Sinus histiocytosis with massive lymphadenopathy: evidence for its relationship to macrophages and for a cytokine‐related disorder

Middel, Peter; Hemmerlein, Bernhard; Fayyazi, Afshin; Kaboth, U; Hj, Radzun

doi:10.1046/j.1365-2559.1999.00746.x

Cited by 92 publications

(70 citation statements)

References 34 publications

(30 reference statements)

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“…Interestingly, that study also found mean variant allele frequencies at levels similar to our study, including a KRAS G12D missense variant in RDD. These very recent findings, in addition to our own, challenge the historical notion that RDD is a purely non-clonal, reactive process [1,3,4]. This case is, to the best of our knowledge, the first report of a KRAS K117N missense variant in RDD.…”

Section: Discussionsupporting

confidence: 64%

“…Historically, RDD is considered non-clonal and reactive [3,4]. However, RDD lesions have been reported to undergo malignant transformation to histiocytic sarcoma [25,26] and high-grade lymphoma [27] indicating their potential for genomic instability.…”

Section: Discussionmentioning

confidence: 99%

“…RDD or sinus histiocytosis with massive lymphadenopathy (SHML) is a rare histiocytic proliferation that is generally considered to be reactive with a benign clinical course [1,3,4]. It typically presents with bilateral cervical lymphadenopathy although extranodal presentations are common (40 % of cases) [1].…”

Section: Introductionmentioning

confidence: 99%

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Rosai–Dorfman Disease Harboring an Activating KRAS K117N Missense Mutation

Shanmugam

Margolskee

Kluk

et al. 2016

Head and Neck Pathol

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Rosai-Dorfman disease (RDD) or sinus histiocytosis with massive lymphadenopathy is a rare histiocytic proliferation that is generally considered to be reactive with a benign clinical course. The etiology of RDD is very poorly understood. Recent studies have shown frequent BRAF, NRAS, KRAS, and PIK3CA activating mutations in several histiocytic neoplasms highlighting the emerging importance of the RAF/MEK/ERK pathway in the pathogenesis of these diseases. Here we report a case of Rosai-Dorfman disease involving the submandibular salivary gland with a KRAS K117N missense mutation discovered by next-generation sequencing. These results suggest that at least a subset of RDD cases may be clonal processes. Further mutational studies on this rare histiocytic disease should be undertaken to better characterize its pathogenesis as well as open up potential avenues for therapy.

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Section: Discussionsupporting

confidence: 64%

Section: Discussionmentioning

confidence: 99%

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Rosai–Dorfman Disease Harboring an Activating KRAS K117N Missense Mutation

Shanmugam

Margolskee

Kluk

et al. 2016

Head and Neck Pathol

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“…Furthermore, its expression by macrophages has been documented in various diseases such as Rosai-Dorfman disease (25), multibacillary leprosy (26), and HIV infection (27,28). In all of these conditions, this apparently aberrant expression was demonstrated to be associated with down-or upregulation of other markers, thereby suggesting functional alterations that are probably related to the underlying immune or infectious disorder (25)(26)(27)(28).…”

Section: Discussionmentioning

confidence: 99%

“…Although the DC origin of MGCs is an attractive supposition, given the lack of specificity of both S-100 protein and fascin, because they are also expressed by macrophages or other cell types (23)(24)(25)(26)(27)(28)38), we think that assessing the DC lineage by merely studying these markers is insufficient to validate such a hypothesis. Whatever their precise ontogeny, the detection of these very characteristic cells in hyperplastic lymphatic tissues of the WR at least has the merit of alerting the pathologist to the possibility of an underlying HIV infection.…”

Section: Discussionmentioning

confidence: 99%

HIV-Associated Multinucleated Giant Cells in Lymphoid Tissue of the Waldeyer's Ring: A Detailed Study

et al. 2000

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Hyperplastic lymphoid tissues of the Waldeyer's ring in human immunodeficiency virus (HIV)-infected patients may occasionally contain multinucleated giant cells (MGCs). These cells, which are unrelated to any opportunistic infection, previously have been demonstrated to harbor significant amounts of HIV. Studies undertaken to characterize these MGCs have generated conflicting results: some reports suggested a macrophage origin, whereas others supported a dendritic cell lineage. This study was performed to determine the occurrence of MGCs in a series of adenoid/tonsil specimens from HIV-seropositive patients showing no histological evidence of opportunistic infection in order to further characterize the phenotype of these cells and to investigate the role of a viral infection in their pathogenesis. Adenoid/tonsil tissue specimens from 21 HIV-seropositive patients with no documented opportunistic infection were scrutinized for the presence of MGCs and evaluated immunohistochemically on paraffin sections by antibodies directed against various macrophage and DC antigens. These antigens included CD68, the macrophage marker 3A5, major histocompatibility complex Class II, S-100 protein, CD1a, and CD83. Additional immunostainings directed at CD21 and CD35 as well as at the HIV-associated p24 antigen were also performed. Finally, the presence of Epstein-Barr virus and human herpesvirus 8 viral sequences was investigated by in situ hybridization and by polymerase chain reaction analysis, respectively. MGCs were found in 14 patients (66.7%), regardless of gender, age, method of viral transmission, CD4 cell count, viral load, or ethnic group. These cells were mostly localized at the lymphoepithelium layer of the tonsillar crypts and, to a lesser extent, in the interfollicular areas of the underlying lymphoid tissue, which consistently exhibited features of follicular hyperplasia. Phenotypically, MGCs were found to be CD68 ؉ , 3A5 ؉ , major histocompatibility complex Class II ؉ , S-100 protein ؉/؊ , CD1a ؊ , CD21 ؊ , CD35 ؊ , and CD83 ؊ . Although the HIV-associated p24 protein was consistently present in the cytoplasm of these cells, no sign of Epstein-Barr virus or human herpesvirus 8 infection could be demonstrated. Consequently, our study didn't show any conclusive evidence to support that MGCs in hyperplastic lymphoid tissues of the Waldeyer's ring from HIV-seropositive patients originated from dendritic cells. The definite nature of these cells has yet to be elucidated, but it is plausible that they simply represent activated macrophages that are infected with HIV present in the oropharyngeal secretions during the circulation of their precursor through the lymphoepithelium area of adenoids and tonsils.

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A Case of Cutaneous Rosai-Dorfman Disease Refractory to Imatinib Therapy

Gebhardt

Averbeck²,

Paasch³

et al. 2009

Arch Dermatol

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Background: Rosai-Dorfman disease is a non-Langerhans cell histiocytosis that recently has been treated successfully with imatinib mesylate in a patient with a systemic variant of the disease. Observations: We describe a 69-year-old man with cutaneous Rosai-Dorfman disease manifesting as progressive, deeply infiltrated skin lesions. Histopathologic examination of the lesions demonstrated dense dermal infiltrate positive for CD68, stabilin-1, and S-100, but not for CD1a. The histiocytes were positive for plateletderived growth factor receptor ␣, the target molecule for imatinib. During the 5-year course of the disease, multiple therapeutic approaches (tuberculostatic drugs, topical and systemic glucocorticoids, thalidomide, isotreti

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Sinus histiocytosis with massive lymphadenopathy: evidence for its relationship to macrophages and for a cytokine‐related disorder

Cited by 92 publications

References 34 publications

Rosai–Dorfman Disease Harboring an Activating KRAS K117N Missense Mutation

Rosai–Dorfman Disease Harboring an Activating KRAS K117N Missense Mutation

HIV-Associated Multinucleated Giant Cells in Lymphoid Tissue of the Waldeyer's Ring: A Detailed Study

A Case of Cutaneous Rosai-Dorfman Disease Refractory to Imatinib Therapy

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