Primary lymphoma of the nose including a relationship to lethal midline granuloma

Eichel, Berkley S.; Harrison, Edgar G.; Devine, Kenneth D.; Scanlon, Paul W.; Brown, Henry A.

doi:10.1016/0002-9610(66)90328-x

Cited by 187 publications

(69 citation statements)

References 10 publications

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“…Pathological characteristics of 42 nasal lymphomas, ie, varying degrees of necrotic change in the upper respiratory tract, and the polymorphous pattern of proliferation were identical with those in LMG of PR type (Eichel et al, 1966;Kassel et al, 1969), which is now classified as an NK/T-or NK-cell lymphoma (Jaffe et al, 1996). Indeed immunohistochemical findings of the present 42 cases were in agreement with those of NK/T-or NK-cell lymphoma, ie, TIA-1 ϩ , CD56 ϩ , CD3 ϩ , or CD43 ϩ .…”

Section: Discussionmentioning

confidence: 74%

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Mutations of the p53 Gene in Nasal NK/T-Cell Lymphoma

Hongyo

Syaifudin

et al. 2000

Laboratory Investigation

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SUMMARY:Mutations of the p53 tumor suppressor gene are reported in various kinds of malignancies including lymphomas.However, p53 gene mutations in nasal NK/T-cell lymphoma have not been reported because most parts of tumors are necrotic and a small amount of living tumor tissues is available for the molecular study. Expression and mutations of the p53 gene were examined in the paraffin-embedded specimens of the nasal lesions from 42 Chinese (Beijing and Chengdu) and Japanese (Okinawa and Osaka) patients with nasal NK/T-cell lymphoma by the immunohistochemistry and single strand conformation polymorphism (SSCP) analysis of polymerase chain reaction (PCR) amplified products followed by direct sequencing. Thirty single-nucleotide substitution mutations were observed in 20 of 42 cases (47.6%). Among the 30 mutations, 18 were missense (mainly G:C to A:T transitions), 9 were silent, and 1 was a nonsense mutation. The remaining 2 mutations involved intron 5 and exon 5 terminal points. Abnormal expression of the p53 protein was also observed in 19 of 42 (45.2%) cases. The incidence was significantly (4-fold) higher in the cases of Osaka than those in other areas, although the incidence of p53 mutations in the cases of Osaka was one-half to one-third of those in the other three areas. The results may suggest some racial, environmental, or lifestyle differences in the cause of nasal tumorigenesis. (Lab Invest 2000, 80:493-499).

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Section: Discussionmentioning

confidence: 74%

“…Thus the term polymorphic reticulosis (PR) was proposed for this condition (Eichel et al, 1966). PR constitutes lethal midline granuloma (LMG), which is characterized by necrotic and granulomatous lesions mainly affecting the nasal cavity.…”

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confidence: 99%

Mutations of the p53 Gene in Nasal NK/T-Cell Lymphoma

Hongyo

Syaifudin

et al. 2000

Laboratory Investigation

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“…This condition is reflected by the plethora of synonyms used for the disorders, such as polymorphous reticulosis, lethal midline granuloma (Eichel et al, 1966;Ratech et al, 1989) and angiocentric immunoproliferative lesion (Lipford et al, 1988;Peiper, 1993). Recent studies have suggested that most of these cases are related to malignant T-cell disorders Kanavaros et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Clonal chromosomal abnormalities as direct evidence for clonality in nasal T/natural killer cell lymphomas

Tien¹,

Su²,

Tang³

et al. 1997

Br J Haematol

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Nasal T/natural killer (NK) cell lymphoma is a distinct clinicopathologic entity which is more prevalent in Asia than in America and Europe. The clonal nature of the infiltrating lymphoid cells is difficult to demonstrate because of the lack of immunologic markers for clonality and the absence of clonal T‐cell receptor gene rearrangement in most cases. In this study, clonal chromosomal abnormalities were detected in the tumour cells from four patients with nasal T/NK cell lymphoma. This finding provided direct evidence for clonality of the disease. Moreover, nonrandom cytogenetic abnormalities, including isochromosome for the short arm (p) of chromosome 6, isochromosome for the long arm (q) of chromosome 1, partial deletion of 6q, and aberrations at 11q, were disclosed. Isochromosome 6p was the sole structural abnormality in one patient, which may be a pathognomonic change in nasal lymphoma.

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“…Clinically, this lymphoma is characterized by progressive necrotic lesions mainly in the nasal cavity and a poor prognosis resulting from rapid progression of the lesion and distinct organs (2,7,8). Histologically, the features of this lymphoma include angiocentric and polymorphous lymphoreticular infiltrates, which are called polymorphic reticulosis (9,10). Original cells of the lymphoma are reported to be of the NK or γδT cell lineages, both of which express the NK cell marker CD56 (2,5,6,11).…”

mentioning

confidence: 99%

Production of Interferon-Inducible Protein-10 and Its Role as an Autocrine Invasion Factor in Nasal Natural Killer/T-Cell Lymphoma Cells

Moriai

Takahara

Ogino

et al. 2009

Clinical Cancer Research

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Purpose: Nasal natural killer (NK)/T-cell lymphoma is associated with Epstein-Barr virus and has poor prognosis because of local invasion and/or multiple dissemination. Recently, the role of chemokines/chemokine receptors in tumor proliferation and invasion has been shown. In this study, we examined whether the specific chemokines were related to the tumor behaviors in nasal NK/T-cell lymphoma. Experimental Design: A chemokine protein array was used to examine specific chemokines produced by SNK-6 and SNT-8 (Epstein-Barr virus-positive nasal NK/T-cell lymphoma lines). The expression of interferon γ-inducible protein 10 (IP-10) and the IP-10 receptor CXCR3 was investigated by ELISA and flow cytometry. Cell growth and invasion were assessed by the MTT and Matrigel invasion assays, respectively. Immunohistologic staining and ELISA were used to examine IP-10 expression in biopsies and sera from patients, respectively. Results: IP-10 was specifically produced by SNK-6 and SNT-8. Moreover, CXCR3 was expressed on the NK cell lines. Functionally, IP-10 did not affect cell proliferation but enhanced cell invasion. In biopsy samples, IP-10 and CXCR3 expressions were detected in the lymphoma cells. Serum IP-10 levels in the patients were much higher than those of healthy controls and the levels were decreased during the complete remission phase after treatments. Conclusions: These results suggest that IP-10 may play an important role in cell invasion in nasal NK/T-cell lymphoma through an autocrine mechanism. (Clin Cancer Res 2009;15(22):6771-9)

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Primary lymphoma of the nose including a relationship to lethal midline granuloma

Cited by 187 publications

References 10 publications

Mutations of the p53 Gene in Nasal NK/T-Cell Lymphoma

Mutations of the p53 Gene in Nasal NK/T-Cell Lymphoma

Clonal chromosomal abnormalities as direct evidence for clonality in nasal T/natural killer cell lymphomas

Production of Interferon-Inducible Protein-10 and Its Role as an Autocrine Invasion Factor in Nasal Natural Killer/T-Cell Lymphoma Cells

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