The bcl-2 and p53 oncoproteins can be modulated by bryostatin 1 and dolastatins in human diffuse large cell lymphoma.

  title={The bcl-2 and p53 oncoproteins can be modulated by bryostatin 1 and dolastatins in human diffuse large cell lymphoma.},
  author={A Maki and Hari H. Diwakaran and Bruce G. Redman and S al-Asfar and George R. Pettit and Ramzi M. Mohammad and Ayad Al-Katib},
  journal={Anti-cancer drugs},
  volume={6 3},
The effects of dolastatin 10 (Dol10) and dolastatin 15 (Dol15) alone, and after treatment with bryostatin 1 (Bryo1), on human diffuse large cell lymphoma cell line (WSU-DLCL2) were studied. At a concentration of 1.0 ng/ml Dol10 and Dol15 showed significant growth inhibition (p < 0.05). This inhibition was intensified when the cells were pretreated for 24 h with 200 nM Bryo1. Bryo1, Dol10 and Dol15 induced apoptosis which was seen on morphological examination, by flow cytometry and DNA… Expand
Bax:Bcl-2 ratio modulation by bryostatin 1 and novel antitubulin agents is important for susceptibility to drug induced apoptosis in the human early pre-B acute lymphoblastic leukemia cell line, Reh.
The ratio of Bax to Bcl-2 protein can determine whether cells will die via apoptosis or be protected from it. Reh was found to express a high basal level of Bcl-2 but was lacking of Bax proteinExpand
Modulation of the expression of Bcl-2 and related proteins in human leukemia cells by protein kinase C activators: relationship to effects on 1-[β-D-arabinofuranosyl]cytosine-induced apoptosis
The findings indicate that the ability of bryostatin 1 to facilitate drug-induced apoptosis in human myeloid leukemia cells involves factors other than quantitative changes in the expression of Bcl-2 family members, and raise the possibility that qualitative alterations in the B cl-2 protein, such as phosphorylation status, may contribute to this capacity. Expand
Bryostatin Induces Protein Kinase C Modulation, Mcl-1 Up-Regulation and Phosphorylation of Bcl-2 Resulting in Cellular Differentiation and Resistance to Drug-induced Apoptosis in B-cell Chronic Lymphocytic Leukemia Cells
Results present an explanation for Bryostatin-induced B-CLL cell survival in which modulation of the PKC pathway couples differentiation with an increase in antiapoptotic protein expression and calls into question the rationale for its use in the treatment of B- CLL. Expand
The antineoplastic agent bryostatin-1 induces proinflammatory cytokine production in human monocytes: synergy with interleukin-2 and modulation of interleukin-2Rgamma chain expression.
It is demonstrated that bryo-1 can potently induce the production of pro-inflammatory cytokines from human peripheral blood monocytes and suggests that stimulation of monokine secretion by bryO-1 may represent at least one of the mechanisms responsible for the in vivo antitumor activity of this drug. Expand
Modulation of ara-C induced apoptosis in leukemia by the PKC activator bryostatin 1.
  • S. Grant
  • Chemistry, Medicine
  • Frontiers in bioscience : a journal and virtual library
  • 1997
Recent evidence suggests that bryostatin 1 may act, through modification of Bcl-2 phosphorylation status, at a distal site in the cell death pathway, which could provide a paradigm important for understanding the mechanism(s) by which agents acting through signal transduction pathways modulate cytotoxic drug-induced cell death. Expand
Role of ubiquitin carboxyl terminal hydrolase in the differentiation of human acute lymphoblastic leukemia cell line, Reh.
The data suggest that TPA-induced apoptosis of Reh cells has a separate pathway from that of differentiation or that UCH-L1 expression is independent of the apoptotic pathway. Expand
Pharmacology and clinical experience with bryostatin 1: a novel anticancer drug.
  • Philip, Zonder
  • Medicine
  • Expert opinion on investigational drugs
  • 1999
There is ample in vitro data demonstrating that bryo 1 can sensitise tumour cells to cytotoxic agents, and recent clinical work has focused on combining b Bryo 1 with traditional chemotherapeutic agents for both haematologic and non-haematological cancers. Expand
Novel marine-derived anticancer agents: a phase I clinical, pharmacological, and pharmacodynamic study of dolastatin 10 (NSC 376128) in patients with advanced solid tumors.
  • T. Madden, H. Tran, +5 authors J. Abbruzzese
  • Medicine
  • Clinical cancer research : an official journal of the American Association for Cancer Research
  • 2000
The available preclinical, pharmacological, and clinical data suggest that further study of escalated DOLA-10 dosing with cytokine support is warranted, and any antitumor activity of this novel agent is documented. Expand
Marine Antitumor Peptide Dolastatin 10: Biological Activity, Structural Modification and Synthetic Chemistry
The biological activity and chemical work of Dol-10 in the advance of antitumor drugs in the last 35 years will be summarized, which will provide the support for pharmaceutical researchers interested in leading exploration of antitUMor marine peptides. Expand
A Phase I trial of bryostatin-1 in children with refractory solid tumors: a Pediatric Oncology Group study.
A Phase I trial of bryostatin-1 was performed in children with solid tumors to establish the dose-limiting toxicity (DLT) and maximum-tolerated dose (MTD); establish the pharmacokinetic profile in children; and document any evidence of antitumor activity. Expand