Hodgkin's disease: The sternberg-reed cell

Bucsky, Peter

doi:10.1007/bf00367457

Cited by 17 publications

(4 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A variety of studies on Hodgkin's disease (HD) have failed to identify the origin of Reed-Sternberg (RS) cells and variants thereof (reviewed in refs. [1][2][3][4][5]. Based on (immuno)electron microscopic,"8 enzyme histo~hemical,~ and immunohistochemical findings,lG13 and on in vitro characterization studies,'&I5 a monocyte/macrophage derivation has been favoured by many investigators.…”

Section: Introductionmentioning

confidence: 99%

Plasmacytoid monocytes (so‐called plasmacytoid T cells) in Hodgkin's disease

Facchetti

Wolf‐Peeters

Desmet

1989

The Journal of Pathology

View full text Add to dashboard Cite

The occurrence and distribution of plasmacytoid monocytes (so-called plasmacytoid T cells) were investigated immunohistochemically in 40 cases of Hodgkin's disease. Large numbers of plasmacytoid monocytes were found in all cases of lymphocyte predominance, nodular sclerosing, and mixed cellularity Hodgkin's disease, characterized by a minor degree of architectural effacement. They occurred at the periphery of lymphoid aggregates which mimic the composite nodule of the reactive lymph node and which contained Reed-Sternberg cells and their variants. Despite some immunophenotypic similarities, no further arguments were found to support a relationship between plasmacytoid monocytes and Reed-Sternberg cells. We conclude that plasmacytoid monocytes represent one of the monocyte-derived cells that contribute to the cellular reaction in Hodgkin's disease.

show abstract

Section: Introductionmentioning

confidence: 99%

Plasmacytoid monocytes (so‐called plasmacytoid T cells) in Hodgkin's disease

Facchetti

Wolf‐Peeters

Desmet

1989

The Journal of Pathology

View full text Add to dashboard Cite

show abstract

“…8,9 Based on these observations, it has been speculated that HRS cells might represent cell fusions. [10][11][12][13] For example, the coexpression of B and dendritic cell markers was taken as an indication that these cells derive from a fusion of a B lymphocyte with a dendritic cell. To clarify this matter, we analyzed single HRS cells from 5 cases of HD with 2 rearranged IgH alleles for the presence of additional IgH alleles in germline configuration as a footprint for a fusion of a B cell with a non-B cell.…”

mentioning

confidence: 99%

Evidence that Hodgkin and Reed-Sternberg cells in Hodgkin disease do not represent cell fusions

Küppers

Bräuninger

Müschen

et al. 2001

Blood

View full text Add to dashboard Cite

IntroductionIn most cases of classical Hodgkin disease (HD), Hodgkin and Reed-Sternberg (HRS) cells carry clonal immunoglobulin (Ig) gene rearrangements and thus derive from B cells. 1 Specifically, the pattern of somatic mutations in the rearranged Ig genes indicates that these cells represent transformed preapoptotic germinal center B cells. 1,2 In rare cases, HRS cells derive from T cells. 3,4 However, the morphology and immunophenotype of HRS cells is untypical for B and also T cells. HRS cells lack expression of most B-cell markers, 5,6 and molecules typical for other lineages are regularly expressed by these cells. 5,7 Another typical feature of HRS cells is their abnormal karyotype. Numerical chromosomal abnormalities with additional copies of several chromosomes are not only observed in the multinucleated Reed-Sternberg cells but also in the mononuclear Hodgkin cells. 8,9 Based on these observations, it has been speculated that HRS cells might represent cell fusions. [10][11][12][13] For example, the coexpression of B and dendritic cell markers was taken as an indication that these cells derive from a fusion of a B lymphocyte with a dendritic cell. To clarify this matter, we analyzed single HRS cells from 5 cases of HD with 2 rearranged IgH alleles for the presence of additional IgH alleles in germline configuration as a footprint for a fusion of a B cell with a non-B cell. Likewise, one case of T-cell-derived HD with 2 rearranged T-cell receptor (TCR)␤ loci was analyzed for additional TCR␤ germline alleles. Study design Patients and tissuesThe 6 cases investigated here were previously analyzed for Ig and/or TCR␤ V gene rearrangements (Table 1). They were selected from a collection of 26 cases of HD analyzed by us. Two V H region genes had been amplified from 5 of the cases, and 1 case analyzed for D H J H joints harbored such a joint besides a V H D H J H joint. Micromanipulation and single-cell PCRSingle HRS cells were micromanipulated from immunostained frozen tissue sections. 2,14 Before gene-specific polymerase chain reaction (PCR) was carried out, genomic DNA of single cells was preamplified with a random 15-mer primer. 15 IgH and TCR␤ VDJ and DJ gene rearrangements and fragments specific for germline configuration of IgH and TCR␤ loci were amplified by seminested PCR and sequenced ( Figure 1). 2,3,16 To rule out that germline polymorphisms at the binding sites for the IgH germlinespecific PCR primers (D H 7-27 and J H 1) hamper amplification of germline fragments, fragments covering these sites were amplified from whole-tissue DNA of cases 2 to 5 (not shown). No polymorphisms were detected at the primer binding sites. In cases 2, 3, and 5, successful amplification of both IgH alleles was confirmed by a polymorphism near the D H 7-27 gene. For patient 1, single micromanipulated T cells of the tumor tissue and, for patient 6, micromanipulated B cells were used for control amplification of germline-specific IgH or TCR␤ fragments. For case 1, IgH germlinespecific amplificates were obtained from 6 of 1...

show abstract

“…Recent studies at the cellular level confirm that HD is a lymphoid neoplasm and investigations at the molecular level suggest that different immunoglobulin gene rearrangements may be linked to the subclasses of HD (Stein et al, 1986;Griesser et al, 1987). The origin of the Reed-Sternberg cell, which distinguishes HD from other lymphomas, remains a controversial issue (Bucsky, 1987, Drexler & Leber, 1988 and cytogenetic studies have so far failed to characterise further this tumour (Kristoffersson et al, 1987;Cabanillas, 1988). Currently no consistent available evidence suggests that the basic Rye classification should be modified.…”

mentioning

confidence: 99%

A specialist leukaemia/lymphoma registry in the UK. Part 1: incidence and geographical distribution of Hodgkin's disease

McKinney

Alexander²,

Ricketts³

et al. 1989

Br J Cancer

View full text Add to dashboard Cite

Summary This paper describes the epidemiology of Hodgkin's disease occurring in parts of the United Kingdom between 1984 and 1986. The cases were carefully diagnosed and the data rigorously cross-checked as part of the larger Leukaemia Research Fund Data Collection Survey of all lymphoid and haematogenous malignancies. The age-specific rates show the lack of an older adult second peak. Spatial variation is examined in some detail. At county and district levels there is little heterogeneity in the distribution of cases. However, at the electoral ward level there were real differences for the younger age group (0-34).

show abstract

Hodgkin's disease: The sternberg-reed cell

Cited by 17 publications

References 48 publications

Plasmacytoid monocytes (so‐called plasmacytoid T cells) in Hodgkin's disease

Plasmacytoid monocytes (so‐called plasmacytoid T cells) in Hodgkin's disease

Evidence that Hodgkin and Reed-Sternberg cells in Hodgkin disease do not represent cell fusions

A specialist leukaemia/lymphoma registry in the UK. Part 1: incidence and geographical distribution of Hodgkin's disease

Contact Info

Product

Resources

About