PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 2475099

Diffuse large cell lymphoma: a teaching hospital experience.

D I Marks·W P Sheridan·D W Ellis·A W Boyd·G Morstyn·M D Green·R M Fox
View original source ↗Export metadata ↓

Abstract

The source did not provide an abstract. Follow the original record for more information.

Explore related subjects

Antigens, CDAntigens, CD19Antigens, CD20Antigens, DifferentiationAntigens, Differentiation, B-LymphocyteAntigens, NeoplasmAntineoplastic Combined Chemotherapy ProtocolsCell Adhesion MoleculesClinical Trials as TopicCyclophosphamideDoxorubicinFemaleHospitals, TeachingHumansLectinsLymphomaMaleNeprilysinPrednisoneSialic Acid Binding Ig-like Lectin 2Time FactorsVincristineClinical TrialJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

D I Marks, W P Sheridan, D W Ellis, A W Boyd, G Morstyn, M D Green, R M Fox. 1989. Diffuse large cell lymphoma: a teaching hospital experience.. https://doi.org/10.1111/j.1445-5994.1989.tb00233.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Autophagic-like cell death in neutrophils induced by autoantibodies.

Human neutrophils undergo autophagic-like cell death following Sialic acid binding immunoglobulin-like lectin-9 (Siglec-9) ligation and concurrent stimulation with certain, but not all, neutrophil survival cytokines. Caspase inhibition by these cytokines is required, but is not sufficient, to trigger this particular form of cell death. Additional mechanisms may involve reactive oxygen species (ROS), and blocking of ROS or prevention of ROS production prevents autophagic-like neutrophil death. Interestingly, human intravenous immunoglobulin (IVIg) preparations contain natural anti-Siglec-9 autoantibodies, which are able to ligate Siglec-9 on neutrophils and induce autophagic-like cell death in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF) and some other survival cytokines. Here, we discuss the pathophysiological and therapeutic implications of these recent findings.

Antigens, CD↗
PubMed2007

Bias in association studies of systemic lupus erythematosus susceptibility due to geographical variation in the frequency of a programmed cell death 1 polymorphism across Europe.

We obtained eight collections of DNA samples from ethnically matched systemic lupus erythematosus (SLE) patients and controls from five European countries totaling 783 patients and 1210 controls. A highly significant cline in the frequency of the PD1.3 A allele was found among controls but not among SLE patients. The frequency of the PD1.3 A allele increased from the Northeast to the Southwest of Europe. The cline was clearly apparent (P=1.2 x 10(-6)) when data from controls of other five SLE susceptibility studies were included in the analysis. This variation has severely biased SLE association studies owing to the lack of parallel changes in SLE patients. As a consequence, the PD1.3 A allele was more common in SLE patients than in controls in the Northeast and Center of Europe, similar to controls in Southeast Europe, and less frequent than in the controls in the Southwest of the Continent. This dissociation in allele frequencies between SLE patients and controls in different subpopulations indicated that programmed cell death 1 variation and disease susceptibility are not independent but the type of relationship is currently unclear. As allele frequency clines are common in other polymorphisms their impact in genetic epidemiology studies should be carefully considered.

Antigens, CD↗