Differential expression of autophagy in hodgkin lymphoma cells treated with various anti-cancer drugs.

Differential expression of autophagy in hodgkin lymphoma cells treated with various anti-cancer drugs. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Differential expression of autophagy in hodgkin lymphoma cells treated with various anti-cancer drugs. Abstract Text:

Amaylia Oehadian,Naoki Koide,Ferdaus Hassan,Shamima Islam,Isamu Mori,Tomoaki Yoshida,Takashi Yokochi,Amaylia Oehadian,Naoki Koide,Ferdaus Hassan,Shamima Islam,Isamu Mori,Tomoaki Yoshida,Takashi Yokochi,

Aim: autophagy is a pivotal physiological process for survival during starvation, differentiation and normal growth control. It is defined as the process of sequestrating cytoplasmic proteins or even entire organelles into the lytic compartment (lysosome/vacuole). This study investigates the expression of autophagy in Hodgkin lymphoma cells treated with various anti-cancer drugs. Methods: Hodgkin's lymphoma cells (HD-My-Z cells) were cultured with various anti-cancer drugs, such as bleomycin, adriamycin, gemcitabine and paclitaxel. Autophagy was detected by fluorescent pattern of light chain 3(LC3) proteins and the apoptotic cell death was determined by annexin V binding. Results: autophagy was detected in HD-My-Z cells treated with gemcitabine, but not with bleomycin, adriamycin and paclitaxel. Adriamycin exhibited the strongest cytotoxic action, and the cytotoxic action of bleomycin and gemcitabine was less marked compared with adriamycin. Paclitaxel did not cause significant cell death in the cells. Conclusion: autophagy was differentially expressed in Hodgkin lymphoma cells treated with anti-cancer drugs and the expression did not correspond to the apoptotic cell death.

Differential expression of autophagy in hodgkin lymphoma cells treated with various anti-cancer drugs. Publishing Authors By Initials

A Oehadian,N Koide,F Hassan,S Islam,I Mori,T Yoshida,T Yokochi,A Oehadian,N Koide,F Hassan,S Islam,I Mori,T Yoshida,T Yokochi,

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

Differential expression of autophagy in hodgkin lymphoma cells treated with various anti-cancer drugs. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Acta medica Indonesiana

VOLUME: 39

Page Numbers: 153-6

Journal Abbreviation:

ISSN: 0125-9326

DAY: 29

MONTH: 11

YEAR: 2007

Differential expression of autophagy in hodgkin lymphoma cells treated with various anti-cancer drugs. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 7901042

Differential expression of autophagy in hodgkin lymphoma cells treated with various anti-cancer drugs. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: Differential expression of autophagy in hodgkin lymphoma cells treated with various anti-cancer drugs. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Differential expression of autophagy in hodgkin lymphoma cells treated with various anti-cancer drugs.

AFFILIATION: Division of Hematology and Medical Oncology, Department of Internal Medicine, Faculty of Medicine, Padjajaran University, Hasan Sadikin Hospital, Bandung.

Country: Indonesia

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: Acta Med Indones

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Differential expression of autophagy in hodgkin lymphoma cells treated with various anti-cancer drugs Related Publications

• Augmented immunological activities of recombinant lipopolysaccharide possessing the mannose homopolymer as the O-specific polysaccharide.
• Differential expression of autophagy in hodgkin lymphoma cells treated with various anti-cancer drugs.
• Discrimination by means of pulsed-field gel electrophoresis between strains of Campylobacter jejuni Lior type 4 derived from sporadic cases and from outbreaks of infection.
• Gamma interferon-induced nitric oxide production in mouse CD5+ B1-like cell line and its association with apoptotic cell death.
• Hydrogen peroxide induces the production of tumor necrosis factor-{alpha} in RAW 264.7 macrophage cells via activation of p38 and stress-activated protein kinase.
• Interleukin-10 inhibits tumor necrosis factor-alpha production in lipopolysaccharide-stimulated RAW 264.7 cells through reduced MyD88 expression.
• Lipopolysaccharide and interferon-gamma enhance Fas-mediated cell death in mouse vascular endothelial cells via augmentation of Fas expression.
• Lipopolysaccharide augments the in vivo lethal action of doxorubicin against mice via hepatic damage.
• Pulsed-field gel electrophoretic analysis of Campylobacter jejuni DNA for use in epidemiological studies.
• Refractory epilepsy accompanying acute encephalitis with multifocal cortical lesions: possible autoimmune etiology.
• Thalidomide inhibits epidermal growth factor-induced cell growth in mouse and human monocytic leukemia cells via Ras inactivation.
• The mechanism of development of acute lung injury in lethal endotoxic shock using alpha-galactosylceramide sensitization.
• Unified synthesis of C19-C26 subunits of amphidinolides B1, B2, and B3 by exploiting unexpected stereochemical differences in Crimmins' and Evans' aldol reactions.
• [Developmental mechanism of pulmonary insufficiency after open heart surgery]
• [Dicor bridge system. Single crowns in practical combinations]
• [Intravenous thrombolytic therapy and its unresolved problems in Japan]