True Histiocytic Lymphoma

2020 ◽  
Author(s):  
Keyword(s):  
Histiocytic Lymphoma

scholarly journals 8a, a New Acridine Antiproliferative and Pro-Apoptotic Agent Targeting HDAC1/DNMT1

2021 ◽  
Vol 22 (11) ◽  
pp. 5516
Author(s):  
Qiting Zhang ◽  
Ziyan Wang ◽  
Xinyuan Chen ◽  
Haoxiang Qiu ◽  
Yifan Gu ◽  
...  
Keyword(s):  
Histone Deacetylase ◽  
Dna Methyltransferase ◽  
Hdac Inhibitors ◽  
Mitochondrial Pathway ◽  
Epigenetic Therapy ◽  
Protein Interaction Data ◽  
Dependent Manner ◽  
Histone Deacetylase 1 ◽  
Histiocytic Lymphoma ◽  
Dose Dependent

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 that 8a mainly passes through the endogenous (mitochondrial) pathway to induce cell apoptosis. From the protein interaction data, we found that 8a also affected the expression of DNA methyltransferase 1 (DNMT1). Therefore, an experiment was performed to assess the binding of 8a to DNMT1 at the molecular and cellular levels. We found that the binding strength of 8a to DNMT1 enhanced in a dose-dependent manner. Additionally, 8a inhibits the expression of DNMT1 mRNA and its protein. These findings suggested that the anti-proliferative and pro-apoptotic activities of 8a against leukemia cells were achieved by targeting HDAC1 and DNMT1.

Richter's syndrome: Diffuse histiocytic lymphoma in patients with chronic lymphocytic leukemia

1980 ◽  
Vol 68 (4) ◽  
pp. 539-548 ◽  
Author(s):  
Donald L. Trump ◽  
Risa B. Mann ◽  
Roger Phelps ◽  
Huw Roberts ◽  
C.Lockard Conley
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Lymphocytic Leukemia ◽  
Histiocytic Lymphoma ◽  
Diffuse Histiocytic Lymphoma ◽  
Richter’S Syndrome

scholarly journals Synthesis, Characterization and Antiproliferative Evaluation of Pt(II) and Pd(II) Complexes with a Thiazine-Pyridine Derivative Ligand

2021 ◽  
Vol 14 (5) ◽  
pp. 395
Author(s):  
Silvia Gutiérrez-Tarriño ◽  
Javier Espino ◽  
Francisco Luna-Giles ◽  
Ana B. Rodríguez ◽  
José A. Pariente ◽  
...  
Keyword(s):  
Cell Lines ◽  
Anticancer Drugs ◽  
Platinum Complexes ◽  
Chemotherapeutic Agents ◽  
Pyridine Derivative ◽  
Cervix Carcinoma ◽  
Multinuclear Complexes ◽  
Histiocytic Lymphoma ◽  
Ovary Adenocarcinoma

Chemical, pharmacological, and clinical research on anticancer coordination complexes has led to noteworthy anticancer drugs such as cisplatin, carboplatin and oxaliplatin. Although these compounds are effective chemotherapeutic agents in the treatment of different tumors, they are associated with high toxicity and numerous side effects. Several studies have shown that the range of platinum complexes with antitumor activity is not limited to structural analogs of cisplatin. Therefore, the development of convenient anticancer drugs that can be effectively used for the treatment of human tumors has become the main goal of most research groups in this field. In this sense, active platinum complexes without NH groups, transplatinum complexes, multinuclear complexes, cationic complexes, and several classes of palladium(II) complexes have emerged. Herein, the synthesis and characterization of two Pt(II) or Pd(II) complexes with PyTz (2-(2-pyridyl)iminotetrahydro-1,3-thiazine), a thiazine derivative ligand, with the formula [MCl2(PyTz)]·C2H6O (M = Pt(II) or Pd(II)) were reported. The potential anticancer ability of both complexes was evaluated in epithelial cervix carcinoma HeLa, human ovary adenocarcinoma SK-OV-3, human histiocytic lymphoma U-937, and human promyelocytic leukemia HL-60 cell lines. Interestingly, the Pt(II) complex showed great cytotoxic potential against all tumor cell lines tested, whereas the Pd(II) complex displayed slight antitumor actions.

scholarly journals Cold Urticaria: An Unusual Manifestation of Histiocytic Lymphoma

1982 ◽  
Vol 68 (4) ◽  
pp. 343-344 ◽  
Author(s):  
Aaron Polliack ◽  
Eldad Ben-Chetrit ◽  
Zvi Stern
Keyword(s):  
Cold Urticaria ◽  
Unusual Manifestation ◽  
Histiocytic Lymphoma

scholarly journals Retinoids downregulate both p60 and p80 forms of tumor necrosis factor receptors in human histiocytic lymphoma U-937 cells

Blood ◽  
1995 ◽  
Vol 85 (12) ◽  
pp. 3547-3555 ◽  
Author(s):  
K Totpal ◽  
MM Chaturvedi ◽  
R LaPushin ◽  
BB Aggarwal
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Leukemia Cell Line ◽  
Cell Surface Expression ◽  
Scatchard Analysis ◽  
Dependent Manner ◽  
Tnf Receptor ◽  
Tnf Receptors ◽  
Histiocytic Lymphoma ◽  
Necrosis Factor

Because retinoids are known to modulate the growth and differentiation effects of tumor necrosis factor (TNF), we investigated the effect of all-trans-retinoic acid (RA) on the cell surface expression of TNF receptors in human histiocytic lymphoma U-937 cells. RA decreased the specific binding of 125I-labeled TNF to these cells in a dose- and time-dependent manner. The maximal decrease occurred when cells were treated with 1 mumol/L RA for 24 hours at 37 degrees C. Scatchard analysis of the binding indicated that the decrease by RA was caused by a decrease in receptor number and not by a decrease in affinity. The downmodulation of TNF receptors was also confirmed by covalent receptor-ligand cross-linking studies. Receptor-mediated internalization of the ligand was also found to be decreased on treatment of cells with RA. Northern blot analysis also indicated a decrease in the transcript of the receptor. By using antibodies specific to either the p60 or p80 form of the TNF receptor, we found that both receptors were downregulated by RA. RA treatment also decreased TNF receptors on acute monocytic leukemia cell line THP-1. Other analogues of RA, specifically 9-cis-RA, (E)-4-[2-(5,6,7,8-tetrahydro-2-naphthalenyl)-1-propenyl]-benzoic acid (TTNPB), and 3-methyl-TTNPB, which differ in their specificity towards different RA receptors, were also active in downregulating TNF receptors. 3-Methyl-TTNPB, which is more specific for the RXR form of the RA receptor, was found to be most potent. The downregulation of TNF receptors by RA correlated with the downmodulation of the antiproliferative effects of TNF against U-937 cells. Overall, our results indicate that RA downmodulates both the p60 and p80 form of the TNF receptor on cells of myeloid origin, which correlates with the cellular response.

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