NDLI: Loss of PU.1 expression is associated with defective immunoglobulin transcription in Hodgkin and Reed-Sternberg cells of classical Hodgkin disease.

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Loss of PU.1 expression is associated with defective immunoglobulin transcription in Hodgkin and Reed-Sternberg cells of classical Hodgkin disease.

Content Provider	Semantic Scholar
Author	Jundt, Franziska Kley, Katharina Anagnostopoulos, Ioannis K. Pröbsting, Kristina Schulze Greiner, Axel Mathas, Stephan Scheidereit, Claus Wirth, Thomas Stein, Harald Doerken, Bernd
Copyright Year	2002
Abstract	Immunoglobulin transcription is impaired in Hodgkin and Reed-Sternberg (HRS) cells of classical Hodgkin disease (cHD). We recently demonstrated that defective immunoglobulin promoter transcription correlates with the down-regulation of the B-cell transcription factors Oct2 and BOB.1/OBF.1. These results prompted us to investigate whether immunoglobulin enhancer activity is also impaired in HRS cells and whether as yet unidentified factors could be necessary for immunoglobulin enhancer activity in HRS cells of cHD. Here we analyzed 30 cases of cHD for expression of the Ets family member PU.1 that is known to collaborate with multiple transcription factors and to regulate expression of immunoglobulin genes. We show that PU.1 is not expressed in primary and cultured HRS cells. Reintroduction of PU.1 and Oct2 in cultured HRS cells restored the activity of cotransduced immunoglobulin enhancer constructs. Our study identifies PU.1 deficiency as a recurrent defect in HRS cells that might contribute to their impairment of immunoglobulin transcription.
Starting Page	364
Ending Page	371
Page Count	8
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://www.bloodjournal.org/content/bloodjournal/99/8/3060.full.pdf?sso-checked=true
PubMed reference number	11929801v1
Volume Number	99
Issue Number	8
Journal	Blood
Language	English
Access Restriction	Open
Subject Keyword	Down-Regulation Enhancer of transcription Genes, Immunoglobulin Hodgkin Disease Leukemia, B-Cell Retreatments SPI1 gene TRANSCRIPTION FACTOR
Content Type	Text
Resource Type	Article

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