Tissue eosinophilia correlates strongly with poor prognosis in nodular sclerosing Hodgkin's disease, allowing for known prognostic factors

被引:145
作者
von Wasielewski, R
Seth, S
Franklin, J
Fischer, R
Hübner, K
Hansmann, ML
Diehl, V
Georgii, A
机构
[1] Hannover Med Sch, Inst Pathol, D-30625 Hannover, Germany
[2] Univ Cologne, Innere Klin 1, D-5000 Cologne 41, Germany
[3] Goethe Univ Frankfurt, D-6000 Frankfurt, Germany
关键词
D O I
10.1182/blood.V95.4.1207.004k34_1207_1213
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Although eosinophilic granulocytes are frequently observed in lymphatic tissue of Hodgkin's patients, no substantial data reveal the prognostic role, if any, of tissue eosinophilia. Thus, eosinophilia was analyzed histologically in 1511 diagnostic biopsy specimens of patients treated under protocol therapy of the German Hodgkin's Lymphoma Study Group between 1988 and 1994. Prominent eosinophilia was seen in 38% of cases, which differed among the histologic types of Hodgkin's disease (HD): none in lymphocyte predominant, 14% in lymphocyte rich classical, 40% in nodular sclerosis grade 1 (NS-I), 55% in nodular sclerosis grade 2, 43% in mixed cellularity (MC), and 54% in lymphocyte depleted, In a multivariate analysis, tissue eosinophilia proved to be the strongest prognostic factor for freedom from treatment failure (P < .001) and overall survival (P < .001) in a stage-stratified model. Among NS-I patients, the effect was highly significant In MC, no significant effect of eosinophilia on survival could be demonstrated, Eosinophils secrete CD30 ligand that is capable of binding to CD30 positive HD cells, The activation of TRAF2, followed by NF-kappaB, which occurs on CD30L/CD30 binding, may explain the neo-plastic proliferation and apoptosis protection of HD cells. TRAF2 is also activated by EBV-LMP expression, which is detectable in the majority of MC but not NS cases, In addition to the possibility that eosinophils are only passive indicators for other unknown prognostic determinants, it may be concluded that the positive clinical outcome of eosinophilia-negative NS cases could be due to lower NF-kappaB activity. (Blood, 2000;95:1207-1213) (C) 2000 by The American Society of Hematology.
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页码:1207 / 1213
页数:7
相关论文
共 65 条
[41]   Gene expression by single Reed-Sternberg cells: Pathways of apoptosis and activation [J].
Messineo, C ;
Jamerson, MH ;
Hunter, E ;
Braziel, R ;
Bagg, A ;
Irving, SG ;
Cossman, J .
BLOOD, 1998, 91 (07) :2443-2451
[42]  
MIR R, 1993, CANCER-AM CANCER SOC, V71, P1857, DOI 10.1002/1097-0142(19930301)71:5<1857::AID-CNCR2820710524>3.0.CO
[43]  
2-B
[44]   THE EPSTEIN-BARR-VIRUS TRANSFORMING PROTEIN LMP1 ENGAGES SIGNALING PROTEINS FOR THE TUMOR-NECROSIS-FACTOR RECEPTOR FAMILY [J].
MOSIALOS, G ;
BIRKENBACH, M ;
YALAMANCHILI, R ;
VANARSDALE, T ;
WARE, C ;
KIEFF, E .
CELL, 1995, 80 (03) :389-399
[45]   Relationship between interleukin-5 and eotaxin in regulating blood and tissue eosinophilia in mice [J].
Mould, AW ;
Matthaei, KI ;
Young, IG ;
Foster, PS .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 99 (05) :1064-1071
[46]   Serum level of the soluble form of the CD30 molecule identifies patients with Hodgkin's disease at high risk of unfavorable outcome [J].
Nadali, G ;
Tavecchia, L ;
Zanolin, E ;
Bonfante, V ;
Viviani, S ;
Camerini, E ;
Musto, P ;
Di Renzo, N ;
Carotenuto, M ;
Chilosi, M ;
Krampera, M ;
Pizzolo, G .
BLOOD, 1998, 91 (08) :3011-3016
[47]   Transmigration of eosinophils through basement membrane components in vitro: Synergistic effects of platelet-activating factor and eosinophil-active cytokines [J].
Okada, S ;
Kita, H ;
George, TJ ;
Gleich, GJ ;
Leiferman, KM .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1997, 16 (04) :455-463
[48]   Eotaxin induces a rapid release of eosinophils and their progenitors from the bone marrow [J].
Palframan, RT ;
Collins, PD ;
Williams, TJ ;
Rankin, SM .
BLOOD, 1998, 91 (07) :2240-2248
[49]  
PASTRNAK A, 1984, NEOPLASMA, V31, P323
[50]   Human eosinophils express functional CD30 ligand and stimulate proliferation of a Hodgkin's disease cell line [J].
Pinto, A ;
Aldinucci, D ;
Gloghini, A ;
Zagonel, V ;
Degan, M ;
Improta, S ;
Juzbasic, S ;
Todesco, M ;
Perin, V ;
Gattei, V ;
Herrmann, F ;
Gruss, HJ ;
Carbone, A .
BLOOD, 1996, 88 (09) :3299-3305