Journal Article

DKFZ-2019-00185

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Oncogene-induced senescence: a potential breakpoint mechanism against malignant transformation in plasma cell disorders.

Lehners, N. (First author)DKFZ* ; Ellert, E. ; Xu, J.DKFZ* ; Hillengass, J. ; Leichsenring, J. ; Stenzinger, A. ; Goldschmidt, H. ; Andrulis, M. ; Raab, M.-S. (Last author)DKFZ*

2018
Taylor & Francis Group London [u.a.]

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Please use a persistent id in citations: doi:10.1080/10428194.2018.1443450

Abstract: Oncogene-induced senescence (OIS) is a cellular tumor-suppressive mechanism present in several premalignant conditions. Here, we analyze the possible impact of OIS on malignant transformation in plasma cell disorders. Tumor samples from 125 patients with different disease stages were analyzed immunohistochemically for expression of senescence markers. Protein expression of cyclin-dependent kinase inhibitor p21Cip1/Waf1 was significantly higher in smoldering multiple myeloma (SMM) compared to monoclonal gammopathy of undetermined significance (MGUS) (p = .02) or symptomatic multiple myeloma (MM) (p = .005). SMM plasma cells expressing p21Cip1/Waf1 were negative for Ki67, consistent with senescence. While p27Kip1 was highly expressed in healthy controls, MGUS and SMM, expression decreased significantly in MM (p = .02). SMM plasma cells displayed a mutually exclusive expression of p21Cip1/Waf1/p27Kip1 suggesting compensatory mechanisms of senescence. In conclusion, we found markers of cellular senescence differentially expressed in SMM compared to MGUS and MM supporting the hypothesis of OIS as a breakpoint mechanism against malignant transformation in plasma cell disorders.

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Contributing Institute(s):

1. Experimentelle Therapien hämatologischer Neoplasien (G170)

Research Program(s):

1. 317 - Translational cancer research (POF3-317) (POF3-317)

Appears in the scientific report 2018

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Database coverage:
; Clarivate Analytics Master Journal List ; Current Contents - Clinical Medicine ; Current Contents - Life Sciences ; Ebsco Academic Search ; IF < 5 ; JCR ; NCBI Molecular Biology Database ; Nationallizenz ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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