Expression of multidrug resistance 1 gene in B‐cell lymphomas: association with follicular dendritic cells. Issue 3 (22nd January 2013)

• Record Type: Journal Article
• Authors: Yagi, Keiko; Yamamoto, Kouhei; Umeda, Shigeaki; Abe, Shinya; Suzuki, Shiho; Onishi, Iichiroh; Kirimura, Susumu; Fukayama, Masashi; Arai, Ayako; Kitagawa, Masanobu; Kurata, Morito
• Is Part Of: Histopathology. Volume 62:Issue 3(2013)
• Page Start: 414
• Page End: 420
• Publication Date: 2013-01-22
• Subjects: Histology, Pathological -- Periodicals; 611.018
• DOI: 10.1111/his.12035
• Languages: English
• ISSNs: 0309-0167

Abstract

<abstract abstract-type="main" xml:lang="en"> <title> <x xml:space="preserve">Abstract</x> </title> <p> <bold>Aims: </bold> Multidrug resistance (MDR) in B‐cell lymphomas still constitutes a major obstacle to the effectiveness of chemotherapy even in the anti‐CD20 antibody therapy era. The aim of this study was to investigate the expression of MDR‐associated molecules in reactive lymphadenopathy (RL), follicular lymphoma (FL), and diffuse large B‐cell lymphoma (DLBCL).</p> <p> <bold>Methods and results: </bold> The expression of mRNA for ABC‐transporter family genes was determined by real‐time RT‐PCR in lymph nodes from RL, FL, and DLBCL cases. <italic>MDR1</italic> exhibited significantly stronger expression in RL, FL, and DLBCL than Raji B‐cell lymphoma cells. RL and FL showed significantly higher expression than DLBCL. Immunohistochemically, MDR1 positive cells were localized in the germinal centers of RL and center of the nodular lesions of FL showing associations with CD21 positive follicular dendritic cells (FDCs). Raji cells were co‐cultured with FDC sarcoma‐derived cells and the expression of <italic>MDR1</italic> and drug resistance were analyzed. The co‐culture of Raji cells with FDCs induced strong expression of <italic>MDR1</italic> and introduced resistance to doxorubicin‐induced apoptosis.</p> <p> <bold>Conclusions: </bold> These results suggest that FDCs induce <italic>MDR1</italic> expression in reactive as well as neoplastic B‐cells. Inhibition of the interaction of FDCs with B‐cells may provide a novel strategy for treating the chemotherapy resistant fraction.</p> </abstract>