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Thematische Bibliographien / Lymphomas leukemia Histone deacetylase / Zeitschriftenartikel

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Zeitschriftenartikel zum Thema „Lymphomas leukemia Histone deacetylase“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 16. Februar 2022

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1

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 &lt; 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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Garcia-Manero, Guillermo, Hui Yang, Carlos Bueso-Ramos, et al. "Phase 1 study of the histone deacetylase inhibitor vorinostat (suberoylanilide hydroxamic acid [SAHA]) in patients with advanced leukemias and myelodysplastic syndromes." Blood 111, no. 3 (2008): 1060–66. http://dx.doi.org/10.1182/blood-2007-06-098061.

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AbstractVorinostat (suberoylanilide hydroxamic acid, SAHA) is a histone deacetylase inhibitor active clinically in cutaneous T-cell lymphoma and preclinically in leukemia. A phase 1 study was conducted to evaluate the safety and activity of oral vorinostat 100 to 300 mg twice or thrice daily for 14 days followed by 1-week rest. Patients with relapsed or refractory leukemias or myelodysplastic syndromes (MDS) and untreated patients who were not candidates for chemotherapy were eligible. Of 41 patients, 31 had acute myeloid leukemia (AML), 4 chronic lymphocytic leukemia, 3 MDS, 2 acute lymphobla

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Chevallier, Nathalie, Connie M. Corcoran, Christine Lennon, et al. "ETO protein of t(8;21) AML is a corepressor for Bcl-6 B-cell lymphoma oncoprotein." Blood 103, no. 4 (2004): 1454–63. http://dx.doi.org/10.1182/blood-2003-06-2081.

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Abstract The multiplicity of transcription factors involved in hematologic malignancies suggests a complicated scenario in which many different molecular mechanisms lead to malignant transformation. We hypothesized that some of these proteins might physically and functionally interact and thus mechanistically link different diseases. The ETO protein of t(8;21) acute myeloid leukemia (AML) is an excellent candidate as a common factor because it is normally expressed in human hematopoietic cells, it binds to histone deacetylases (HDACs), and it interacts with the PLZF protein of t(11;17) acute p

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Okabe, Seiichi, Testuzo Tauchi, Akihiro Nakajima, et al. "Analysis of Histone Deacetylase Inhibitor, FK228, Effect on Chronic Myelogenous Leukemia Cell Line." Blood 104, no. 11 (2004): 4675. http://dx.doi.org/10.1182/blood.v104.11.4675.4675.

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Abstract Chronic myelogenous leukemia (CML) results from transformation of hematopoietic cells by the BCR/ABL gene. Although high rates of hematologic responses to imatinib therapy, the acquired resistance to imatinib has been recognized as a major problem in the treatment of CML Histone deacetylases (HDACs) and histone acetyltransferases (HATs) regulate gene expression and cell growth. Recently, HDAC inhibitors have known as a new class of anti-cancer drugs. One of the HDAC inhibitor, FK228 (FR901228, depsipeptide) is now doing the clinical trial for the treatment of patients, such as periphe

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Kozako, Tomohiro, Makoto Yoshimitsu, Yohann White, et al. "Overexpression of SIRT1, a Longevity Gene-Encoded Protein, and Induction of Apoptosis by Its Inhibition In Adult T-Cell Leukemia Cells." Blood 116, no. 21 (2010): 2768. http://dx.doi.org/10.1182/blood.v116.21.2768.2768.

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Abstract Abstract 2768 Adult T-cell leukemia-lymphoma (ATL) is an aggressive peripheral T-cell neoplasm developing after a long-term infection with human T-cell leukemia virus (HTLV-1), in which NF-kB is also implicated as an exacerbation factor. Despite recent progress in both chemotherapy and supportive care for hematological malignancies, the prognosis of ATL is still poor; overall survival at 3 years is only 24%. New strategies for the therapy and prophylaxis of ATL (e.g., vaccines and novel molecular target agents) are still required. SIRT1, an NAD+-dependent histone/protein deacetylase,

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Mori, Naoki, Takehiro Matsuda, Masayuki Tadano, et al. "Apoptosis Induced by the Histone Deacetylase Inhibitor FR901228 in Human T-Cell Leukemia Virus Type 1-Infected T-Cell Lines and Primary Adult T-Cell Leukemia Cells." Journal of Virology 78, no. 9 (2004): 4582–90. http://dx.doi.org/10.1128/jvi.78.9.4582-4590.2004.

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ABSTRACT Inhibition of histone deacetylase (HDAC) activity induces growth arrest, differentiation, and, in certain cell types, apoptosis. FR901228, FK228, or depsipeptide, is an HDAC inhibitor effective in T-cell lymphomas. Adult T-cell leukemia (ATL) is caused by human T-cell leukemia virus type 1 (HTLV-1) and remains incurable. We examined whether FR901228 is effective for treatment of ATL by assessing its ability to induce apoptosis of HTLV-1-infected T-cell lines and primary leukemic cells from ATL patients. FR901228 induced apoptosis of Tax-expressing and -unexpressing HTLV-1-infected T-c

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Cea, Michele, Antonia Cagnetta, Floriana Fruscione, et al. "Deacetylase Inhibitor Cocktails Provide Striking Synergistic Interactions in Human Leukemia Cells." Blood 114, no. 22 (2009): 4404. http://dx.doi.org/10.1182/blood.v114.22.4404.4404.

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Abstract Abstract 4404 Cancer cells almost invariably exhibit aberrant histone deacetylase (HDAC) activity leading to changes in chromatine structure, altered gene expression, poor differentiation, impaired apoptosis and increased proliferation. Accordingly, virtually all the HDAC inhibitors currently available show some degree of antitumor activity in preclinical cancer models and several of these compounds are currently under investigation or already approved for the treatment of human malignancies. Such is the case of the hydroxamic acid derivative suberoylanilide hydroxamic acid (Vorinosta

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South, Gina, Jessica Haladyna, Kirk Hansen, and Kathrin M. Bernt. "Histone Profiling in Leukemia Using LC-MS/MS." Blood 124, no. 21 (2014): 2202. http://dx.doi.org/10.1182/blood.v124.21.2202.2202.

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Abstract It has become increasingly evident that epigenetic changes, including aberrant histone modifications, play a crucial role in malignant transformation and may contribute to relapsed and refractory disease. There are over 160 known histone modifications, most of which remain poorly explored. Post-translational histone modifications (PTMs) have been shown to be altered in hematologic malignancies, and the protein network that regulates these PTMs offers potential therapeutic opportunities through pharmacologic inhibition. Prominent examples include aberrant histone acetylation in multipl

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Okabe, Seiichi, Tetsuzo Tauchi, Eishi Ashihara, Shinya Kimura, Taira Maekawa, and Kazuma Ohyashiki. "Activity of the Histone Deacetylase Inhibitor, Vorinostat, Against BCR-ABL Positive Leukemia Cells with Random Mutagenesis and In Combination with Nilotinib." Blood 116, no. 21 (2010): 4460. http://dx.doi.org/10.1182/blood.v116.21.4460.4460.

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Abstract Abstract 4460 The clinical use of imatinib, a specific BCR-ABL tyrosine kinase inhibitor (TKI) is effective in inducing a complete hematological and cytogenetic remission in a high percentage of chronic myeloid leukemia (CML) and Philadelphia chromosome (Ph) positive acute lymphoblastic leukemia (ALL) patients. However, imatinib does not efficiently kill leukemic stem cells and is limited by the emergence of resistance due to the point mutations in the BCR-ABL kinase domain. Histone acetyltransferases (HAT) and histone deacetylases (HDAC) control the acetylation of histones and intrac

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Reyes-Garau, Ribeiro, and Roué. "Pharmacological Targeting of BET Bromodomain Proteins in Acute Myeloid Leukemia and Malignant Lymphomas: From Molecular Characterization to Clinical Applications." Cancers 11, no. 10 (2019): 1483. http://dx.doi.org/10.3390/cancers11101483.

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Alterations in protein-protein and DNA-protein interactions and abnormal chromatin remodeling are a major cause of uncontrolled gene transcription and constitutive activation of critical signaling pathways in cancer cells. Multiple epigenetic regulators are known to be deregulated in several hematologic neoplasms, by somatic mutation, amplification, or deletion, allowing the identification of specific epigenetic signatures, but at the same time providing new therapeutic opportunities. While these vulnerabilities have been traditionally addressed by hypomethylating agents or histone deacetylase

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Marchi, Enrica, Danielle C. Bongero, Matko Kalac, Luigi Scotto, and Owen A. O'Connor. "The Combination of Histone Deacetylase Inhibitors and Hypomethylating Agents Exhibits Marked Synergy In Preclinical Models of T-Cell Lymphoma." Blood 116, no. 21 (2010): 3937. http://dx.doi.org/10.1182/blood.v116.21.3937.3937.

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Abstract Abstract 3937 CHOP and CHOP-like chemotherapy programs remain the most commonly used regimens for the treatment of peripheral T-cell lymphomas (PTCLs) despite often sub-optimal results. Histone deacetylase inhibitors (HDACIs) are epigenetic agents known to be active in T-cell lymphoma. Recently romidepsin (R) was approved for patients with relapsed or refractory CTCL. Both R and belinostat (B) are being investigated in patients with relapsed or refractory PTCL. We have previously shown that hypomethylating agents as decitabine (D) produce synergistic interactions with HDACIs in B-cell

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Balasubramanian, Sriram, Susanne Steggerda, Mint Sirisawad, Marshall Schreeder, Luke Doiron, and Joseph J. Buggy. "The Histone Deacetylase-8 (HDAC8) Selective Inhibitor PCI-34051 Decreases Interleukin-1 Beta Secretion in Vitro and Reduces Inflammation in Vivo." Blood 112, no. 11 (2008): 2581. http://dx.doi.org/10.1182/blood.v112.11.2581.2581.

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Abstract Inhibitors of histone deacetylases (HDACs) which are currently in clinical testing for treating various cancers typically inhibit multiple isoforms of the 11-member HDAC family. We have developed an isoform-selective HDAC inhibitor, PCI-34051, that inhibits HDAC8 with a Ki of 10 nM and greater than 200-fold selectivity over other HDAC isoforms (Balasubramanian et al. (2008) Leukemia,22:1026–34). We have shown that PCI-34051 selectively induced apoptosis in cell lines derived from T-cell lymphomas and leukemias, but not in other tumor or normal cell types. Here we show that it potently

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Ribrag, Vincent, Won Seog Kim, Reda Bouabdallah, et al. "Safety and Efficacy of Abexinostat, a Pan-Histone Deacetylase (HDAC) Inhibitor, in Non-Hodgkin Lymphoma and Chronic Lymphocytic Leukemia: Results of an Ongoing Phase 2 Study." Blood 126, no. 23 (2015): 256. http://dx.doi.org/10.1182/blood.v126.23.256.256.

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Abstract Introduction: Histone deacetylase (HDAC) inhibitors, by blocking HDAC enzymes, can regulate acetylation states of histones and other non-histone proteins. Hyperacetylation of histones in cells can cause transcriptional activation of tumor suppressor genes, as well as genes involved in cell cycle control, cell division, and apoptosis, resulting in antitumor activity. Currently, 3 HDAC inhibitors (HDACi), vorinostat, romidepsin, and belinostat, are approved for the treatment of relapsed or refractory peripheral or cutaneous T-cell lymphoma (T-CL). HDACi in development also show promisin

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Okabe, Seiichi, Tetsuzo Tauchi, Hal E. Broxmeyer, and Kazuma Ohyashiki. "Depsipeptide (FK228) Preferntially Induces Apoptosis in Acute T-Cell Leukemia Cell Lines Mediated by CD45 and Src Kinase." Blood 108, no. 11 (2006): 4468. http://dx.doi.org/10.1182/blood.v108.11.4468.4468.

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Abstract Histone acetyltransferases (HAT) and histone deacetylases (HDAC) control the acetylation of histones and intracellular proteins, and regulate the transcription and function of the proteins. One histone deacetylase inhibitor, depsipeptide (FK228) has shown clinical activity in a subset of resistant patients with T-cell lymphoma. However the mechanism of depsipeptide-induced apoptosis in acute T-cell leukemia cells has not yet been fully elucidated. To evaluate the mechanisms of action of depsipeptide, we utilized the acute T-cell leukemia cell line, Jurkat. Treatment with depsipeptide

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Kozako, Tomohiro, Teruhisa Shoji, Akiyoshi Aikawa, et al. "SIRT1, a Longevity Gene Encoded Protein, Regulates Apoptosis of Adult T-Cell Leukemia Cells and Its Inhibition by Sirtinol Induces Apoptosis." Blood 114, no. 22 (2009): 3684. http://dx.doi.org/10.1182/blood.v114.22.3684.3684.

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Abstract Abstract 3684 Poster Board III-620 Adult T-cell leukemia-lymphoma (ATL) is an aggressive peripheral T-cell neoplasm with a poor prognosis developing after long-term infection with human T-cell leukemia virus-1 (HTLV-1). HTLV-1 Tax is closely related to leukemic cell proliferation through nuclear factor-kappa B (NF-ƒÈB) activation. Recent studies have demonstrated that histone deacetylase class I/II inhibitors induce growth arrest and apoptosis of HTLV-1-infected T-cells via blockade of NF-ƒÈB signaling. SIRT1, an NAD(+)-dependent class III histone deacetylase, is widely recognized f

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Miller, Claudia P., Kechen Ban, Melanie E. Dujka, et al. "NPI-0052, a novel proteasome inhibitor, induces caspase-8 and ROS-dependent apoptosis alone and in combination with HDAC inhibitors in leukemia cells." Blood 110, no. 1 (2007): 267–77. http://dx.doi.org/10.1182/blood-2006-03-013128.

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The proteasome has been successfully targeted for the treatment of multiple myeloma and mantle cell lymphoma; however, in other hematologic malignancies, bortezomib has been less effective as a single agent. Here, we describe effects of NPI-0052, a novel proteasome inhibitor, in leukemia model systems. In cell lines, NPI-0052 inhibits all 3 proteolytic activities associated with the proteasome: chymotrypsin-, trypsin-, and caspase-like. NPI-0052 also induces DNA fragmentation in leukemia lines and in mononuclear cells from a Ph + acute lymphoblastic leukemia (ALL) patient. Caspase-3 activation

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Merimi, Makram, Pavel Klener, Maud Szynal, et al. "Suppression of Viral Gene Expression in Bovine Leukemia Virus-Associated B-Cell Malignancy: Interplay of Epigenetic Modifications Leading to Chromatin with a Repressive Histone Code." Journal of Virology 81, no. 11 (2007): 5929–39. http://dx.doi.org/10.1128/jvi.02606-06.

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ABSTRACT Ovine leukemia/lymphoma resulting from bovine leukemia virus infection of sheep offers a large animal model for studying mechanisms underlying leukemogenesis. Silencing of viral information including Tax, the major contributor to the oncogenic potential of the virus, is critical if not mandatory for tumor progression. In this study, we have identified epigenetic mechanisms that govern the complete suppression of viral expression, using a lymphoma-derived B-cell clone carrying a silent provirus. Silencing was not relieved by injection of the malignant B cells into sheep. However, exoge

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Sharma, Vasundhara, Lanzhu Yue, Nathan P. Horvat, et al. "Selective Targeting of Histone Deacetylase 11 Disables Metabolism of Myeloproliferative Neoplasms." Blood 134, Supplement_1 (2019): 474. http://dx.doi.org/10.1182/blood-2019-127235.

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Introduction: Acetylated histone and non-histone proteins are pharmacologic targets for both solid and hematological cancers including myeloproliferative neoplasms (MPNs), a group of clonal hematological malignancies driven by aberrant JAK2/STAT signaling. MPNs are characterized by epigenetic alterations, including aberrant acetylation, which makes this disease particularly interesting for targeting with HDAC inhibitors. Four classes of histone deacetylases (Class I-IV HDACs) regulate gene transcription and modulate cellular processes that drive the initiation and progression of cancer. Pan-HD

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Dong, Li, Shu Cheng, Zhong Zheng, et al. "Histone deacetylase inhibitor potentiated the ability of MTOR inhibitor to induce autophagic cell death in Burkitt leukemia/lymphoma." Journal of Hematology & Oncology 6, no. 1 (2013): 53. http://dx.doi.org/10.1186/1756-8722-6-53.

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Spurgeon, Stephen, Andy I. Chen, Craig Okada, et al. "A Phase I/II Study of Vorinostat (SAHA), Cladribine (2-CdA), and Rituximab Shows Significant Activity in Previously Untreated Mantle Cell Lymphoma." Blood 118, no. 21 (2011): 441. http://dx.doi.org/10.1182/blood.v118.21.441.441.

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Abstract Abstract 441 Background: Despite significant progress in the treatment of mantle cell lymphoma (MCL), relapse remains the norm and additional therapies are needed especially for patients who are not candidates for aggressive treatment approaches. Increasingly, it has become evident that epigenetic modifications, including DNA hypomethylation and histone deacetylase inhibition, are critical to the pathogenesis and treatment of hematologic malignancies; important to cancer biology; and may be essential to the development of treatment resistance in B-cell malignancies. Further developmen

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Kano, Yasuhiko, Miyuki Akutsu, Saburo Tsunoda, et al. "Cytotoxic effects of histone deacetylase inhibitor FK228 (depsipeptide, formally named FR901228) in combination with conventional anti-leukemia/lymphoma agents against human leukemia/lymphoma cell lines." Investigational New Drugs 25, no. 1 (2006): 31–40. http://dx.doi.org/10.1007/s10637-006-9000-0.

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Ramirez, Lorimar, Melissa Singh, and Joya Chandra. "HDAC and LSD1 Inhibitors Synergize to Induce Cell Death in Acute Leukemia Cells." Blood 118, no. 21 (2011): 1427. http://dx.doi.org/10.1182/blood.v118.21.1427.1427.

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Abstract Abstract 1427 Histone deacetylase inhibitors (HDACi) are a class of emerging epigenetic therapies which are being used to treat cancer. Two HDACi (vorinostat and romidepsin) are FDA approved for cutaneous T-cell lymphoma. HDACi have been employed in clinical trials for acute leukemia, but single agent activity has been limited. Improved efficacy is observed when combined with other anticancer agents. In the current study we addressed acute leukemia models using vorinostat, a pan-HDACi that inhibits HDAC class I, II, and IV and entinostat, a newer HDACi that inhibits HDAC class I more

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Wang, Kai, Deborah Morosini, Roman Yelensky, et al. "Genomic Alterations of Histone Modification Genes Are Significantly Less Common in Non-Hodgkin Lymphomas of Adolescents and Young Adults Compared to Older Patients." Blood 124, no. 21 (2014): 1684. http://dx.doi.org/10.1182/blood.v124.21.1684.1684.

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Abstract Background: Non-Hodgkin lymphoma (NHL) is a large group of hematolymphoid malignant neoplasms that can occur at any age. Genomic alterations of histone modifying genes and the NF-kB signaling pathway are characteristic of NHLs. Histone deacetylase and methyltransferase inhibitors including the EZH2 inhibitors E7438, GSK126 and El1 have shown anti-tumor activity in NHLs (PMID: 24217204). Cancers arising in adolescent and young adults (age 15-39, AYA) often exhibit different clinical and biological features than older adults. However, there is very limited information on age-related gen

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Tsukasaki, Kunihiro, and Kensei Tobinai. "Clinical Trials and Treatment of ATL." Leukemia Research and Treatment 2012 (January 16, 2012): 1–12. http://dx.doi.org/10.1155/2012/101754.

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ATL is a distinct peripheral T-lymphocytic malignancy associated with human T-cell lymphotropic virus type I (HTLV-1). The diversity in clinical features and prognosis of patients with this disease has led to its subtype-classification into four categories, acute, lymphoma, chronic, and smoldering types, defined by organ involvement, and LDH and calcium values. In case of acute, lymphoma, or unfavorable chronic subtypes (aggressive ATL), intensive chemotherapy like the LSG15 regimen (VCAP-AMP-VECP) is usually recommended if outside of clinical trials, based on the results of a phase 3 trial. I

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Ma, Helen, Enrica Marchi, Bin Cheng, Govind Bhagat, and Owen A. O'Connor. "Novel Drugs and Clinical Trial-Based Treatments Prolong Survival of Peripheral T-Cell Lymphomas (PTCL) Patients: Single Institution Retrospective Analysis." Blood 134, Supplement_1 (2019): 3486. http://dx.doi.org/10.1182/blood-2019-123587.

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Introduction Peripheral T-cell lymphomas (PTCL) are a group of rare and heterogeneous diseases associated with unfavorable prognoses. Conventional chemotherapy has been the standard of care, but is considered marginally effective. This outcome has been attributed to the fact that most PTCL treatments are derived from the management of aggressive B-cell lymphomas. While relapse is common, subsequent line therapies are heterogeneous, and can include many lines of non-specific chemotherapy. Recently approved novel agents, such as pralatrexate and histone deacetylase (HDAC) inhibitors, and clinica

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Du, Jinwei, Shigemi Matsuyama, and Yu-Chung Yang. "CITED2 Facilitates Apoptosis Induced By Histone Deacetylase Inhibitor SAHA In Human Pediatric Pre-B Acute Lymphoblastic Leukemia Cells." Blood 122, no. 21 (2013): 2913. http://dx.doi.org/10.1182/blood.v122.21.2913.2913.

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Abstract Acute lymphoblastic leukemia (ALL) is the most common malignancy in childhood, representing 31% of all tumors, and about 85% of children with ALL have B-cell ALL. Although the survival rate is approaching 90%, ALL remains the main cause of death from disease in children and young adults. The activity of histone deacetylases (HDAC) in childhood ALL is increased compared with that in normal peripheral blood mononuclear cells or bone marrow cells. Treatment of mice engrafted with T or B-ALL cells with HDAC inhibitor (HDACi) increases the acetylation of Histone 3 and Histone 4 and prolong

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Yves, Plumelle, Michel Stephane, Banydeen Rishika, Delaunay Christine, and Panelatti Gérard. "Characteristics of Adult T-Cell Leukemia/Lymphoma Patients with Long Survival: Prognostic Significance of Skin Lesions and Possible Beneficial Role of Valproic Acid." Leukemia Research and Treatment 2015 (June 14, 2015): 1–9. http://dx.doi.org/10.1155/2015/476805.

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We describe the clinical and biological features of ten patients with a survival superior to ten years (long survival), out of 175 patients diagnosed with Adult T-cell Leukemia/Lymphoma (ATL) in Martinique (1983–2013). There were 5 lymphoma and 5 chronic subtypes. Five of them (3 chronic, 2 lymphoma) had been treated with valproic acid (VA) for neurological disorders developed before or after ATL diagnosis, suggesting a beneficial role for VA as a histone deacetylase inhibitor (HDI) in ATL treatment. Total duration of uninterrupted VA treatment ranged from 8 to 37 years. Overall, the 175 incid

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O'Connor, Owen A., Mark L. Heaney, Lawrence Schwartz, et al. "Clinical Experience With Intravenous and Oral Formulations of the Novel Histone Deacetylase Inhibitor Suberoylanilide Hydroxamic Acid in Patients With Advanced Hematologic Malignancies." Journal of Clinical Oncology 24, no. 1 (2006): 166–73. http://dx.doi.org/10.1200/jco.2005.01.9679.

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Purpose To document the toxicity and activity of the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) in patients with pretreated hematologic malignancies. Patients and Methods Two formulations of SAHA (intravenous [IV] and oral) have been assessed in two consecutive phase I trials. In both trials, dose escalation was performed in parallel and independently in patients with solid tumors and hematologic malignancies. Eligible patients were required to have adequate hepatic and renal function, an absolute neutrophil count ≥ 500/μL and a platelet count more than 25,000/mL. All

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Zhang, Q.-L., L. Wang, Y.-W. Zhang, et al. "The proteasome inhibitor bortezomib interacts synergistically with the histone deacetylase inhibitor suberoylanilide hydroxamic acid to induce T-leukemia/lymphoma cells apoptosis." Leukemia 23, no. 8 (2009): 1507–14. http://dx.doi.org/10.1038/leu.2009.41.

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Bommert, Kurt, Stefan Knop, Janine Arts, et al. "Novel, 2ND Generation Histone Deacetylase (HDAC) Inhibitor JNJ-26481585 Exhibits Potent Antitumor Activity Against Chronic Lymphocytic Leukemia Cells In-Vitro and Ex-Vivo." Blood 110, no. 11 (2007): 4679. http://dx.doi.org/10.1182/blood.v110.11.4679.4679.

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Abstract Chronic lymphocytic leukemia (CLL), the most frequent lymphoproliferative disease is characterized by the insidious accumulation of mature-appearing lymphocytes predominantely in bone marrow, blood and lymphatic tissues. Despite a generally indolent course the vast majority of subjects diagnosed with CLL eventually require treatment. Apart from cytostatic drugs recently antibodies have been added to the therapeutic armamentarium. However, only a minority of patients will enjoy long-term disease-free intervals thus making further intervention of therapy highly desirable. Histone deacet

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Li, Xinyao, Dan Ma, Tingting Lu, et al. "Regulation of HACE1 Expression Enhances HDAC Inhibitor Lmk-235-Mediated Apoptosis in Diffuse Large B-Cell Lymphoma Cells." Blood 132, Supplement 1 (2018): 5299. http://dx.doi.org/10.1182/blood-2018-99-117842.

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Abstract Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of non-Hodgkin's lymphoma (NHL). It is a group of adult lymphomas with a large clinical presentation and prognosis heterogeneity. In order to improve the cure rate of diffuse large B-cell lymphoma, it is necessary to find a new DLBCL treatment plan that can control the progression of the disease and explore its unknown potential therapeutic targets. Epigenetic modification has become a new treatment for leukemia in recent years, and histone deacetylase inhibitor (HDACi) is a novel drug for the treatment of DLBCL in recen

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Willenbacher, Ella, Karin Jöhrer, Wolfgang Willenbacher, Brigitte Flögel, Richard Greil, and Brigitte Kircher. "Pixantrone demonstrates significant in vitro activity against multiple myeloma and plasma cell leukemia." Annals of Hematology 98, no. 11 (2019): 2569–78. http://dx.doi.org/10.1007/s00277-019-03797-6.

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Abstract Treatment results for multiple myeloma and plasma cell leukemia have considerably improved, but cure remains elusive and establishing new therapeutic approaches constitutes a major unmet clinical need. We analyzed the anti-myeloma properties of the aza-anthracenedione pixantrone which has been successfully used in a phase III study for the treatment of patients with aggressive non-Hodgkin’s lymphoma as monotherapy as well as in combination regimes in vitro and in an adapted in vivo model (ex ovo chicken chorioallantoic membrane (CAM) assay). Pixantrone significantly inhibited prolifer

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Kalac, Matko, Enrica Marchi, Luigi Scotto, et al. "Synergistic Combinations of Histone Deacetylase Inhibitors and Decitabine Induce a Unique Gene Expression and Epigenetic Profile In Models of Diffuse Large B-Cell Lymphoma." Blood 116, no. 21 (2010): 435. http://dx.doi.org/10.1182/blood.v116.21.435.435.

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Abstract Abstract 435 Diffuse large B-cell lymphoma (DLBCL) is the most common type of lymphoid malignancy, representing approximately 30–40% of all lymphomas. While significant progress has been made in treating this disease over the past decade, it is still regarded as a heterogeneous disease which, after being classified as relapsed or refractory, is fatal in about one-third of patients. Histone deacetylase inhibitors (HDACI) are presently approved for the treatment of relapsed or refractory cutaneous T- cell lymphomas (CTCL), and have marked activity in peripheral T-cell lymphomas (PTCL),

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Bhalla, Kapil N. "Epigenetic Dysregulation in Lymphoid Malignancies." Blood 116, no. 21 (2010): SCI—29—SCI—29. http://dx.doi.org/10.1182/blood.v116.21.sci-29.sci-29.

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Abstract Abstract SCI-29 Greater understanding of the role of the epigenetic mechanisms and cancer cell epigenome in the pathogenesis of cancer in general and lymphoid malignancies in particular has emerged, which is yielding insights into how to therapeutically target these novel mechanisms. Epigenetic mechanisms include histone modifications, DNA methylation, nucleosome remodeling and small non-coding RNAs. In transformed cells, the methylome involves global DNA hypomethylation mostly targeting DNA repeats, and hypermethylation of CpG islands in the promoter regions of TSGs. For example, met

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Jo, Tatsuro, Takahiro Sakai, Kaori Matsuzaka, et al. "Successful Treatment of a Patient with Brentuximab Vedotin-Refractory ALK-Negative Anaplastic Large Cell Lymphoma with Romidepsin." Case Reports in Oncology 13, no. 3 (2020): 1402–9. http://dx.doi.org/10.1159/000511111.

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We present the case of a 78-year-old male patient who was diagnosed with anaplastic lymphoma kinase (ALK)-negative, CC chemokine receptor 4 (CCR4)-negative, and CD30-positive anaplastic large cell lymphoma (ALCL). The patient had a past medical history of adult T-cell leukemia/lymphoma and colon cancers that had developed simultaneously approximately 2 years prior to the development of ALCL that were treated with immunochemotherapy and resection, respectively. Initial treatment for ALCL included brentuximab vedotin, an anti-CD30 monoclonal antibody-monomethyl auristatin E conjugate; however, w

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Toomey, Ngoc, and Juan Carlos Ramos. "The Combination of Belinostat with Zidovudine for Treatment of HTLV-I Related Adult T-Cell Leukemia-Lymphoma." Blood 126, no. 23 (2015): 1562. http://dx.doi.org/10.1182/blood.v126.23.1562.1562.

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Abstract Adult T-cell leukemia-lymphoma (ATLL) is an aggressive malignancy with poor prognosis that is incurable by conventional drugs. Histone deacetylase (HDAC) inhibitors (HDIs) are broadly active anti-neoplastic agents that can be cautiously exploited in the treatment of ATLL. The HTLV-I provirus is clonally integrated in virtually all ATLL cells. The HTLV-I 5'LTR promoter is trans -activated by the viral protein Tax through binding of CREB and p300/CBP. Tax binding enhances p300/CBP histone acetyl transferase (HAT) activity resulting in histone acetylation, chromatin unwinding, and transc

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Schnell, Annika P., Stephan Kohrt, and Andrea K. Thoma-Kress. "Latency Reversing Agents: Kick and Kill of HTLV-1?" International Journal of Molecular Sciences 22, no. 11 (2021): 5545. http://dx.doi.org/10.3390/ijms22115545.

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Human T-cell leukemia virus type 1 (HTLV-1), the cause of adult T-cell leukemia/lymphoma (ATLL), is a retrovirus, which integrates into the host genome and persistently infects CD4+ T-cells. Virus propagation is stimulated by (1) clonal expansion of infected cells and (2) de novo infection. Viral gene expression is induced by the transactivator protein Tax, which recruits host factors like positive transcription elongation factor b (P-TEFb) to the viral promoter. Since HTLV-1 gene expression is repressed in vivo by viral, cellular, and epigenetic mechanisms in late phases of infection, HTLV-1

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Sahakian, Eva, Bijal D. Shah, John Powers, et al. "The Opposing Role of Histone Deacetylase 10 (HDAC10) and HDAC11 in Proliferation/Survival of Mantle Cell Lymphoma (MCL) and Chronic Lymphocytic Leukemia (CLL)." Blood 118, no. 21 (2011): 1363. http://dx.doi.org/10.1182/blood.v118.21.1363.1363.

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Abstract Abstract 1363 The role of HDACs in cell biology, initially limited to their effects upon histones, encompasses now more complex regulatory functions that are dependent on their tissue expression, cellular compartment distribution and the stage of cellular differentiation. Not surprisingly, HDACs have been shown to play important roles in normal B-cell biology and, aberrant expression of these proteins has been found in some B-cell malignancies1. However, the role of specific HDACs in regulation of pro-survival and cell-cycling genes in MCL and CLL still remains poorly understood. We t

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Kozako, Tomohiro, Makoto Yoshimitsu, Naomichi Arima, et al. "Induction of Apoptosis and Autophagy By Nampt Inhibition in Adult T-Cell Leukemia/Lymphoma and Leukemic Cell Lines." Blood 128, no. 22 (2016): 2327. http://dx.doi.org/10.1182/blood.v128.22.2327.2327.

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Abstract Introduction: Adult T-cell leukemia/lymphoma (ATL) is an aggressive peripheral T-cell neoplasm that develops after long-term infection with human T-cell leukemia virus type I (HTLV-1). Despite the recent advances in chemotherapy, allogeneic hematopoietic stem cell transplantation, and supportive care, the prognosis for patients with acute, lymphoma, or unfavorable chronic subtypes is one of the poorest among hematological malignancies. The identification of new molecular targets for ATL prevention and treatment is desired. SIRT1, a nicotinamide adenine dinucleotide (NAD+)-dependent hi

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Ma, Helen, Bin Cheng, and Owen A. O'Connor. "Survival outcomes of patients with peripheral T-cell lymphomas (PTCL) treated with chemotherapy and/or novel agents: The Columbia University experience." Journal of Clinical Oncology 37, no. 15_suppl (2019): e19049-e19049. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e19049.

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e19049 Background: CHOP-based regimens have been considered the standard of care for PTCL despite disappointing results. Several lines of evidence, including the regulatory approval of novel drugs since 2009, raise the question as to whether these drugs are changing the natural history of relapsed PTCL. Recent molecular insights into the pathogenesis of PTCL, especially in angioimmunoblastic T-cell lymphoma (AITL), have revealed a number of genetic lesions that might portend a unique vulnerability to select agents, such as histone deacetylase inhibitors (HDACi). Methods: This is a retrospectiv

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Marchi, Enrica, Matko Kalac, Danielle Bongero, et al. "Effect of a combination of epigenetic agents on the malignant phenotype in models of T-cell lymphoma." Journal of Clinical Oncology 30, no. 15_suppl (2012): e13569-e13569. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e13569.

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e13569 Background: CHOP and CHOP-like chemotherapy are the most used regimens for the treatment of peripheral T-cell lymphomas (PTCLs) despite sub-optimal results. Histone deacetylase inhibitors (HDACIs) have shown class activity in PTCLs. The interaction between the HDACIs (depsipeptide (R), belinostat (B), vorinostat (V) and panobinostat (P)) and a DNMT inhibitor (decitabine (D) was investigated in vitro, in vivo and at the molecular level in T-cell lymphoma and leukemia cell lines (H9, HH, P12, PF-382). Methods: For cytotoxicity assays, luminescence cell viability assay was used (CellTiter-

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