PATHOLOGY & ONCOLOGY RESEARCHVol. 3 No. 2, 1997

 Article

Regulation of Differentiation, Proliferation and Drug-Induced Apoptosis in HT58 Lymphoma Cells

Rudolf MIHALIK1, Ferenc UHER2, István PETÁK1, Anna SEBESTYÉN1, László KOPPER1

11st Institute of Pathology and Experimental Cancer Research, Semmelweis University Medicine, Budapest, Hungary
2National Institute of Hematology and Immunology, Budapest, Hungary

 

Recently, it has been suggested, that differentiated cells are more resistant to the apoptotic effect of DNA damaging agents possibly due to the decreased activity of ''damage detecting / apoptosis triggering'' mechanism. Previously, we have shown, that PMA pretreatment reduced etoposide- (ETO) but enhanced staurosporine- (STA) -induced apoptosis in HT58 cells. Data presented here show that the HT58 human, ''mature'' B-lymphoma cells exposed to PMA secrete more IgM into the supernatant indicating commitment of cells to perform differentiated function. The sensitivity of HT58 cells to ETO- or STA-induced apoptosis is influenced diversely with PMA pre- or posttreatment. Interestingly, the DNA damage (gamma radiation, bleomycin, ETO) or okadaic acic (30 nM) reduced the [PMA+STA] - induced apoptosis. Pathology & Oncology Research, Vol 3, Nr 2, 100-105, 1997

Key words: apoptosis; lymphoma; differentiation; etoposide; staurosporine; PMA


Received: Apr 22, 1997; accepted: Jun 12, 1997
Correspondence: László KOPPER, 1st Institute of Pathology and Experimental Cancer Research, Semmelweis University Medicine, Üllõi út 26. Budapest H-1085, Hungary; Tel: 36-1-1170891, Fax: 36-1-1170891; E-mail: kopper@korb1.sote.hu

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