues. We have previously reported that the gene encoding the pro-apoptotic BH3-only protein Bim is frequently inactivated by genetic and epigenetic mechanisms that substantially vary among the different B-cell lymphoma subgroups. Further scr
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Buggy, Joseph, Sriram Balasubramanian, Jason Ramos, Mint Sirisawad, and Louie Naumovski. "Histone Deacetylase Inhibitor, PCI-24781, Induces Growth Inhibition and Apoptosis in Hematopoietic Tumor-Derived Cell Lines and Primary Leukemia Cells." Blood 108, no. 11 (2006): 4399. http://dx.doi.org/10.1182/blood.v108.11.4399.4399.

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Abstract Histone deacetylase (HDAC) inhibitors are a new class of anticancer drugs that have shown promising activity in clinical trials. PCI-24781 (formerly CRA-024781) is a novel, hydroxamic acid-based HDAC inhibitor that is currently under evaluation in phase I clinical trials in patients with refractory solid malignancies and lymphomas. In this study, we show that PCI-24781 inhibits growth and induces apoptosis in a variety of hematopoietic cell lines derived from B-, T- and myeloid malignancies. Growth inhibition and apoptosis were noted at drug concentrations < 0.125 μM and were a
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Bieszczad, Bartosz, Damian Garbicz, Marta Świtalska, et al. "Improved HDAC Inhibition, Stronger Cytotoxic Effect and Higher Selectivity against Leukemias and Lymphomas of Novel, Tricyclic Vorinostat Analogues." Pharmaceuticals 14, no. 9 (2021): 851. http://dx.doi.org/10.3390/ph14090851.

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Histone deacetylase (HDAC) inhibitors are a class of drugs used in the cancer treatment. Here, we developed a library of 19 analogues of Vorinostat, an HDAC inhibitor used in lymphomas treatment. In Vorinostat, we replaced the hydrophobic phenyl group with various tricyclic ‘caps’ possessing a central, eight-membered, heterocyclic ring, and investigated the HDAC activity and cytotoxic effect on the cancer and normal cell lines. We found that 3 out of the 19 compounds, based on dibenzo[b,f]azocin-6(5H)-one, 11,12-dihydrodibenzo[b,f]azocin-6(5H)-one, and benzo[b]naphtho[2,3-f][1,5]diazocine-6,14
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Zhang, Qiting, Ziyan Wang, Xinyuan Chen, et al. "8a, a New Acridine Antiproliferative and Pro-Apoptotic Agent Targeting HDAC1/DNMT1." International Journal of Molecular Sciences 22, no. 11 (2021): 5516. http://dx.doi.org/10.3390/ijms22115516.

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Epigenetic therapy using histone deacetylase (HDAC) inhibitors has become an attractive project in new drug development. However, DNA methylation and histone acetylation are important epigenetic ways to regulate the occurrence and development of leukemia. Given previous studies, N-(2-aminophenyl)benzamide acridine (8a), as a histone deacetylase 1 (HDAC1) inhibitor, induces apoptosis and shows significant anti-proliferative activity against histiocytic lymphoma U937 cells. HDAC1 plays a role in the nucleus, which we confirmed by finding that 8a entered the nucleus. Subsequently, we verified tha
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Perez-Salvia, Montserrat, Aldaba Eneko, Vara Yosu, et al. "Efficacy of a New Small-Molecule Inhibitor of Histone Deacetylase 6 (HDAC6) in Preclinical Models of B-Cell Lymphoma and Acute Myeloid Leukemia." Blood 132, Supplement 1 (2018): 5383. http://dx.doi.org/10.1182/blood-2018-99-111578.

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Abstract Histone deacetylase 6 (HDAC6) is a protein modifier that is an increasingly attractive pharmacological target. Interestingly, the observation that the HDAC6 knock-out mouse is not lethal, in contrast to those undergoing complete loss of class I, II and III HDACs, suggests that specific HDAC6 inhibitors may be better tolerated than pan-HDAC inhibitors or drugs that target the other HDAC classes. In this regard, the compound ACY-1215 (Rocilinostat), the described selective HDAC6 inhibitors, is undergoing clinical trials for the treatment of multiple myeloma. Taking into account the prev
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Dissertationen zum Thema "Lymphomas leukemia Histone deacetylase"

1

Kam, Kevin. "Therapeutic potential of demethylation agents and histone deaceytlase inhibitors in NK-cell lymphoma and leukemia /." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38657922.

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Kam, Kevin, and 甘季燐. "Therapeutic potential of demethylation agents and histone deaceytlase inhibitors in NK-cell lymphoma and leukemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B45011564.

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Petruccelli, Luca. "Histone deacetylase inhibitors induce reactive oxygen species and DNA damage, and display enhanced activity in DNA repair deficient acute myeloid leukemia expressing leukemia associated fusion proteins." Thesis, McGill University, 2014. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=121176.

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Histone deacetylase inhibitors (HDI) have shown promising antitumor activity in preclinical and clinical studies for a broad range of hematological and solid malignancies. Nonetheless, the percentage of patients in any given malignancy who experience a meaningful clinical response remains small. While initial studies with HDIs focused on utilizing these agents to re-sensitize leukemic cells to differentiating stimuli, recent studies have shown HDIs to display significant cytotoxic activity in malignant cells by a number of different mechanisms. One proposed mechanism is the accumulation of DNA
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Qi, Huiling. "Modulation of Folate Receptor Beta for Drug Targeting in Acute Myelogenous Leukemia." University of Toledo Health Science Campus / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=mco1147304406.

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Borutinskaite, Veronika Viktorija. "Characterization of proteins involved in differentiation and apoptosis of human leukemia and epithelial cancer cells." Doctoral thesis, Linköpings universitet, Klinisk mikrobiologi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-11741.

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Today, cancer is understood as an epigenetic as well as a genetic disease. The main epigenetic hallmarks of the cancer cell are DNA methylation and histone modifications. The latter changes may be an optimal target for novel anticancer agents. The main goal of using histone deacetylase inhibitors (HDACIs) would be restoration of gene expression of those tumor-suppressor genes that have been transcriptionally silenced by promoter-associated histone deacetylation. However, HDACIs have pleiotropic effects that we are only just starting to understand. These may also be responsible for the inductio
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Lin, Hsiu-Pen, and 林秀盆. "Characterization of the Histone Deacetylase Inhibitor (Valproic Acid) on the Growth, Apoptosis and Differentiation of Acute Myeloid Leukemia." Thesis, 2004. http://ndltd.ncl.edu.tw/handle/09494105893442684201.

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碩士<br>臺北醫學大學<br>醫學技術學系<br>93<br>Abstract Epigenetic control of gene expression plays an important role in hematopoiesis and leukemogenesis. One of the major components in epigenetic regulation of gene expression is histone acetylation.Recent studies have shown that histone deacetylase inhibitors (HDACIs) might be useful for treating hematopoietic malignancies. However the effects of these HDACIs on human acute myeloid leukemia (AML) have not been studied comprehensively. In this study, we examined the effects of several clinically available HDACIs on the proliferation, differentiati
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Trus, Michael. "Altering retinoid sensitivity in acute myeloblastic leukemia cells by treatment with the histone deacetylase inhibitor, valproic acid, and the inhibitor of DNA methyltransferase activity, 5-aza-2'-deoxycytidine /." 2006. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=442548&T=F.

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Bücher zum Thema "Lymphomas leukemia Histone deacetylase"

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Trus, Michael. Altering retinoid sensitivity in acute myeloblastic leukemia cells by treatment with the histone deacetylase inhibitor, valproic acid, and the inhibitor of DNA methyltransferase activity, 5-aza-2'-deoxycytidine. 2006.

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Buchteile zum Thema "Lymphomas leukemia Histone deacetylase"

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Kalac, Matko, and Owen A. O’Connor. "The Emerging Role of Histone Deacetylase Inhibitors in the Treatment of Lymphoma." In Innovative Leukemia and Lymphoma Therapy. CRC Press, 2019. http://dx.doi.org/10.1201/9780429114670-10.

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Konferenzberichte zum Thema "Lymphomas leukemia Histone deacetylase"

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Villanueva, Lorea, Montserrat Perez-Salvia, Eneko Aldaba, et al. "Abstract 4725: Efficacy of a new small-molecule inhibitor of histone deacetylase 6 (HDAC6) in preclinical models of B-cell lymphoma and acute myeloid leukemia." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4725.

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Villanueva, Lorea, Montserrat Perez-Salvia, Eneko Aldaba, et al. "Abstract 4725: Efficacy of a new small-molecule inhibitor of histone deacetylase 6 (HDAC6) in preclinical models of B-cell lymphoma and acute myeloid leukemia." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4725.

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Sahakian, Eva, Kamira Maharaj, John Powers, et al. "Abstract 4485: Regulation of chronic lymphocytic leukemia (CLL) immunobiology by histone deacetylase 6 (HDAC6)." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4485.

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Wang, Xiaoguang, Brittany C. Waschke, Rachel A. Woolaver, et al. "Abstract PO-54: Mechanistic consequences of histone-deacetylase inhibition towards sensitizing PD1 blockade-resistant B-cell lymphomas." In Abstracts: AACR Virtual Meeting: Advances in Malignant Lymphoma; August 17-19, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2643-3249.lymphoma20-po-54.

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Petruccelli, Luca A., Filippa Pettersson, Daphne Dupere‐Richer, Kim L. Rice, Jonathan D. Licht, and Wilson H. Miller. "Abstract A189: Expression of fusion proteins in acute myeloid leukemia cells increases sensitivity to histone deacetylase inhibitors." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-a189.

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Petruccelli, Luca A., Kim L. Rice, Filippa Pettersson, et al. "Abstract 2136: Expression of fusion proteins in acute myeloid leukemia cells increases sensitivity to histone deacetylase inhibitors." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2136.

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Mensah, Afua A., Eugenio Gaudio, Ivo Kwee, et al. "Abstract A129: Novel histone deacetylase inhibitors ITF-A and ITF-B exhibit efficacy in preclinical models of mature B-cell lymphomas." 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-a129.

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Matthews, Geoffrey M., Leonie Cluse, Eric Wang, et al. "Abstract 5533: RNAi-mediated depletion of histone deacetylases highlights the potential for isoform-specific inhibitors in B-cell lymphoma and acute myeloid leukemia." 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.am2014-5533.

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Kane, Shriya, Jonathon L. Payne, Mario Soliman, et al. "Abstract 1513: Epigenetic regulation of CD117 expression in B-cell acute lymphoblastic leukemia by Ikaros and histone deacetylase HDAC1." 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.am2018-1513.

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Maharaj, Kamira, John Powers, Alex Achille, Eva Sahakian, and Javier Pinilla-Ibarz. "Abstract 4723: Combinatorial efficacy of anti-PD1 treatment and selective histone deacetylase 6 (HDAC6) inhibition in chronic lymphocytic leukemia (CLL)." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4723.

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Berichte der Organisationen zum Thema "Lymphomas leukemia Histone deacetylase"

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Bhalla, Kapil. Combinations of Novel Histone Deacetylase and Bcr-Abl Inhibitors in the Therapy of Imatinib Mesylate-Sensitive and Refractory Bcr-Abl Expressing Leukemia. Defense Technical Information Center, 2007. http://dx.doi.org/10.21236/ada484223.

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Bhalla, Kapil. Combinations of Novel Histone Deacetylase and Bcr-Abl Inhibitors in the Therapy of Imatinib Mesylate-Sensitive and -Refractory Bcr-Abl Expressing Leukemia. Defense Technical Information Center, 2008. http://dx.doi.org/10.21236/ada517391.

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