TY - JOUR
T1 - Gene expression by single Reed-Sternberg cells
T2 - Pathways of apoptosis and activation
AU - Messineo, Christina
AU - Jamerson, M. Hunter
AU - Hunter, Eileen
AU - Braziel, Rita
AU - Bagg, Adam
AU - Irving, Steven G.
AU - Cossman, Jeffrey
N1 - Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 1998/4/1
Y1 - 1998/4/1
N2 - Although Hodgkin's disease is highly responsive to treatments that cause apoptosis, it remains resistant to the physiological mechanisms intended to cause call death. Presumably, the Reed-Sternberg call defies endogenous apoptosis, persists, accumulates, and manifests the malignant disorder seen clinically. The Reed-Sternberg cell expresses several members of the tumor necrosis factor receptor superfamily. This family of receptors is involved in both activation and proliferation of cells, as well as either protection from or initiation of apoptosis in calls expressing these surface proteins. Signals from these receptors affect transcription. We reasoned that the activation state and resistance to apoptosis of Reed-Sternberg calls might be attributable to dysregulation of genes controling these processes. To determine gene expression by Reed-Sternberg calls, we developed a method of micromanipulation, global reverse transcription, and the reverse transcription-polymerase chain reaction and applied it to 51 single Reed- Sternberg cells and their variants from six cases of Hodgkin's disease. This report analyzes the gene expression of bcl-xs, bcl-xl, bax-α, bax-β, fadd, fas, fas ligand (fas L), ice, TNF-α, TNF-β, TNFR1, TNFR2, TRAF1, TRAF2, TRAF3, cIAP2, and tradd at the level of mRNA in the single Reed-Sternberg cells and their variants. The findings here suggest a molecular mechanism for the activated state and in vivo survival occurring in untreated Reed- Sternberg calls of Hodgkin's disease.
AB - Although Hodgkin's disease is highly responsive to treatments that cause apoptosis, it remains resistant to the physiological mechanisms intended to cause call death. Presumably, the Reed-Sternberg call defies endogenous apoptosis, persists, accumulates, and manifests the malignant disorder seen clinically. The Reed-Sternberg cell expresses several members of the tumor necrosis factor receptor superfamily. This family of receptors is involved in both activation and proliferation of cells, as well as either protection from or initiation of apoptosis in calls expressing these surface proteins. Signals from these receptors affect transcription. We reasoned that the activation state and resistance to apoptosis of Reed-Sternberg calls might be attributable to dysregulation of genes controling these processes. To determine gene expression by Reed-Sternberg calls, we developed a method of micromanipulation, global reverse transcription, and the reverse transcription-polymerase chain reaction and applied it to 51 single Reed- Sternberg cells and their variants from six cases of Hodgkin's disease. This report analyzes the gene expression of bcl-xs, bcl-xl, bax-α, bax-β, fadd, fas, fas ligand (fas L), ice, TNF-α, TNF-β, TNFR1, TNFR2, TRAF1, TRAF2, TRAF3, cIAP2, and tradd at the level of mRNA in the single Reed-Sternberg cells and their variants. The findings here suggest a molecular mechanism for the activated state and in vivo survival occurring in untreated Reed- Sternberg calls of Hodgkin's disease.
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U2 - 10.1182/blood.v91.7.2443
DO - 10.1182/blood.v91.7.2443
M3 - Article
C2 - 9516144
AN - SCOPUS:0032055536
SN - 0006-4971
VL - 91
SP - 2443
EP - 2451
JO - Blood
JF - Blood
IS - 7
ER -