Genetic analysis of sorted Hodgkin and Reed-Sternberg cells using comparative genomic hybridization

Ohshima, Koichi; Ishiguro, Masako; Ohgami, Akiko; Sugihara, Midori; Haraoka, Seiji; Suzumiya, Junji; Kikuchi, Masahiro

doi:10.1002/(sici)1097-0215(19990719)82:2<250::aid-ijc16>3.3.co;2-c

Cited by 8 publications

(17 citation statements)

References 15 publications

(24 reference statements)

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“…6,15,16 The lymph nodes were fixed in buffered formalin and embedded in paraffin. Lymphocyte predominance (LP) and lymphocyte depletion (LD) subtypes were excluded from the present study.…”

Section: Methodsmentioning

confidence: 87%

“…In addition, the cases with LOH showed one or more clonal LOH, in which the signal of the second allele of H&RS cells was completely absent. 6 In the present study, LOH of 16q, especially 16q21-23, seemed to be a common phenomenon in H&RS cells. At present, development of human tumor is thought to occur through accumulation of genetic changes within a cell lineage.…”

Section: Analysis Of Chromosome 16mentioning

confidence: 99%

“…Cytogenetic analysis of HD is considered to be difficult, because H&RS cells are few in number and have a low mitotic rate. 6 To confirm that the lymphocytes in the background were reactive, we performed CGH with B cells and T cells. [1][2][3] Comparative genomic hybridization (CGH) is a recently developed molecular cytogenetic method that allows, in a single experiment, the detection of genetic imbalances in tumors and their mapping on normal reference metaphase spreads.…”

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confidence: 99%

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Chromosome 16q deletion and loss of E-cadherin expression in Hodgkin and Reed-Sternberg cells

et al. 2001

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Hodgkin and Reed‐Sternberg (H&RS) cells are generally considered to be the neoplastic cells of Hodgkin's disease (HD); however, such H&RS cells are a few in number due to the numerous reactive cells. Very few data have so far been published on the cytogenetic abnormalities in HD. We have previously used the analysis of comparative genomic hybridization (CGH), employing sorted H&RS cells. The most commonly observed genetic aberrations were a loss on 16q11/21, a gain on 1p13 and a gain on 7q35/36. To confirm the loss of 16q, we analyzed the loss of heterozygosity (LOH) using the regions D16S3075 (16p13), D16S3068 (16q11), D16S3136 (16q12), D16S503 (16q13), D16S515 (16q21), D16S3091 (16q23) and D16S520 (16q24). A total of 100 sorted H&RS cells were compared with a similar number of sorted reactive T cells in 15 cases with HD, including 5 cases with nodular sclerosis (NS) type and 10 cases with mixed cellularity (MC) type. LOHs of 16q, especially 16q21‐23, were frequently detected, but 16p deletions were infrequent. Analysis of 16q21 showed LOH in 12 of 15 cases with HD (80%), including 9 cases with MC type (90%) and 3 cases with NS type (60%). 16q23 showed LOH in 9 of 15 cases with HD (60%), including 5 cases with MC type (50%) and 4 cases with NS (80%). On the other hand, 16p13 showed LOH in 3 of 15 cases with HD (20%). Immunohistochemical staining showed that H&RS cells rarely expressed E‐cadherin, which is located on 16q. Our findings suggest that 16q deletion, especially 16q21‐23, is probably involved in H&RS giant cell formation and tumorigenesis. © 2001 Wiley‐Liss, Inc.

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“…6,15,16 The lymph nodes were fixed in buffered formalin and embedded in paraffin. Lymphocyte predominance (LP) and lymphocyte depletion (LD) subtypes were excluded from the present study.…”

Section: Methodsmentioning

confidence: 87%

Section: Analysis Of Chromosome 16mentioning

confidence: 99%

mentioning

confidence: 99%

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Chromosome 16q deletion and loss of E-cadherin expression in Hodgkin and Reed-Sternberg cells

et al. 2001

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“…Malpighi alluded to this entity in 1666, but the disease's eponym honors the English physician who first described the clinical presentation, gross anatomy, mode of spread, and propensity for splenic involvement that are characteristic of this disease. 204 Studies have clearly demonstrated that the neoplastic cells of Hodgkin's lymphoma are clonally derived from germinal center B cells that have lost the capacity to express immunoglobulin. Cytogenetic studies clearly established the neoplastic nature of Hodgkin's lymphoma.…”

Section: Hodgkin's Lymphomamentioning

confidence: 99%

Lymph Nodes

Chang¹,

Arber²,

Weiss³

2009

Modern Surgical Pathology

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“…Microdissection of HRSC enables the use of genomic techniques, such as comparative genomic hybridisation (CGH), by providing an enriched population of tumour cells. Multiple chromosomal imbalances in tumour biopsies (Ohshima et al , ; Hartmann et al , ) and HRSC cell lines (Joos et al , ) have been reported. In summary, HRSC harbour tremendous cytogenetic complexity with frequent, reoccurring chromosomal imbalances affecting multiple oncogenic pathways (Borchmann & Engert, ).…”

Section: The Genomic Landscapementioning

confidence: 99%

The translational science of hodgkin lymphoma

et al. 2018

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Summary Hodgkin Lymphoma (HL) is an unusual B‐cell lymphoma because the malignant cells exist as a minority population in a densely cellular microenvironment. The microenvironment is comprised predominately of inflammatory and immune cells with fibrosis in some cases. There are multiple dysregulated signalling pathways that sustain HL within this microenvironment, such as the Nuclear factor‐κB and Janus kinase/signal transducers and activators of transcription pathways. Advances in genomic medicine have enabled a better characterisation of the rare tumour cells and improved our understanding of the signalling mechanisms that exist between the malignant cell and its microenvironment. Current therapy for HL produces excellent clinical outcomes in most younger patients. However, problems with current treatment approaches include poorer outcomes in the elderly, toxicity of highly‐effective combination chemotherapy regimens and relapse in high‐risk patients. Better understanding of disease biology aids in upfront prognostication of patients, defines new methods for treatment monitoring and assists in the recognition of novel targets for therapy. Biology‐driven therapies, including anti‐CD30 antibody conjugates, cellular immunotherapies and immune modulation, particularly with checkpoint inhibitors, have changed treatment algorithms for relapsed/refractory patients. Future challenges exist in incorporating immune‐based therapies earlier in treatment algorithms to reduce toxicity and prevent relapse for patients with HL.

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Genetic analysis of sorted Hodgkin and Reed-Sternberg cells using comparative genomic hybridization

Cited by 8 publications

References 15 publications

Chromosome 16q deletion and loss of E-cadherin expression in Hodgkin and Reed-Sternberg cells

Chromosome 16q deletion and loss of E-cadherin expression in Hodgkin and Reed-Sternberg cells

Lymph Nodes

The translational science of hodgkin lymphoma

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