Cytogenetic investigations in Hodgkin's disease: I. Involvement of specific chromosomes in marker formation

Fonatsch, Christa; Diehl, Volker; Schaadt, M.; Burrichter, H.; Kirchner, Hartmut

doi:10.1016/0165-4608(86)90106-8

Cited by 44 publications

(13 citation statements)

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“…An interesting new finding, however, was the remarkable overrepresentation of grains on a small, till then unidentified, marker chromosome. This marker XI, which had been interpreted before as being derived from a chromosome 21 (Fonatsch et al 1986) (Fig. 1), showed significant labeling with silver grains above the centromere region in XIp after ISH using the probe pmetH (33 of 372 grains, 8.9%) with a statistical probability of P < 0.0001 (Table 2, Fig.…”

Section: Resultsmentioning

confidence: 99%

“…L540 was established from bone marrow from a 20-yearold woman affected by Hodgkin's disease (clinical stage IVB) of the histological nodular sclerosing type. Morphology, growth behavior, cytochemical and immunological characteristics (Diehl et al 1981), and the karyotypic peculiarities of L540 ceUs have been thoroughly described (Fonatsch et al 1986) (Fig. 1).…”

Section: Cet/smentioning

confidence: 99%

“…Moreover, L540 cells showed expression of MET, an oncogene detected after transformation of a human osteosarcoma cell Offprint requests to: C. Fonatsch line (HOS) by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) (Cooper et al 1984). Interestingly, nucleolus organizer regions carrying genes for ribosomal RNA are involved in the formation of two marker chromosomes of L540 (Fonatsch et al 1986). …”

Section: Introductionmentioning

confidence: 99%

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Chromosomal in situ hybridization of a Hodgkin's disease-derived cell line (L540) using DNA probes for TCRA, TCRB, MET, and rRNA

et al. 1990

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The Hodgkin's lymphoma-derived cell line L540, which exhibits multiple marker chromosomes and a genotype characteristic of T-cell origin, showed expression of MET oncogene. L540 was studied by in situ hybridization for chromosomal rearrangements concerning the regions where genes for TCRA and TCRB chains, for MET oncogene, and for rRNA are located. All four genes were demonstrated to be involved in the formation of marker chromosomes. Especially remarkable was the participation of rDNA-bearing regions in two different translocations.

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Section: Resultsmentioning

confidence: 99%

Section: Cet/smentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Chromosomal in situ hybridization of a Hodgkin's disease-derived cell line (L540) using DNA probes for TCRA, TCRB, MET, and rRNA

et al. 1990

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“…No significant differences between the aberrations reported in recurrent as compared with untreated cases were found. The authors also noted that cell lines established from pleural effusions, or bone marrow and peripheral blood, from four patients with Hodgkin's disease by Fonatsch et al (1986) yielded a set of breakpoints that, with the exception of 14q32, were different from those observed in the 40 cases in which fresh tumor tissue was examined.…”

Section: Chromosome Banding Studiesmentioning

confidence: 99%

Cytogenetics of Hodgkin’s disease

Atkin

1998

Cytogenet Genome Res

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Cytogenetic studies over the past 35 years have made a major contribution towards the understanding of the nature of Hodgkin’s disease by demonstrating unequivocally the consistent presence of a clonal population of cells that have the cardinal features of malignancy e.g. more or less gross aneuploidy, frequently with complex chromosomal changes and showing considerable variation from case to case, thus comparable to the findings in carcinomas and other solid cancers. The mode is frequently in the triploid-tetraploid region, as we found in 17 of 27 cases studied in this laboratory by Feulgen microspectrophotometry, compared to only 10 cases with neardiploid modes. It is disappointing that no specific change, such as a translocation that could give a clue to the chromosomal location of a gene or genes involved in the etiology of Hodgkin’s disease, has yet been found. Nevertheless it is clear that a number of nonrandom changes, including several that are also common in other malignancies including the non-Hodgkin’s lymphomas, are frequently present, e.g., deletions of 1p, 6q, and 7q. Interestingly, deletions of 4q, with loss of 4q25→q27, that have also been reported may show some specificity for Hodgkin’s disease.

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“…The CD30 and CD30L genes have been mapped to the chromosome 1 short arm (lp36) and chromosome 9 long arm (9q33), respectively [33,106]. Structural abnormalities at microscopic level at lp36 have been detected in some HD, AML (M7), and in MDS [25,32,100]; the dysplastic or neoplastic cells in latter two types of diseases are usually CD30-.…”

Section: Expression Of Cd30 By H-rs Cells and Alcl Cellsmentioning

confidence: 99%

Hodgkin's Disease and Anaplastic Large Cell Lymphoma Revisited

Waldron¹,

Xie²,

Hsu³

et al. 1995

J Biomed Sci

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In cultures, and in tissues as well, Hodgkin’s and Reed-Stemberg (H-RS) cells and anaplastic large cell lymphoma (ALCL) cells are known to express a variety of cytokines, including IL-1, -5, -6, -8, -9, TNF-α, GM-CSF, M-CSF, TGF-β, CD70, CD80, and CD86. Various numbers of H-RS/ALCL cells may express cytokine receptors (R), such as CD30, CD40, IL-2R (CD25/CD122), IL-6R (CD 126), IL-7R (CD 127), TNF-R (CD 120), TGF-ß-R (CD105/endo- glin), M-CSF-R (CD115), and SCF-R (CD117/c-kit receptor). All of these cytokines and cytokine receptors are implicated in the growth regulation of H-RS/ALCL cells, the histopathologic alterations in tissues, and the clinical manifestations in patients with Hodgkin’s disease (HD) or ALCL. Many of these cytokines or cytokine receptors also play an important role in the pathogenesis of other types of lymphomas. In this review, we describe the cytokine or cytokine-receptor expression that is diacritic for H-RS/ALCL cells. The identification of such unique cytokine-cytokine receptor interactions is likely to explain the biologic property that distinguishes HD/ALCL from other types of lymphomas. These interactions include those of CD30L-CD30, CD40L- CD40, CD70-CD27, CD80/CD86-CD28, SCF-CD117, IL-9-IL9R, and IL-7- IL-7R. The H-RS/ALCL cells express IL-9 and two cytokine receptors, CD30 and CD 117, which are observed infrequently in NHLs. Although IL-7 expression is not restricted to H-RS/ALCL cells, the expression of IL-7 in conjunction with IL-9 and/or CD117 may be regarded as unique for HD/ALCL because of an unusual combination and a synergistic activity among these cytokines. The expression of CD70 and CD80/CD86 (as cytokines) may exert a unique effect in HD because of intimate contact between H-RS cells and CD27/CD28-positive T cells. The expression of these costimulators (CD70 and CD80/CD86) and other adhesion/constimulator molecules such as CD54 and CD58, along with the secretion of soluble cytokines such as IL-1, IL-6, IL-7, or TNFs by H-RS/ALCL cells, could result in the profound T-cell proliferation often seen in lymph nodes involved by HD and some ALCL. On the other hand, the expression of CD30L and CD40L by surrounding T cells may affect the proliferation of H-RS/ALCL cells. The cytokine-cytokine receptor interaction between H-RS cells and T cells via direct cell-cell contact is bidirectional, a situation not commonly seen in NHLs.

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Cytogenetic investigations in Hodgkin's disease: I. Involvement of specific chromosomes in marker formation

Cited by 44 publications

References 13 publications

Chromosomal in situ hybridization of a Hodgkin's disease-derived cell line (L540) using DNA probes for TCRA, TCRB, MET, and rRNA

Chromosomal in situ hybridization of a Hodgkin's disease-derived cell line (L540) using DNA probes for TCRA, TCRB, MET, and rRNA

Cytogenetics of Hodgkin’s disease

Hodgkin's Disease and Anaplastic Large Cell Lymphoma Revisited

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